2011 ACCF/AHA/SCAI Guideline for Percutaneous Coronary Intervention
Table of Contents
Preamble . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .e576
References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .e620
Appendix 1. Author Relationships With Industry and
Other Entities (Relevant) . . . . . . . . . . . . .e643
Appendix 2. Reviewer Relationships With Industry and Other Entities (Relevant) . . . . . . . . .e645
Appendix 3. Abbreviation List . . . . . . . . . . . . . . . . . .e648
Appendix 4. Additional Tables/Figures . . . . . . . . . . . .e649
The medical profession should play a central role in evaluating the evidence related to drugs, devices, and procedures for the detection, management, and prevention of disease. When properly applied, expert analysis of available data on the benefits and risks of these therapies and procedures can improve the quality of care, optimize patient outcomes, and favorably affect costs by focusing resources on the most effective strategies. An organized and directed approach to a thorough review of evidence has resulted in the production of clinical practice guidelines that assist physicians in selecting the best management strategy for an individual patient. Moreover, clinical practice guidelines can provide a foundation for other applications, such as performance measures, appropriate use criteria, and both quality improvement and clinical decision support tools.
The American College of Cardiology Foundation (ACCF) and the American Heart Association (AHA) have jointly produced guidelines in the area of cardiovascular disease since 1980. The ACCF/AHA Task Force on Practice Guidelines (Task Force), charged with developing, updating, and revising practice guidelines for cardiovascular diseases and procedures, directs and oversees this effort. Writing committees are charged with regularly reviewing and evaluating all available evidence to develop balanced, patient-centric recommendations for clinical practice.
Experts in the subject under consideration are selected by the ACCF and AHA to examine subject-specific data and write guidelines in partnership with representatives from other medical organizations and specialty groups. Writing committees are asked to perform a formal literature review; weigh the strength of evidence for or against particular tests, treatments, or procedures; and include estimates of expected outcomes where such data exist. Patient-specific modifiers, comorbidities, and issues of patient preference that may influence the choice of tests or therapies are considered. When available, information from studies on cost is considered, but data on efficacy and outcomes constitute the primary basis for the recommendations contained herein.
In analyzing the data and developing recommendations and supporting text, the writing committee uses evidence-based methodologies developed by the Task Force.1 The Class of Recommendation (COR) is an estimate of the size of the treatment effect considering risks versus benefits in addition to evidence and/or agreement that a given treatment or procedure is or is not useful/effective or in some situations may cause harm. The Level of Evidence (LOE) is an estimate of the certainty or precision of the treatment effect. The writing committee reviews and ranks evidence supporting each recommendation with the weight of evidence ranked as LOE A, B, or C according to specific definitions that are included in Table 1. Studies are identified as observational, retrospective, prospective, or randomized where appropriate. For certain conditions for which inadequate data are available, recommendations are based on expert consensus and clinical experience and are ranked as LOE C. When recommendations at LOE C are supported by historical clinical data, appropriate references (including clinical reviews) are cited if available. For issues for which sparse data are available, a survey of current practice among the clinicians on the writing committee is the basis for LOE C recommendations and no references are cited. The schema for COR and LOE is summarized in Table 1, which also provides suggested phrases for writing recommendations within each COR. A new addition to this methodology is separation of the Class III recommendations to delineate if the recommendation is determined to be of “no benefit” or is associated with “harm” to the patient. In addition, in view of the increasing number of comparative effectiveness studies, comparator verbs and suggested phrases for writing recommendations for the comparative effectiveness of one treatment or strategy versus another have been added for COR I and IIa, LOE A or B only.
In view of the advances in medical therapy across the spectrum of cardiovascular diseases, the Task Force has designated the term guideline-directed medical therapy (GDMT) to represent optimal medical therapy as defined by ACCF/AHA guideline recommended therapies (primarily Class I). This new term, GDMT, will be used herein and throughout all future guidelines.
Because the ACCF/AHA practice guidelines address patient populations (and healthcare providers) residing in North America, drugs that are not currently available in North America are discussed in the text without a specific COR. For studies performed in large numbers of subjects outside North America, each writing committee reviews the potential influence of different practice patterns and patient populations on the treatment effect and relevance to the ACCF/AHA target population to determine whether the findings should inform a specific recommendation.
The ACCF/AHA practice guidelines are intended to assist healthcare providers in clinical decision making by describing a range of generally acceptable approaches to the diagnosis, management, and prevention of specific diseases or conditions. The guidelines attempt to define practices that meet the needs of most patients in most circumstances. The ultimate judgment regarding care of a particular patient must be made by the healthcare provider and patient in light of all the circumstances presented by that patient. As a result, situations may arise for which deviations from these guidelines may be appropriate. Clinical decision making should involve consideration of the quality and availability of expertise in the area where care is provided. When these guidelines are used as the basis for regulatory or payer decisions, the goal should be improvement in quality of care. The Task Force recognizes that situations arise in which additional data are needed to inform patient care more effectively; these areas will be identified within each respective guideline when appropriate.
Prescribed courses of treatment in accordance with these recommendations are effective only if followed. Because lack of patient understanding and adherence may adversely affect outcomes, physicians and other healthcare providers should make every effort to engage the patient's active participation in prescribed medical regimens and lifestyles. In addition, patients should be informed of the risks, benefits, and alternatives to a particular treatment and be involved in shared decision making whenever feasible, particularly for COR IIa and IIb, where the benefit-to-risk ratio may be lower.
The Task Force makes every effort to avoid actual, potential, or perceived conflicts of interest that may arise as a result of industry relationships or personal interests among the members of the writing committee. All writing committee members and peer reviewers of the guideline are asked to disclose all such current relationships, as well as those existing 12 months previously. In December 2009, the ACCF and AHA implemented a new policy for relationships with industry and other entities (RWI) that requires the writing committee chair plus a minimum of 50% of the writing committee to have no relevant RWI (Appendix 1 for the ACCF/AHA definition of relevance). These statements are reviewed by the Task Force and all members during each conference call and/or meeting of the writing committee and are updated as changes occur. All guideline recommendations require a confidential vote by the writing committee and must be approved by a consensus of the voting members. Members are not permitted to write, and must recuse themselves from voting on, any recommendation or section to which their RWI apply. Members who recused themselves from voting are indicated in the list of writing committee members, and section recusals are noted in Appendix 1. Authors' and peer reviewers' RWI pertinent to this guideline are disclosed in Appendixes 1 and 2, respectively. Additionally, to ensure complete transparency, writing committee members' comprehensive disclosure information—including RWI not pertinent to this document—is available as an online supplement. Comprehensive disclosure information for the Task Force is also available online at www.cardiosource.org/ACC/About-ACC/Leadership/Guidelines-and-Documents-Task-Forces.aspx. The work of the writing committee was supported exclusively by the ACCF, AHA, and the Society for Cardiovascular Angiography and Interventions (SCAI) without commercial support. Writing committee members volunteered their time for this activity.
In an effort to maintain relevance at the point of care for practicing physicians, the Task Force continues to oversee an ongoing process improvement initiative. As a result, in response to pilot projects, several changes to these guidelines will be apparent, including limited narrative text, a focus on summary and evidence tables (with references linked to abstracts in PubMed) and more liberal use of summary recommendation tables (with references that support LOE) to serve as a quick reference.
In April 2011, the Institute of Medicine released 2 reports: Finding What Works in Health Care: Standards for Systematic Reviews and Clinical Practice Guidelines We Can Trust.2,3 It is noteworthy that the ACCF/AHA guidelines were cited as being compliant with many of the standards that were proposed. A thorough review of these reports and of our current methodology is under way, with further enhancements anticipated.
The recommendations in this guideline are considered current until they are superseded by a focused update or the full-text guideline is revised. Guidelines are official policy of both the ACCF and AHA.
1.1. Methodology and Evidence Review
The recommendations listed in this document are, whenever possible, evidence based. An extensive evidence review was conducted through November 2010, as well as selected other references through August 2011. Searches were limited to studies, reviews, and other evidence conducted in human subjects and that were published in English. Key search words included but were not limited to the following: ad hoc angioplasty, angioplasty, balloon angioplasty, clinical trial, coronary stenting, delayed angioplasty, meta-analysis, percutaneous transluminal coronary angioplasty, randomized controlled trial (RCT), percutaneous coronary intervention (PCI) and angina, angina reduction, antiplatelet therapy, bare-metal stents (BMS), cardiac rehabilitation, chronic stable angina, complication, coronary bifurcation lesion, coronary calcified lesion, coronary chronic total occlusion (CTO), coronary ostial lesions, coronary stent (BMS and drug-eluting stents [DES]; and BMS versus DES), diabetes, distal embolization, distal protection, elderly, ethics, late stent thrombosis, medical therapy, microembolization, mortality, multiple lesions, multi-vessel, myocardial infarction (MI), non–ST-elevation myocardial infarction (NSTEMI), no-reflow, optical coherence tomography, proton pump inhibitor (PPI), return to work, same-day angioplasty and/or stenting, slow flow, stable ischemic heart disease (SIHD), staged angioplasty, STEMI, survival, and unstable angina (UA). Additional searches cross-referenced these topics with the following subtopics: anticoagulant therapy, contrast nephropathy, PCI-related vascular complications, unprotected left main PCI, multivessel coronary artery disease (CAD), adjunctive percutaneous interventional devices, percutaneous hemodynamic support devices, and secondary prevention. Additionally, the committee reviewed documents related to the subject matter previously published by the ACCF and AHA. References selected and published in this document are representative and not all-inclusive.
To provide clinicians with a comprehensive set of data, whenever deemed appropriate or when published, the absolute risk difference and number needed to treat or harm will be provided in the guideline, along with confidence intervals (CIs) and data related to the relative treatment effects such as odds ratio (OR), relative risk, hazard ratio (HR), or incidence rate ratio. The focus of this guideline is the safe, appropriate, and efficacious performance of PCI. The risks of PCI must be balanced against the likelihood of improved survival, symptoms, or functional status. This is especially important in patients with SIHD.
1.2. Organization of the Writing Committee
The committee was composed of physicians with expertise in interventional cardiology, general cardiology, critical care cardiology, cardiothoracic surgery, clinical trials, and health services research. The committee included representatives from the ACCF, AHA, and SCAI.
1.3. Document Review and Approval
This document was reviewed by 2 official reviewers nominated by the ACCF, AHA, and SCAI, as well as 21 individual content reviewers (including members of the ACCF Interventional Scientific Council and ACCF Surgeons' Scientific Council). All information on reviewers' RWI was distributed to the writing committee and is published in this document (Appendix 2). This document was approved for publication by the governing bodies of the ACCF, AHA, and SCAI.
1.4. PCI Guidelines: History and Evolution
In 1982, a 2-page manuscript titled “Guidelines for the Performance of Percutaneous Transluminal Coronary Angioplasty” was published in Circulation.4 The document, which addressed the specific expertise and experience physicians should have to perform balloon angioplasty, as well as laboratory requirements and the need for surgical support, was written by an ad hoc group whose members included Andreas Grüntzig. In 1980, the ACC and the AHA established the Task Force on Assessment of Diagnostic and Therapeutic Cardiovascular Procedures, which was charged with the development of guidelines related to the role of new therapeutic approaches and of specific noninvasive and invasive procedures in the diagnosis and management of cardiovascular disease. The first ACC/AHA Task Force report on guidelines for coronary balloon angioplasty was published in 1988.5 The 18-page document discussed and made recommendations about lesion classification and success rates, indications for and contraindications to balloon angioplasty, institutional review of angioplasty procedures, ad hoc angioplasty after angiography, and on-site surgical backup. Further iterations of the guidelines were published in 1993,6 2001,7 and 2005.8 In 2007 and 2009, focused updates to the guideline were published to expeditiously address new study results and recent changes in the field of interventional cardiology.9,10 The 2009 focused update is notable in that there was direct collaboration between the writing committees for the STEMI guidelines and the PCI guidelines, resulting in a single publication of focused updates on STEMI and PCI.10
The evolution of the PCI guideline reflects the growth of knowledge in the field and parallels the many advances and innovations in the field of interventional cardiology, including primary PCI, BMS and DES, intravascular ultrasound (IVUS) and physiologic assessments of stenosis, and newer antiplatelet and anticoagulant therapies. The 2011 iteration of the guideline continues this process, addressing ethical aspects of PCI, vascular access considerations, CAD revascularization including hybrid revascularization, revascularization before noncardiac surgery, optical coherence tomography, advanced hemodynamic support devices, no-reflow therapies, and vascular closure devices. Most of this document is organized according to “patient flow,” consisting of preprocedural considerations, procedural considerations, and postprocedural considerations. In a major undertaking, the STEMI, PCI, and coronary artery bypass graft (CABG) surgery guidelines were written concurrently, with additional collaboration with the SIHD guideline writing committee, allowing greater collaboration between the different writing committees on topics such as PCI in STEMI and revascularization strategies in patients with CAD (including unprotected left main PCI, multivessel disease revascularization, and hybrid procedures).
In accordance with direction from the Task Force and feedback from readers, in this iteration of the guideline, the text has been shortened, with an emphasis on summary statements rather than detailed discussion of numerous individual trials. Online supplemental evidence and summary tables have been created to document the studies and data considered for new or changed guideline recommendations.
2. CAD Revascularization
Recommendations and text in this section are the result of extensive collaborative discussions between the PCI and CABG writing committees, as well as key members of the SIHD and UA/NSTEMI writing committees. Certain issues, such as older versus more contemporary studies, primary analyses versus subgroup analyses, and prospective versus post hoc analyses, have been carefully weighed in designating COR and LOE; they are addressed in the appropriate corresponding text. The goals of revascularization for patients with CAD are to 1) improve survival and/or 2) relieve symptoms.
Revascularization recommendations in this section are predominantly based on studies of patients with symptomatic SIHD and should be interpreted in this context. As discussed later in this section, recommendations on the type of revascularization are, in general, applicable to patients with UA/NSTEMI. In some cases (eg, unprotected left main CAD), specific recommendations are made for patients with UA/NSTEMI or STEMI.
Historically, most studies of revascularization have been based on and reported according to angiographic criteria. Most studies have defined a “significant” stenosis as ≥70% diameter narrowing; therefore, for revascularization decisions and recommendations in this section, a “significant” stenosis has been defined as ≥70% diameter narrowing (≥50% for left main CAD). Physiological criteria, such as an assessment of fractional flow reserve (FFR), has been used in deciding when revascularization is indicated. Thus, for recommendations about revascularization in this section, coronary stenoses with FFR ≤0.80 can also be considered to be “significant.”11,12
As noted, the revascularization recommendations have been formulated to address issues related to 1) improved survival and/or 2) improved symptoms. When one method of revascularization is preferred over the other for improved survival, this consideration, in general, takes precedence over improved symptoms. When discussing options for revascularization with the patient, he or she should understand when the procedure is being performed in an attempt to improve symptoms, survival, or both.
Although some results from the SYNTAX (Synergy between Percutaneous Coronary Intervention with TAXUS and Cardiac Surgery) study are best characterized as subgroup analyses and “hypothesis generating,” SYNTAX nonetheless represents the latest and most comprehensive comparison of PCI and CABG.13,14 Therefore, the results of SYNTAX have been considered appropriately when formulating our revascularization recommendations. Although the limitations of using the SYNTAX score for certain revascularization recommendations are recognized, the SYNTAX score is a reasonable surrogate for the extent of CAD and its complexity and serves as important information that should be considered when making revascularization decisions. Recommendations that refer to SYNTAX scores use them as surrogates for the extent and complexity of CAD.
Revascularization recommendations to improve survival and symptoms are provided in the following text and are summarized in Tables 2 and 3. References to studies comparing revascularization with medical therapy are presented when available for each anatomic subgroup.
See Online Data Supplements 1 and 2 for additional data regarding the survival and symptomatic benefits with CABG or PCI for different anatomic subsets.
2.1. Heart Team Approach to Revascularization Decisions: Recommendations
One protocol used in RCTs14–16,23 often involves a multidisciplinary approach referred to as the Heart Team. Composed of an interventional cardiologist and a cardiac surgeon, the Heart Team 1) reviews the patient's medical condition and coronary anatomy, 2) determines that PCI and/or CABG are technically feasible and reasonable, and 3) discusses revascularization options with the patient before a treatment strategy is selected. Support for using a Heart Team approach comes from reports that patients with complex CAD referred specifically for PCI or CABG in concurrent trial registries have lower mortality rates than those randomly assigned to PCI or CABG in controlled trials.15,16
The SIHD, PCI, and CABG guideline writing committees endorse a Heart Team approach in patients with unprotected left main CAD and/or complex CAD in whom the optimal revascularization strategy is not straightforward. A collaborative assessment of revascularization options, or the decision to treat with GDMT without revascularization, involving an interventional cardiologist, a cardiac surgeon, and (often) the patient's general cardiologist, followed by discussion with the patient about treatment options, is optimal. Particularly in patients with SIHD and unprotected left main and/or complex CAD for whom a revascularization strategy is not straightforward, an approach has been endorsed that involves terminating the procedure after diagnostic coronary angiography is completed: this allows a thorough discussion and affords both the interventional cardiologist and cardiac surgeon the opportunity to discuss revascularization options with the patient. Because the STS score and the SYNTAX score have been shown to predict adverse outcomes in patients undergoing CABG and PCI, respectively, calculation of these scores is often useful in making revascularization decisions.13,14,17–22
2.2. Revascularization to Improve Survival: Recommendations
Left Main CAD Revascularization
Class III: HARM
Non–Left Main CAD Revascularization
Class III: HARM
2.3. Revascularization to Improve Symptoms: Recommendations
Class III: HARM
2.4. CABG Versus Contemporaneous Medical Therapy
In the 1970s and 1980s, 3 RCTs established the survival benefit of CABG compared with contemporaneous (although minimal by current standards) medical therapy without revascularization in certain subjects with stable angina: the Veterans Affairs Cooperative Study,114 European Coronary Surgery Study,55 and CASS (Coronary Artery Surgery Study).115 Subsequently, a 1994 meta-analysis of 7 studies that randomized a total of 2649 patients to medical therapy or CABG30 showed that CABG offered a survival advantage over medical therapy for patients with left main or 3-vessel CAD. The studies also established that CABG is more effective than medical therapy for relieving anginal symptoms. These studies have been replicated only once during the past decade. In MASS II (Medicine, Angioplasty, or Surgery Study II), patients with multivessel CAD who were treated with CABG were less likely than those treated with medical therapy to have a subsequent MI, need additional revascularization, or experience cardiac death in the 10 years after randomization.104
Surgical techniques and medical therapy have improved substantially during the intervening years. As a result, if CABG were to be compared with GDMT in RCTs today, the relative benefits for survival and angina relief observed several decades ago might no longer be observed. Conversely, the concurrent administration of GDMT may substantially improve long-term outcomes in patients treated with CABG in comparison with those receiving medical therapy alone. In the BARI 2D (Bypass Angioplasty Revascularization Investigation 2 Diabetes) trial of patients with diabetes mellitus, no significant difference in risk of mortality in the cohort of patients randomized to GDMT plus CABG or GDMT alone was observed, although the study was not powered for this endpoint, excluded patients with significant left main CAD, and included only a small percentage of patients with proximal LAD artery disease or LV ejection fraction (LVEF) <0.50.116 The PCI and CABG guideline writing committees endorse the performance of the ISCHEMIA (International Study of Comparative Health Effectiveness with Medical and Invasive Approaches) trial, which will provide contemporary data on the optimal management strategy (medical therapy or revascularization with CABG or PCI) of patients with SIHD, including multivessel CAD, and moderate to severe ischemia.
2.5. PCI Versus Medical Therapy
Although contemporary interventional treatments have lowered the risk of restenosis compared with earlier techniques, meta-analyses have failed to show that the introduction of BMS confers a survival advantage over balloon angioplasty117–119 or that the use of DES confers a survival advantage over BMS.119,120
No study to date has demonstrated that PCI in patients with SIHD improves survival rates.26,53,56,82,116,119,121–124 Neither COURAGE (Clinical Outcomes Utilizing Revascularization and Aggressive Drug Evaluation)82 nor BARI 2D,116 which treated all patients with contemporary optimal medical therapy, demonstrated any survival advantage with PCI, although these trials were not specifically powered for this endpoint. Although 1 large analysis evaluating 17 RCTs of PCI versus medical therapy (including 5 trials of subjects with acute coronary syndromes [ACS]) found a 20% reduction in death with PCI compared with medical therapy,123 2 other large analyses did not.119,122 An evaluation of 13 studies reporting the data from 5442 patients with nonacute CAD showed no advantage of PCI over medical therapy for the individual endpoints of all-cause death, cardiac death or MI, or nonfatal MI.124 Evaluation of 61 trials of PCI conducted over several decades shows that despite improvements in PCI technology and pharmacotherapy, PCI has not been demonstrated to reduce the risk of death or MI in patients without recent ACS.119
The findings from individual studies and systematic reviews of PCI versus medical therapy can be summarized as follows:
2.6. CABG Versus PCI
The results of 26 RCTs comparing CABG and PCI have been published: Of these, 9 compared CABG with balloon angioplasty,75,105,128–142 14 compared CABG with BMS implantation,88,143–160 and 3 compared CABG with DES implantation.14,161,162
2.6.1. CABG Versus Balloon Angioplasty or BMS
A systematic review of the 22 RCTs comparing CABG with balloon angioplasty or BMS implantation concluded the following163:
Survival was similar for CABG and PCI (with balloon angioplasty or BMS) at 1 year and 5 years. Survival was similar for CABG and PCI in subjects with 1-vessel CAD (including those with disease of the proximal portion of the LAD artery) or multivessel CAD.
Incidence of MI was similar at 5 years after randomization.
Procedural stroke occurred more commonly with CABG than with PCI (1.2% versus 0.6%).
Relief of angina was accomplished more effectively with CABG than with PCI 1 year after randomization and 5 years after randomization.
During the first year after randomization, repeat coronary revascularization was performed less often after CABG than after PCI (3.8% versus 26.5%). This was also demonstrated after 5 years of follow-up (9.8% versus 46.1%). This difference was more pronounced with balloon angioplasty than with BMS.
A collaborative analysis of data from 10 RCTs comparing CABG with balloon angioplasty (6 trials) or with BMS implantation (4 trials)164 permitted subgroup analyses of the data from the 7812 patients. No difference was noted with regard to mortality rate 5.9 years after randomization or the composite endpoint of death or MI. Repeat revascularization and angina were noted more frequently in those treated with balloon angioplasty or BMS implantation.164 The major new observation of this analysis was that CABG was associated with better outcomes in patients with diabetes mellitus and in those >65 years old. Of interest, the relative outcomes of CABG and PCI were not influenced by other patient characteristics, including the number of diseased coronary arteries.
Many trials did not report outcomes for other important patient subsets. For example, the available data are insufficient to determine if race, obesity, renal dysfunction, peripheral arterial disease, or previous coronary revascularization affected the comparative outcomes of CABG and PCI.
Most of the patients enrolled in these trials were male, and most had 1- or 2-vessel CAD and normal LV systolic function (EF >50%)—subjects known to be unlikely to derive a survival benefit and less likely to experience complications after CABG.30
The patients enrolled in these trials represented only a small fraction (generally <5% to 10%) of those who were screened. For example, most screened patients with 1-vessel CAD and many with 3-vessel CAD were not considered for randomization.
See Online Data Supplements 3 and 4 for additional data comparing CABG with PCI.
2.6.2. CABG Versus DES
Although the results of 9 observational studies comparing CABG and DES implantation have been published,32,165–172 most of them had short (12 to 24 months) follow-up periods. In a meta-analysis of 24 268 patients with multivessel CAD treated with CABG or DES,173 the incidences of death and MI were similar for the 2 procedures, but the frequency with which repeat revascularization was performed was roughly 4 times higher after DES implantation. Only 1 large RCT comparing CABG and DES implantation has been published. The SYNTAX trial randomly assigned 1800 patients (of a total of 4337 who were screened) to receive DES or CABG.14,46 Major adverse cardiac events (MACE), a composite of death, stroke, MI, or repeat revascularization during the 3 years after randomization, occurred in 20.2% of CABG patients and 28.0% of those undergoing DES implantation (P<0.001). The rates of death and stroke were similar; however, MI (3.6% for CABG, 7.1% for DES) and repeat revascularization (10.7% for CABG, 19.7% for DES) were more likely to occur with DES implantation.46
In SYNTAX, the extent of CAD was assessed using the SYNTAX score, which is based on the location, severity, and extent of coronary stenoses, with a low score indicating less complicated anatomic CAD. In post hoc analyses, a low score was defined as ≤22; intermediate, 23 to 32; and high, ≥33. The occurrence of MACE correlated with the SYNTAX score for DES patients but not for those undergoing CABG. At 12-month follow-up, the primary endpoint was similar for CABG and DES in those with a low SYNTAX score. In contrast, MACE occurred more often after DES implantation than after CABG in those with an intermediate or high SYNTAX score.14 At 3 years of follow-up, the mortality rate was greater in subjects with 3-vessel CAD treated with PCI than in those treated with CABG (6.2% versus 2.9%). The differences in MACE between those treated with PCI or CABG increased with an increasing SYNTAX score (Figure 1).46
Although the utility of using a SYNTAX score in everyday clinical practice remains uncertain, it seems reasonable to conclude from SYNTAX and other data that outcomes of patients undergoing PCI or CABG in those with relatively uncomplicated and lesser degrees of CAD are comparable, whereas in those with complex and diffuse CAD, CABG appears to be preferable.46
See Online Data Supplements 5 and 6 for additional data comparing CABG with DES.
2.7. Left Main CAD
2.7.1. CABG or PCI Versus Medical Therapy for Left Main CAD
CABG confers a survival benefit over medical therapy in patients with left main CAD. Subgroup analyses from RCTs performed 3 decades ago included 91 patients with left main CAD in the Veterans Administration Cooperative Study.28 A meta-analysis of these trials demonstrated a 66% reduction in relative risk in mortality with CABG, with the benefit extending to 10 years.30 The CASS Registry24 contained data from 1484 patients with ≥50% diameter stenosis left main CAD initially treated surgically or nonsurgically. Median survival duration was 13.3 years in the surgical group; and 6.6 years in the medical group. The survival benefit of CABG over medical therapy appeared to extend to 53 asymptomatic patients with left main CAD in the CASS Registry.29 Other therapies that subsequently have been shown to be associated with improved long-term outcome, such as the use of aspirin, statins, and internal mammary artery grafting, were not widely used in that era.
RCTs and subgroup analyses that compare PCI with medical therapy in patients with “unprotected” left main CAD do not exist.
2.7.2. Studies Comparing PCI Versus CABG for Left Main CAD
Of all subjects undergoing coronary angiography, approximately 4% are found to have left main CAD,175 >80% of whom have significant (≥70% diameter) stenoses in other epicardial coronary arteries.
Published cohort studies have found that major clinical outcomes are similar with PCI or CABG 1 year after revascularization and that mortality rates are similar at 1, 2, and 5 years of follow-up; however, the risk of needing target-vessel revascularization is significantly higher with stenting than with CABG.
In the SYNTAX trial, 45% of screened patients with unprotected left main CAD had complex disease that prevented randomization; 89% of these underwent CABG.13,14 In addition, 705 of the 1800 patients who were randomized had revascularization for unprotected left main CAD. The majority of patients with left main CAD and a low SYNTAX score had isolated left main CAD or left main CAD plus 1-vessel CAD; the majority of those with an intermediate score had left main CAD plus 2-vessel CAD; and most of those with a high SYNTAX score had left main CAD plus 3-vessel CAD. At 1 year, rates of all-cause death and MACE were similar for the 2 groups.13 Repeat revascularization rates were higher in the PCI group than the CABG group (11.8% versus 6.5%), but stroke occurred more often in the CABG group (2.7% versus 0.3%). At 3 years of follow-up, the incidence of death in those undergoing left main CAD revascularization with low or intermediate SYNTAX scores (≤32) was 3.7% after PCI and 9.1% after CABG (P=0.03), whereas in those with a high SYNTAX score (≥33), the incidence of death after 3 years was 13.4% after PCI and 7.6% after CABG (P=0.10).46 Because the primary endpoint of SYNTAX was not met (ie, noninferiority comparison of CABG and PCI), these subgroup analyses need to be considered in that context.
In the LE MANS (Study of Unprotected Left Main Stenting Versus Bypass Surgery) trial,23 105 patients with left main CAD were randomized to receive PCI or CABG. Although a low proportion of patients treated with PCI received DES (35%) and a low proportion of patients treated with CABG received internal mammary grafts (72%), the outcomes at 30 days and 1 year were similar between the groups. In the PRECOMBAT (Premier of Randomized Comparison of Bypass Surgery versus Angioplasty Using Sirolimus-Eluting Stent in Patients with Left Main Coronary Artery Disease) trial of 600 patients with left main disease, the composite endpoint of death, MI, or stroke at 2 years occurred in 4.4% of patients treated with PCI patients and 4.7% of patients treated with CABG, but ischemia-driven target-vessel revascularization was more often required in the patients treated with PCI (9.0% versus 4.2%).52
The results from these 3 RCTs suggest (but do not definitively prove) that major clinical outcomes in selected patients with left main CAD are similar with CABG and PCI at 1- to 2-year follow-up, but repeat revascularization rates are higher after PCI than after CABG. RCTs with extended follow-up of ≥5 years are required to provide definitive conclusions about the optimal treatment of left main CAD. In a meta-analysis of 8 cohort studies and 2 RCTs,41 death, MI, and stroke occurred with similar frequency in the PCI- and CABG-treated patients at 1, 2, and 3 years of follow-up. Target-vessel revascularization was performed more often in the PCI group at 1 year (OR: 4.36), 2 years (OR: 4.20), and 3 years (OR: 3.30).
See Online Data Supplements 7 to 12 for additional data comparing PCI with CABG for left main CAD.
2.7.3. Revascularization Considerations for Left Main CAD
Although CABG has been considered the “gold standard” for unprotected left main CAD revascularization, more recently PCI has emerged as a possible alternative mode of revascularization in carefully selected patients. Lesion location is an important determinant when considering PCI for unprotected left main CAD. Stenting of the left main ostium or trunk is more straightforward than treating distal bifurcation or trifurcation stenoses, which generally requires a greater degree of operator experience and expertise.176 In addition, PCI of bifurcation disease is associated with higher restenosis rates than when disease is confined to the ostium or trunk.39,177 Although lesion location influences technical success and long-term outcomes after PCI, location exerts a negligible influence on the success of CABG. In subgroup analyses, patients with left main CAD and a SYNTAX score ≥33 with more complex or extensive CAD had a higher mortality rate with PCI than with CABG.46 Physicians can estimate operative risk for all CABG candidates using a standard instrument, such as the risk calculator from the STS database. The above considerations are important factors when choosing among revascularization strategies for unprotected left main CAD and have been factored into revascularization recommendations. Use of a Heart Team approach has been recommended in cases in which the choice of revascularization is not straightforward. As discussed in Section 2.9.7, the ability of the patient to tolerate and comply with dual antiplatelet therapy (DAPT) is also an important consideration in revascularization decisions.
The 2005 PCI guideline8 recommended routine angiographic follow-up 2 to 6 months after stenting for unprotected left main CAD. However, because angiography has limited ability to predict stent thrombosis and the results of SYNTAX suggest good intermediate-term results for PCI in subjects with left main CAD, this recommendation was removed in the 2009 STEMI/PCI focused update.10
Experts have recommended immediate PCI for unprotected left main CAD in the setting of STEMI.51 The impetus for such a strategy is greatest when left main CAD is the site of the culprit lesion, antegrade coronary flow is diminished (eg, TIMI flow grade 0, 1, or 2), the patient is hemodynamically unstable, and it is believed that PCI can be performed more quickly than CABG. When possible, the interventional cardiologist and cardiac surgeon should decide together on the optimal form of revascularization for these subjects, although it is recognized that these patients are usually critically ill and therefore not amenable to a prolonged deliberation or discussion of treatment options.
2.8. Proximal LAD Artery Disease
A cohort study53 and a meta-analysis30 from the 1990s suggested that CABG confers a survival advantage over contemporaneous medical therapy for patients with disease in the proximal segment of the LAD artery. Cohort studies and RCTs30,133,146,148,161,178–181 as well as collaborative- and meta-analyses164,182–184 showed that PCI and CABG result in similar survival rates in these patients.
See Online Data Supplement 13 for additional data regarding proximal LAD artery revascularization.
2.9. Clinical Factors That May Influence the Choice of Revascularization
2.9.1. Diabetes Mellitus
An analysis performed in 2009 of data on 7812 patients (1233 with diabetes) in 10 RCTs demonstrated a worse long-term survival rate in patients with diabetes mellitus after balloon angioplasty or BMS implantation than after CABG.164 The BARI 2D trial116 randomly assigned 2368 patients with type 2 diabetes and CAD to undergo intensive medical therapy or prompt revascularization with PCI or CABG, according to whichever was thought to be more appropriate. By study design, those with less extensive CAD more often received PCI, whereas those with more extensive CAD were more likely to be treated with CABG. The study was not designed to compare PCI with CABG. At 5-year follow-up, no difference in rates of survival or MACE between the medical therapy group and those treated with revascularization was noted. In the PCI stratum, no significant difference in MACE between medical therapy and revascularization was demonstrated (DES in 35%; BMS in 56%); in the CABG stratum, MACE occurred less often in the revascularization group. One-year follow-up data from the SYNTAX study demonstrated a higher rate of repeat revascularization in patients with diabetes mellitus treated with PCI than with CABG, driven by a tendency for higher repeat revascularization rates in those with higher SYNTAX scores undergoing PCI.76 In summary, in subjects requiring revascularization for multivessel CAD, current evidence supports diabetes mellitus as an important factor when deciding on a revascularization strategy, particularly when complex or extensive CAD is present (Figure 2).
See Online Data Supplements 14 and 15 for additional data regarding diabetes mellitus.
2.9.2. Chronic Kidney Disease
Cardiovascular morbidity and mortality rates are markedly increased in patients with chronic kidney disease (CKD) when compared with age-matched controls without CKD. The mortality rate for patients on hemodialysis is >20% per year, and approximately 50% of deaths among these patients are due to a cardiovascular cause.187,188
To date, randomized comparisons of coronary revascularization (with CABG or PCI) and medical therapy in patients with CKD have not been reported. Some, but not all, observational studies or subgroup analyses have demonstrated an improved survival rate with revascularization compared with medical therapy in patients with CKD and multivessel CAD,189–191 despite the fact that the incidence of periprocedural complications (eg, death, MI, stroke, infection, renal failure) is increased in patients with CKD compared with those without renal dysfunction. Some studies have shown that CABG is associated with a greater survival benefit than PCI among patients with severe renal dysfunction.190–196
2.9.3. Completeness of Revascularization
Most patients undergoing CABG receive complete or nearly complete revascularization, which seems to influence long-term prognosis positively.197 In contrast, complete revascularization is accomplished less often in subjects receiving PCI (eg, in <70% of patients), but the extent to which the absence of complete initial revascularization influences outcome is less clear. Rates of late survival and survival free of MI appears to be similar in patients with and without complete revascularization after PCI. Nevertheless, the need for subsequent CABG is usually higher in those whose initial revascularization procedure was incomplete (compared with those with complete revascularization) after PCI.198–200
2.9.4. LV Systolic Dysfunction
Several older studies and a meta-analysis of the data from these studies reported that patients with LV systolic dys-function (predominantly mild to moderate in severity) had better survival with CABG than with medical therapy alone.30,64–68 For patients with more severe LV systolic dysfunction, however, the evidence that CABG results in better survival compared with medical therapy is lacking. In the STICH (Surgical Treatment for Ischemic Heart Failure) trial of subjects with LVEF <35% with or without viability testing, CABG and GDMT resulted in similar rates of survival (death from any cause, the study's primary outcome) after 5 years of follow-up. For a number of secondary outcomes at this time point, including 1) death from any cause or hospitalization for heart failure, 2) death from any cause or hospitalization for cardiovascular causes, 3) death from any cause or hospitalization for any cause, or 4) death from any cause or revascularization with PCI or CABG, CABG was superior to GDMT. Although the primary outcome (death from any cause) was similar in the 2 treatment groups after an average of 5 years of follow-up, the data suggest the possibility that outcomes would differ if the follow-up were longer in duration; as a result, the study is being continued to provide follow-up for up to 10 years.83,84
Only very limited data comparing PCI with medical therapy in patients with LV systolic dysfunction are available.68 In several ways, these data are suboptimal, in that many studies compared CABG with balloon angioplasty, many were retrospective, and many were based on cohort or registry data. Some of the studies demonstrated a similar survival rate in patients having CABG and PCI,71,164,201–203 whereas others showed that those undergoing CABG had better outcomes.32 The data that exist at present on revascularization in patients with CAD and LV systolic dysfunction are more robust for CABG than for PCI, although data from contemporary RCTs in this patient population are lacking. Therefore, the choice of revascularization in patients with CAD and LV systolic dysfunction is best based on clinical variables (eg, coronary anatomy, presence of diabetes mellitus, presence of CKD), magnitude of LV systolic dysfunction, patient preferences, clinical judgment, and consultation between the interventional cardiologist and the cardiac surgeon.
2.9.5. Previous CABG
In patients with recurrent angina after CABG, repeat revascularization is most likely to improve survival in subjects at highest risk, such as those with obstruction of the proximal LAD artery and extensive anterior ischemia.85–93 Patients with ischemia in other locations and those with a patent LIMA to the LAD artery are unlikely to experience a survival benefit from repeat revascularization.92
Cohort studies comparing PCI and CABG among post-CABG patients report similar rates of mid- and long-term survival after the 2 procedures.85,88–91,93,204 In the patient with previous CABG who is referred for revascularization for medically refractory ischemia, factors that may support the choice of repeat CABG include vessels unsuitable for PCI, number of diseased bypass grafts, availability of the internal mammary artery for grafting chronically occluded coronary arteries, and good distal targets for bypass graft placement. Factors favoring PCI over CABG include limited areas of ischemia causing symptoms, suitable PCI targets, a patent graft to the LAD artery, poor CABG targets, and comorbid conditions.
2.9.6. Unstable Angina/Non–ST-Elevation Myocardial Infarction
The main difference between management of the patient with SIHD and the patient with UA/NSTEMI is that the impetus for revascularization is stronger in the setting of UA/NSTEMI, because myocardial ischemia occurring as part of an ACS is potentially life threatening, and associated anginal symptoms are more likely to be reduced with a revascularization procedure than with GDMT.205–207 Thus, the indications for revascularization are strengthened by the acuity of presentation, the extent of ischemia, and the ability to achieve full revascularization. The choice of revascularization method is generally dictated by the same considerations used to decide on PCI or CABG for patients with SIHD.
2.9.7. DAPT Compliance and Stent Thrombosis: Recommendation
Class III: HARM
The risk of stent thrombosis is increased dramatically in patients who prematurely discontinue DAPT, and stent thrombosis is associated with a mortality rate of 20% to 45%.208 Because the risk of stent thrombosis with BMS is greatest in the first 14 to 30 days, this is the generally recommended minimum duration of DAPT therapy for these individuals. Consensus in clinical practice is to treat DES patients for at least 12 months with DAPT to avoid late (after 30 days) stent thrombosis.208,212 Therefore, the ability of the patient to tolerate and comply with at least 30 days of DAPT with BMS treatment and at least 12 months of DAPT with DES treatment is an important consideration in deciding whether to use PCI to treat patients with CAD.
2.10. TMR as an Adjunct to CABG
TMR has been used on occasion in patients with severe angina refractory to GDMT in whom complete revascularization cannot be achieved with PCI and/or CABG. Although the mechanism by which TMR might be efficacious in these patients is unknown,213,214 several RCTs of TMR as sole therapy demonstrated a reduction in anginal symptoms compared with intensive medical therapy alone.109–111,215–217 A single randomized multicenter comparison of TMR (with a holmium:YAG laser) plus CABG and CABG alone in patients in whom some myocardial segments were perfused by arteries considered not amenable to grafting112 showed a significant reduction in perioperative mortality rate (1.5% versus 7.6%, respectively), and the survival benefit of the TMR–CABG combination was present after 1 year of follow-up.112 At the same time, a large retrospective analysis of data from the STS National Cardiac Database as well as a study of 169 patients from the Washington Hospital Center who underwent combined TMR–CABG, showed no difference in adjusted mortality rate compared with CABG alone.113,218 In short, a TMR–CABG combination does not appear to improve survival compared with CABG alone. In selected patients, however, such a combination may be superior to CABG alone in relieving angina.
2.11. Hybrid Coronary Revascularization: Recommendations
Hybrid coronary revascularization, defined as the planned combination of LIMA-to-LAD artery grafting and PCI of ≥1 non-LAD coronary arteries,226 is intended to combine the advantages of CABG (ie, durability of the LIMA graft) and PCI.227 Patients with multivessel CAD (eg, LAD and ≥1 non-LAD stenoses) and an indication for revascularization are potentially eligible for this approach. Hybrid revascularization is ideal in patients in whom technical or anatomic limitations to CABG or PCI alone may be present and for whom minimizing the invasiveness (and therefore the risk of morbidity and mortality) of surgical intervention is preferred221 (eg, patients with severe preexisting comorbidities, recent MI, a lack of suitable graft conduits, a heavily calcified ascending aorta, or a non-LAD coronary artery unsuitable for bypass but amenable to PCI, and situations in which PCI of the LAD artery is not feasible because of excessive tortuosity or CTO).
Hybrid coronary revascularization may be performed in a hybrid suite in one operative setting or as a staged procedure (ie, PCI and CABG performed in 2 different operative suites, separated by hours to 2 days, but typically during the same hospital stay). Because most hospitals lack a hybrid operating room, staged procedures are usually performed. With the staged procedure, CABG before PCI is preferred, because this approach allows the interventional cardiologist to 1) verify the patency of the LIMA-to-LAD artery graft before attempting PCI of other vessels and 2) minimize the risk of perioperative bleeding that would occur if CABG were performed after PCI (ie, while the patient is receiving DAPT). Because minimally invasive CABG may be associated with lower graft patency rates compared with CABG performed through a midline sternotomy, it seems prudent to angiographically image all grafts performed through a minimally invasive approach to confirm graft patency.221
To date, no RCTs involving hybrid coronary revascularization have been published. Over the past 10 years, several small, retrospective series of hybrid revascularization using minimally invasive CABG and PCI have reported low mortality rates (0 to 2%) and event-free survival rates of 83% to 92% at 6 to 12 months of follow-up. The few series that have compared the outcomes of hybrid coronary revascularization with standard CABG report similar outcomes at 30 days and 6 months.219–225
3. PCI Outcomes
3.1. Definitions of PCI Success
The success of a PCI procedure is best defined by 3 interrelated components: angiographic findings, procedural events, and clinical outcomes.
3.1.1. Angiographic Success
A successful PCI produces sufficient enlargement of the lumen at the target site to improve coronary artery blood flow. A successful balloon angioplasty is defined as the reduction of a minimum stenosis diameter to <50% with a final TIMI flow grade 3 (visually assessed by angiography) without side branch loss, flow-limiting dissection, or angio-graphic thrombus.7 For coronary stents, a minimum stenosis diameter of <20% (as visually assessed by angiography) has previously been the clinical benchmark of an optimal angiographic result. Given improvements in technology and techniques, as well as recognition of the importance of an adequately deployed stent to decrease the risks of stent restenosis and thrombosis,12,228,229 the writing committee concluded that a minimum diameter stenosis of <10% (with an optimal goal of as close to 0% as possible) should be the new benchmark for lesions treated with coronary stenting. As with balloon angioplasty, there should be final TIMI flow grade 3, without occlusion of a significant side branch, flow-limiting dissection, distal embolization, or angiographic thrombus. Problems with determining angiographic success include disparities between the visual assessment and computer-aided quantitative stenosis measurement and self-reporting of success in clinical reports or databases.
3.1.2. Procedural Success
A successful PCI should achieve angiographic success without associated in-hospital major clinical complications (eg, death, MI, stroke, emergency CABG).7,8 Issues regarding the diagnosis and prognostic implications of procedure-related MI are discussed in Sections 3.3 and 5.10.
3.1.3. Clinical Success
In the short term, a clinically successful PCI requires both anatomic and procedural success along with relief of signs and/or symptoms of myocardial ischemia. Long-term clinical success requires that the short-term clinical success remain durable and that relief of signs and symptoms of myocardial ischemia persist >9 months after the procedure. Restenosis is the principal cause of lack of long-term clinical success after a short-term clinical success has been achieved. Restenosis is not a complication; it is the expected biological response to vascular injury. The frequency of clinically important restenosis may be judged by the frequency with which subsequent revascularization procedures are performed on target arteries after the index procedure.
3.2. Predictors of Clinical Outcome After PCI
Factors associated with increased PCI complication rates include advanced age, diabetes, CKD, ACS, congestive heart failure, and multivessel CAD.8,230–232 Several models have been developed and refined over the past 2 decades to predict mortality with PCI.230,233–236 At present, perhaps the best accepted system is from the ACC National Cardiovascular Data Registry (NCDR) CathPCI Risk Score system, which uses clinical variables and PCI setting to predict inpatient mortality (Appendix 4A).236 In general, these models perform very well (C statistic: approximately 0.90), although predictive capability decreases in high-risk patients.
Models have also been developed to predict procedural success. Presently, the modified ACC/AHA score230 and the SCAI score (Appendix 4B)237 are both in use, with the latter slightly outperforming the former. Discrimination as measured by the C statistic is generally good to very good (0.70 to 0.82), depending on the outcome variable and patient population.
The angiographic SYNTAX score238 has been developed to predict long-term risk of MACE after multivessel intervention. The SYNTAX score and its potential utility in helping guide revascularization strategies are discussed in Section 2. Composite models including angiographic and clinical variables have been developed but generally require validation in larger cohorts of patients.
3.3. PCI Complications
In an analysis of the NCDR CathPCI database of patients undergoing PCI between 2004 and 2007, the overall inhospital mortality rate was 1.27%, ranging from 0.65% in elective PCI to 4.81% in STEMI.236 Factors associated with an increased risk of PCI-related death include advanced age, comorbidities (eg, diabetes, CKD, congestive heart failure), multivessel CAD, high-risk lesions, and the setting of PCI (eg, STEMI, urgent or emergency procedure, cardiogenic shock).56,230–232,236
Causes of procedural and periprocedural MI include acute artery closure, embolization and no-reflow, side branch occlusion, and acute stent thrombosis. The incidence of procedure-related MI depends to a great degree on the definition of MI used, the patient population studied, and whether or not cardiac biomarkers are routinely assessed after PCI. The definition and clinical significance of PCI-related MI have been controversial. Criteria for defining a PCI-related MI have evolved over time.8,239,240 The 2007 universal definition of MI240 states that after PCI, elevations of cardiac biomarkers above the 99th percentile upper reference limit indicate periprocedural myocardial necrosis. Increases of biomarkers >3 times the 99th percentile upper reference limit were designated as defining PCI-related MI.240 According to this definition, ≥15% of patients undergoing PCI would be defined as having periprocedural MI.241,242 Issues in procedure-related MI are discussed in Section 5.10.
The need for emergency CABG has dramatically decreased with advances in PCI technology, particularly coronary stents.243,244 Recently the NCDR reported the rate of emergency CABG at 0.4%.244 Procedure-related indications for CABG in 1 large series included coronary dissection (27%), acute artery closure (16%), perforation (8%), and failure to cross the lesion (8%).245 The strongest predictors of the need for emergency CABG in several analyses are cardiogenic shock (OR: 11.4), acute MI or emergency PCI (OR: 3.2 to 3.8), multivessel disease (OR: 2.3 to 2.4), and type C lesion (OR: 2.6).243,245 In-hospital mortality for emergency CABG ranges from 7.8% to 14%.243,245,246
In a contemporary analysis from the NCDR, the incidence of PCI-related stroke was 0.22%.247 In-hospital mortality in patients with PCI-related stroke is 25% to 30%.247,248 Factors associated with an increased risk of stroke include fibrinolytic therapy administered before PCI (OR: 4.7), known cerebrovascular disease (OR: 2.20), STEMI as the indication for PCI (OR: 3.2), use of an intra-aortic balloon pump (IABP) (OR: 2.6), older age (OR: 1.17 per 5-year increase), and female sex.247–249 Initial imaging after a stroke in 1 small series revealed hemorrhagic etiology in 18%, ischemic etiology in 58%, and no clear etiology in 24%.248 One potential algorithm for the treatment of catheterization-related stroke has been recently proposed.250 This document includes no specific recommendations for the management of PCI-related stroke but refers the reader to the AHA/American Stroke Association guidelines for the management of adults with stroke.251
Vascular complications from PCI are primarily related to vascular access. Important femoral vascular complications include access site hematoma, retroperitoneal hematoma, pseudoaneurysm, arteriovenous fistula, and arterial dissection and/or occlusion.252 The incidence of these vascular complications in various reports generally ranges from 2% to 6% and has decreased with time.249,253–257 Factors associated with an increased risk of vascular complication include age ≥70 years, body surface area <1.6 m2, emergency procedures, peripheral artery disease, periprocedural use of glycoprotein (GP) IIb/IIIa inhibitors, and female sex (if not corrected for body surface area).249,253,254,257,258 Ultrasound guidance has been used for femoral artery access to potentially decrease complications.259 As discussed in Section 5.11, vascular closure devices have not been clearly demonstrated to decrease vascular complication rates. Radial site access decreases the rate of access-related bleeding and complications compared with femoral access.255,260 Loss of the radial pulse has been reported in ≤5% of radial procedures.261 Infrequent to rare complications occurring with the radial artery approach include compartment syndrome, pseudoaneurysm (<0.01%), and sterile abscess (occurring with previous-generation hydrophilic sheaths).262 Radial artery spasm may occur and treatment at times may be challenging. Local hematomas may occur from small-branch vessel hydrophilic wire perforation or inexperience with wristband use.
The risk of coronary perforation is approximately 0.2%, most commonly by wire perforation during PCI for CTO or by ablative or oversized devices during PCI of heavily diseased or tortuous coronary arteries.263 The risk of tamponade and management of the perforation varies with the type of perforation.264
Periprocedural bleeding is now recognized to be associated with subsequent mortality,265,266 and the avoidance of bleeding complications has become an important consideration in performing PCI. The risk of bleeding is associated with patient factors (eg, advanced age, low body mass index, CKD, baseline anemia), as well as the degree of platelet and thrombin inhibition, vascular access site, and sheath size.267–269 Issues of periprocedural bleeding are discussed in Section 4.7.
The incidence of contrast-induced acute kidney injury (AKI) or “contrast nephropathy” in published reports depends on the definition of contrast nephropathy used and the frequency of risk factors for contrast-induced AKI in the patient population studied. Important risk factors for contrast-induced AKI include advanced age, CKD, congestive heart failure, diabetes, and the volume of contrast administered. Contrast-induced AKI and strategies to prevent it are discussed in Section 4.4.
4. Preprocedural Considerations
Table 4 contains recommendations for preprocedural considerations and interventions in patients undergoing PCI.
4.1. Cardiac Catheterization Laboratory Requirements
Defibrillators are considered by The Joint Commission to be life-support equipment requiring routine assessment and completion of appropriate logs. Many hospitals require periodic inspection of consoles for ancillary devices used in coronary intervention (eg, Doppler wires, pressure-tipped sensor wires, and IVUS catheters). Point-of-care testing devices (eg, activated clotting time and arterial blood gas machines) require routine calibration. Duration of storage of digital cine images is often mandated by law. Operating parameters for x-ray imaging equipment are adjusted at installation and periodically assessed by a qualified physicist in cooperation with the equipment manufacturer. Familiarity with radiation dose–reducing features of catheterization laboratory equipment and assistance from a qualified physicist are important for radiation dose minimization and image optimization.
An interventional cardiologist must be present in the laboratory for the duration of each procedure and is responsible for procedure outcome. Nursing and technical personnel are also required to be present in the catheterization laboratory, with specific staffing dependent on state requirements and laboratory caseload and mix. Catheterization laboratory technical staff may include nurse practitioners, registered nurses, licensed vocational or practical nurses, physician assistants, nursing assistants, radiology technicians, or catheterization laboratory technicians. All catheterization laboratory staff are usually certified in basic life support, advanced cardiovascular life support, and, where appropriate, pediatric advanced life support. Catheterization laboratory personnel have a nursing degree/certification or invasive cardiovascular credentials such as registered cardiovascular invasive specialist or American Society of Radiation technologists.305
4.1.3. ‘Time-Out' Procedures
In 2003, The Joint Commission mandated a universal protocol requiring proper preoperative identification of the patient by the members of the catheterization laboratory team, marking of the operative site, and a final time-out just before the procedure.306 Although initially intended to prevent wrong-site surgery, this has been expanded to include all invasive procedures despite limited scientific evidence of its effectiveness.307 The intent of the time-out is for all members of the team to improve patient care by collectively discussing the case. The content of a time-out includes confirmation of the correct patient, correct side and site, agreement on the procedure to be performed, correct patient position, and availability of needed equipment, supplies, and implants. The timeout may be checklist driven or conversational, depending on laboratory preferences.308 The writing committee strongly endorses the practice of conducting a time-out before all PCI procedures.
4.2. Ethical Aspects
The 3 principles of medical ethics are beneficence, autonomy, and justice. Beneficence involves the physician's duty to act in the best interests of the patient and avoid maleficence, or harm (primum non nocere). Autonomy describes the physician's duty to help the patient maintain control over his or her medical treatments. Justice describes the physician's duty to treat the individual patient responsibly with due consideration of other patients and stakeholders in the healthcare system. Ethical considerations specific to PCI have been previously discussed309 and are highlighted below:
Place the patient's best interest first and foremost when making clinical decisions (beneficence).
Ensure that patients actively participate in decisions affecting their care (autonomy).
Consider how decisions regarding one patient may also affect other patients and providers (justice).
Plan and perform procedures and provide care with the intention of improving the patient's quality of life and/or decreasing the risk of mortality, independent of reimbursement considerations and without inappropriate bias or influence from industry, administrators, referring physicians, or other sources.
Before performing procedures, obtain informed con sent after giving an explanation regarding the details of the procedure and the risks and benefits of both the procedure and alternatives to the procedure.
Plan and perform procedures according to standards of care and recommended guidelines, and deviate from them when appropriate or necessary in the care of individual patients.
Seek advice, assistance, or consultation from colleagues when such consultation would benefit the patient.
4.2.1. Informed Consent
Obtaining informed consent for procedures is a legal and ethical necessity. Ideally, informed consent is obtained long enough before the procedure that the patient can fully consider informed consent issues and discuss them with family or other providers, avoiding any sense of coercion. Ad hoc PCI, or PCI immediately following diagnostic procedures, presents special problems. When informed consent for PCI is obtained before diagnostic catheterization is performed, it is impossible to predict the levels of risk and benefit from an ad hoc PCI.310,311 If diagnostic catheterization reveals anatomy that poses a particularly high risk or for which the superiority of PCI compared with other strategies is unclear, the precatheterization informed consent discussion may be inadequate. In such cases, deferral of PCI until additional informed consent discussions and/or consultations occur may be appropriate, even though it inconveniences the patient and the healthcare system. It is the responsibility of the interventionalist to act in the patient's best interest in these circumstances.
Informed consent before emergency procedures is particularly difficult.312–314 The patient presenting with STEMI is usually in distress and often sedated, making true informed consent impossible. Rapid triage, transport, and treatment of STEMI patients create a pressured atmosphere that by necessity limits a prolonged and detailed informed consent process. Nevertheless, the interventionist must attempt to provide information about the risks and benefits of different strategies to the patient and family and balance the benefit of thorough discussion with the benefits of rapid intervention.
4.2.2. Potential Conflicts of Interest
Decisions about the performance and timing of PCI may pose additional ethical dilemmas. When considering whether to perform multivessel PCI in 1 stage versus 2 stages, safety and convenience for the patient must guide the decision, regardless of payment policies that maximize reimbursement when PCI is staged.311 A separate issue is self-referral, through which diagnostic catheterization often leads seamlessly to PCI by the same operator.315 The interventionist has an ethical obligation to the patient to consider all treatment options, consult with additional specialists (eg, cardiac surgeons) when their input would be helpful to the patient, avoid unnecessary interventional procedures, and allow the patient to consult family members and other physicians.311
4.3. Radiation Safety: Recommendation
The issue of radiation exposure during imaging procedures has received increased attention, and the writing committee believes that radiation safety should be addressed in this guideline. Current standards for cardiac catheterization laboratories include the following:
Specific procedures and policies are in place to mini mize patient (and operator) risk.
A radiation safety officer coordinates all radiation safety issues and works conjointly with the medical or health physicist.
Patient radiation exposure is reduced to as low a level as reasonably can be achieved.
Patients at increased risk for high procedural radiation exposure are identified.
Informed consent includes radiation safety informa tion, particularly for the high-risk patient.
A basic primer on the physics of x-ray imaging, essential to the safe practice of radiation dose management, has been published in an ACCF/AHA/Heart Rhythm Society/SCAI clinical competence statement.316Appendix 4C summarizes strategies to minimize patient and operator radiation exposure. Adverse radiation effects are now well recognized as infrequent but potentially serious complications of prolonged interventional procedures.317 Fluoroscopic time does not include cine acquisition imaging and is therefore not an accurate measure of patient radiation dose. Total air kerma at the interventional reference point (Ka,r, in Gy) and air kerma area product (PKA, in Gycm2) are required to be reported on interventional x-ray systems since 2006. These are useful in the assessment of potential tissue adverse effects or long-term radiation sequelae, respectively, and it is reasonable to include them in the catheterization record at the conclusion of each procedure. Appendix 4D summarizes considerations for patient follow-up based on radiation dose during the procedure.317
4.4. Contrast-Induced AKI: Recommendations
Class III: NO BENEFIT
See Online Data Supplements 16 to 18 for additional data regarding contrast-induced AKI.
Contrast-induced AKI or “contrast nephropathy” is one of the leading causes of hospital-acquired AKI. Major risk factors for contrast-induced AKI include advanced age, CKD, congestive heart failure, diabetes, and the volume of contrast administered. A risk-scoring system is available to predict the risk of contrast nephropathy using these risk factors and additional variables.270 Thus far, the only strategies clearly shown to reduce the risk of contrast-induced AKI are hydration and minimizing the amount of contrast media. Other than saline hydration, measures that were believed to reduce the risk of contrast-induced AKI have been found to be neutral, to have deleterious effects, or to be characterized by heterogeneous and conflicting data.
Studies of hydration to reduce the risk of contrast-induced AKI suggest that isotonic saline is preferable to half isotonic saline, intravenous (IV) hydration is preferable to oral hydration, hydration for hours before and after exposure to contrast media is preferable to a bolus administration of saline immediately before or during contrast media exposure, and administration of isotonic saline alone is preferable to administration of isotonic saline plus mannitol or furosemide.272–275,320 On the basis of these studies, a reasonable hydration regimen would be isotonic crystalloid (1.0 to 1.5 mL/kg per hour) for 3 to 12 hours before the procedure and continuing for 6 to 24 hours after the procedure.272–275,284,320,321
Prior studies of N-acetyl-L-cysteine and sodium bicarbonate have produced conflicting results. Some, often small, earlier studies suggested benefit, but many other more contemporary studies and meta-analyses found no clear evidence of benefit, and there are potential issues of publication bias and poor methodology issues in several analyses.279–282,322–332 The recently completed largest randomized study on N-acetyl-L-cysteine and contrast nephropathy in patients undergoing angiographic procedures, ACT (Acetylcysteine for Contrast-Induced Nephropathy Trial), demonstrated no benefit in primary or secondary endpoints. An updated meta-analysis using only high-quality trials similarly demonstrated no benefit.283 Taken as a whole, these studies do not support any recommendation for the use of N-acetyl-L-cysteine, they do, however, provide sufficient data to conclude that N-acetyl-L-cysteine does not prevent contrast-induced AKI in patients undergoing angiographic procedures.
The correlation between the volume of contrast media and the risk of contrast-induced AKI has been documented in several studies.276,277 Thus, minimization of contrast media volume is important to prevent contrast-induced AKI in patients undergoing angiography. The volume of contrast already administered during diagnostic catheterization is an important factor when considering possible “ad hoc” PCI.
Comparative studies of different contrast media (eg, low-osmolar versus iso-osmolar, one agent versus another agent) have produced variable and sometimes contradictory results.334–339 Thus, current data are insufficient to justify specific recommendations about low- and isoosmolar contrast media. This issue is discussed in detail in the 2011 UA/NSTEMI focused update.340 For a further discussion of contrast media and PCI, the reader is referred to a position statement by the SCAI.284
4.5. Anaphylactoid Reactions: Recommendations
Class III: NO BENEFIT
The incidence of anaphylactoid reactions to contrast media is ≤1%, and the incidence of severe reactions may be as low as 0.04%.284 Limited data suggest that in patients with a history of prior anaphylactoid reaction, the recurrence rate without prophylaxis is in the range of 16% to 44%.341 Adequate pretreatment of patients with prior anaphylactoid reactions reduces the recurrence rate to close to zero.284–286 A regimen of 50 mg of prednisone administered 13 hours, 7 hours, and 1 hour before the procedure (as well as 50 mg of diphenhydramine 1 hour before the procedure) has been shown to reduce the risk of recurrent anaphylactoid reaction.286 In practice, a regimen of 60 mg of prednisone the night before and morning of the procedure (as well as 50 mg of diphenhydramine 1 hour before the procedure) is often used.252 There are minimal data on the “pretreatment” of patients undergoing emergency PCI.342 One group has suggested IV steroids (eg, 80 mg to 125 mg of methylprednisolone, 100 mg of hydrocortisone sodium succinate), as well as oral or IV diphenhydramine and possible IV cimetidine.284 For a more detailed discussion of issues related to contrast-induced anaphylactoid reactions, the reader is referred to several dedicated discussions on contrast agents.284,341
There are no data to suggest that those patients with seafood or shellfish allergies are at risk for an anaphylactoid reaction from exposure to contrast media. Iodine does not mediate seafood, shellfish, or contrast media reactions. The common misconception that seafood allergies and contrast reactions are cross-reactions to iodine probably arose from a survey published in 1975 in which 15% of patients with a history of contrast reaction reported a personal history of shellfish allergy, but nearly identical proportions of patients reported allergies to other foods, such as milk and egg, in the same survey.287 Pretreatment of patients with steroids based only on a history of seafood or shellfish allergy has a small but non-zero risk of adverse effect (eg, hyperglycemia in a patient with diabetes) without any demonstrated benefit.288,289
4.6. Statin Treatment: Recommendation
See Online Data Supplement 19 for additional data regarding preprocedural statin treatment.
Statins have long-term benefits in patients with CAD343,344 and ACS.345,346 The benefits of statins in ACS begin early, before substantial lipid lowering has occurred,345,347 suggesting pleiotropic effects of statins. These might include anti-inflammatory effects, improvement of endothelial function, decrease of oxidative stress, or inhibition of thrombogenic responses.348 Statins were beneficial when pretreatment was started from 7 days to just before PCI.290–297
4.7. Bleeding Risk: Recommendation
Periprocedural bleeding is now recognized as a major risk factor for subsequent mortality.265,266 Bleeding may lead to mortality directly (because of the bleeding event) or through ischemic complications that occur when antiplatelet or anticoagulant agents are withdrawn in response to the bleeding. Bleeding may also be a marker of comorbidities associated with worse prognosis (eg, occult cancer). The risk of bleeding is associated with a number of patient factors (eg, advanced age, low body mass index, CKD, baseline anemia), as well as the degree of platelet and thrombin inhibition, vascular access site, and sheath size.267–269 The overall approach to PCI should be individualized to minimize both ischemic and bleeding risks.
Measures to minimize the risks of bleeding complications are discussed in several sections of this guideline. These include use of anticoagulation regimens associated with a lower risk of bleeding, weight-based dosing of heparin and other agents, use of activated clotting times to guide unfractionated heparin (UFH) dosing, avoidance of excess anticoagulation,349 dosing adjustments in patients with CKD (eg, eptifibatide, tirofiban, bivalirudin),350 use of radial artery access site,255 and avoidance of femoral vein cannulation when possible. Vascular closure devices have not been clearly demonstrated to decrease bleeding complications and are discussed in detail in Section 5.11.
4.8. PCI in Hospitals Without On-Site Surgical Backup: Recommendations
Class III: HARM
See Online Data Supplement 20 for additional data regarding hospitals without on-site surgical backup.
Primary and elective PCI can be performed at hospitals without on-site cardiac surgical backup with a high success rate, low in-hospital mortality rate, and low rate for emergency CABG.351,353,354 The best outcomes for patients with STEMI are achieved at hospitals with 24/7 access to primary PCI.355 Criteria for the performance of PCI without on-site surgical backup have been proposed in an SCAI expert consensus document.352 Consideration of elective PCI without on-site cardiac surgical backup is thought to be appropriate only when performed by experienced operators with complication rates and outcomes equivalent or superior to national benchmarks. Accurate assessment of complication rates and patient outcomes via a regional or national data registry, so that outcomes can be compared with established benchmarks, is an important quality control component of any PCI program. Desires for personal or institutional financial gain, prestige, market share, or other similar motives are not appropriate considerations for initiation of PCI programs without on-site cardiac surgery. It is only appropriate to consider initiation of a PCI program without on-site cardiac surgical backup if this program will clearly fill a void in the healthcare needs of the community. Competition with another PCI program in the same geographic area, particularly an established program with surgical backup, may not be in the best interests of the community.
Tables 5 and 6 list the SCAI expert consensus document requirements for PCI programs without on-site surgical backup. Table 7 gives the requirements for primary PCI and emergency CABG at hospitals without on-site cardiac surgery, and Table 8 lists the requirements for patient and lesion selection and backup strategy for nonemergency PCI.352
|Experienced nursing and technical laboratory staff with training in interventional laboratories. Personnel must be comfortable treating acutely ill patients with hemodynamic and electrical instability.|
|On-call schedule with operation of laboratory 24 h/d, 365 d/y.*|
|Experienced coronary care unit nursing staff comfortable with invasive hemodynamic monitoring, operation of temporary pacemaker, and management of IABP. Personnel capable of endotracheal intubation and ventilator management both on-site and during transfer if necessary.|
|Full support from hospital administration in fulfilling the necessary institutional requirements, including appropriate support services (eg, respiratory care, blood bank).|
|Written agreements for emergency transfer of patients to a facility with cardiac surgery. Transport protocols should be developed and tested a minimum of 2 times per year.|
|Well-equipped and maintained cardiac catheterization laboratory with high-resolution digital imaging capability and IABP equipment compatible with transport vehicles. The capability for real-time transfer of images and hemodynamic data (via T-1 transmission line) as well as audio and video images to review terminals for consultation at the facility providing surgical backup support is ideal.|
|Appropriate inventory of interventional equipment, including guide catheters, balloons, and stents in multiple sizes; thrombectomy and distal protection devices; covered stents; temporary pacemakers; and pericardiocentesis trays. Pressure wire device and IVUS equipment are optimal but not mandatory. Rotational or other atherectomy devices should be used cautiously in these facilities because of the greater risk of perforation.|
|Meticulous clinical and angiographic selection criteria for PCI (Tables 6 and 7).|
|Performance of primary PCI as the treatment of first choice for STEMI to ensure streamlined care paths and increased case volumes. Door-to-balloon times should be tracked, and <90 min outlier cases should be carefully reviewed for process improvement opportunities.|
|On-site rigorous data collection, outcomes analysis, benchmarking, quality improvement, and formalized periodic case review.|
|Participation in a national data registry where available, such as the ACC NCDR in the United States.|
|Avoid intervention in patients with
|Transfer emergently for coronary bypass surgery patients with
|Patient risk: expected clinical risk in case of occlusion caused by procedure|
| High patient risk: Patients with any of the following
|Lesion risk: probability that procedure will cause acute vessel occlusion|
| Increased lesion risk: lesions in open vessels with any of the following characteristics
|Strategy for surgical backup based on lesion and patient risk
5. Procedural Considerations
5.1. Vascular Access: Recommendation
See Online Data Supplement 21 for additional data regarding radial access.
Femoral artery access remains the most commonly used approach in patients undergoing PCI in the United States. Choosing a femoral artery puncture site is facilitated by fluoroscopic landmark identification or ultrasound guidance. Low punctures have a high incidence of peripheral artery complications, whereas high punctures have an increased risk of retroperitoneal hemorrhage. In patients with a synthetic graft, arterial access is possible after the graft is a few months old and complication rates are not increased.254
Radial site access is used frequently in Europe and Canada but not in the United States.260 A learning curve exists for the radial approach that will affect procedure time and radiation dose, with a trend toward lower procedural success rates for radial versus femoral access.255 However, compared with femoral access, radial access decreases the rate of access-related bleeding and complications.255,260,363 In a recent large RCT comparing radial and femoral access in patients with ACS undergoing PCI, there was no difference in the primary composite endpoint (death, MI, stroke, major bleeding), although there was a lower rate of vascular complications with the use of radial access.362 Radial artery access is particularly appealing in patients with coagulopathy, elevated international normalized ratio due to warfarin, or morbid obesity.
5.2. PCI in Specific Clinical Situations
5.2.1. UA/NSTEMI: Recommendations
Class III: NO BENEFIT
The goals of coronary angiography and revascularization in UA/NSTEMI patients are to reduce the risk of death and MI and provide symptom relief. To improve prognosis, early risk stratification is essential for selection of medical and/or invasive treatment strategies. Indications for revascularization depend on the patient's clinical risk characteristics and coronary anatomy and are in general stronger in the presence of high-risk clinical presentation (eg, dynamic electrocardiogram [ECG] changes, elevated troponin, high Global Registry of Acute Coronary Events score), recurrent symptoms, threatened viable myocardium, CKD, and larger ischemic burden (Appendix 4E). For choice of revascularization technique, the anatomical considerations are generally those used for stable CAD, although PCI may initially be performed in the index lesion to stabilize the patient (Section 2).
Contemporary studies variably comparing strategies of very early (within hours of admission), early (within 24 hours of admission), and delayed (1 to 7 days after admission) cardiac catheterization and revascularization support a strategy of early angiography and revascularization to reduce the risk of recurrent ischemia and MI, particularly among those at high risk (eg, Global Registry of Acute Coronary Events score >140),367,369,370 whereas a delayed approach is reasonable in low-intermediate risk patients (based on clinical course). There is no evidence that incremental benefit is derived by angiography and PCI performed within the first few hours of hospital admission.207,367,371–378
5.2.2. ST-Elevation Myocardial Infarction
188.8.131.52. Coronary Angiography Strategies in STEMI: Recommendations
Class III: NO BENEFIT
The historical reperfusion strategies of “primary PCI,” “immediate PCI,” “rescue PCI,” “deferred PCI,” “facilitated PCI,” and the “pharmacoinvasive strategy” have evolved in parallel with advances in antithrombotic therapy and STEMI prehospital and hospital systems of care. The clinical challenge in primary PCI is achieving rapid time to treatment and increasing patient access to this preferred reperfusion strategy. The clinical challenge in patients treated with fibrinolytic therapy is deciding for whom and when to perform coronary angiography.
In unstable patients (eg, severe heart failure or cardiogenic shock, hemodynamically compromising ventricular arrhythmias) not treated initially with primary PCI, a strategy of immediate coronary angiography with intent to perform PCI is implemented unless invasive management is considered futile or unsuitable given the clinical circumstances.383,384
In stable patients treated with fibrinolytic therapy and clinical suspicion of reperfusion failure, a strategy of immediate coronary angiography followed by PCI improves outcome in those at high risk.385,386 Such a strategy is also implemented in patients with evidence for infarct artery reocclusion (Table 9). The clinical diagnosis of failed fibrinolysis is difficult but is best made when there is <50% ST-segment resolution 90 minutes after initiation of therapy in the lead showing the greatest degree of ST-segment elevation at presentation. Given the association between bleeding events and adverse cardiac events, a reasonable approach is to select moderate- and high-risk patients for PCI and treat low-risk patients with medical therapy. ECG and clinical findings of anterior MI or inferior MI with right ventricular involvement or precordial ST-segment depression, as well as ongoing pain, usually predicts increased risk and the greatest potential benefit.392 Conversely, patients with symptom resolution, improving ST-segment elevation, or inferior MI localized to 3 ECG leads probably gain little benefit.
In stable patients treated with fibrinolytic therapy and clinical evidence for successful reperfusion, an early invasive strategy with cardiac catheterization performed within 24 hours decreases reinfarction and recurrent ischemic events.388,390,391 Because of the associated increased bleeding risk, very early (<2 to 3 hours) catheterization after administration of fibrinolytic therapy with intent to perform revascularization should be reserved for patients with evidence of failed fibrinolysis and significant myocardial jeopardy for whom immediate angiography and revascularization would be appropriate.393
184.108.40.206. Primary PCI of the Infarct Artery: Recommendations
Class III: HARM
Primary PCI is preferred to fibrinolytic therapy when time-to-treatment delays are short and the patient presents to a high-volume, well-equipped center staffed with expert interventional cardiologists and skilled support staff. Compared with fibrinolytic therapy in RCTs, primary PCI produces higher rates for infarct artery patency, TIMI flow grade 3, and lower rates for recurrent ischemia, reinfarction, emergency repeat revascularization procedures, intracranial hemorrhage, and death.379 Early, successful PCI also greatly decreases the complications of STEMI that result from longer ischemic times or unsuccessful fibrinolytic therapy, allowing earlier hospital discharge and resumption of daily activities. The greatest mortality benefit of primary PCI is in high-risk patients. PCI outcomes may not be as successful with prolonged time-to-treatment or low-volume hospitals and operators (Table 10).
Several reports have shown excellent outcomes for patients with STEMI undergoing interhospital transfer where first medical contact–to-door balloon time modestly exceeded the systematic goal of <90 minutes.396–398,409 In these reports, the referring hospital and the receiving hospital established a transfer protocol that minimized transfer delays, and outcomes were similar to those of direct-admission patients. On the basis of these results, the PCI and STEMI guideline writing committees have modified the first medical contact–to-device time goal from 90 minutes to 120 minutes for interhospital transfer patients,397 while emphasizing that systems should continue to strive for times ≤90 minutes. Hospitals that cannot meet these criteria should use fibrinolytic therapy as their primary reperfusion strategy.
PCI of a noninfarct artery at the time of primary PCI in stable patients is associated with worse clinical outcomes unless the patient is in cardiogenic shock where PCI of a severe stenosis in a coronary artery supplying a large territory of myocardium might improve hemodynamic stability.404,406,408 Delayed PCI can be performed in noninfarct arteries at a later time if clinically indicated.410–412
220.127.116.11. Delayed or Elective PCI in Patients With STEMI: Recommendations
Class III: NO BENEFIT
Studies and meta-analyses suggest potential benefit for PCI in fibrinolytic failure.385,386 In stable patients treated with fibrinolytic therapy and clinical evidence for successful reperfusion, an early invasive strategy with cardiac catheterization performed within 24 hours decreases reinfarction and recurrent ischemic events.388,390,391
PCI for a hemodynamically significant stenosis in a patent infarct artery >24 hours after STEMI as part of a revascularization strategy improves outcome.410,411,413–417 PCI of an occluded infarct artery 1 to 28 days after MI in asymptomatic patients without evidence of myocardial ischemia has no incremental benefit beyond optimal medical therapy with aspirin, beta blockers, angiotensin-converting enzyme inhibitors, and statins in preserving LV function and preventing subsequent cardiovascular events.418–420 It is important to note that elective PCI of an occluded infarct artery has not been studied in patients with New York Heart Association functional class III or IV heart failure, rest angina, serum creatinine >2.5 mg/dL, left main or 3-vessel CAD, clinical instability, or severe inducible ischemia on stress testing in an infarct zone that is not akinetic or dyskinetic.
5.2.3. Cardiogenic Shock: Recommendations
See Online Data Supplement 22 for additional data regarding cardiogenic shock.
Cardiogenic shock is the leading cause of in-hospital mortality complicating STEMI. Revascularization is the only treatment proven to decrease mortality rates.384,421–423 Although revascularization is almost always accomplished through PCI, selected patients with severe 3-vessel or left main disease can benefit from emergency CABG. Revascularization attempts may be futile and not indicated in cases of severe multiorgan failure.427 Patient selection for revascularization is more important in the elderly, but several observational reports demonstrate acceptable outcomes in patients with few comorbidities and a reasonable potential for survival.428–431 Patients who present to hospitals without PCI capability are usually emergently transported to a PCI center, because mortality without transfer is markedly elevated.432
18.104.22.168. Procedural Considerations for Cardiogenic Shock
Patients with cardiogenic shock should receive standard pharmacological therapies, including aspirin, a P2Y12 receptor antagonist, and anticoagulation.427,433 Inotropic and vasopressor therapy improves perfusion pressure. Historically, negative inotropes and vasodilators are avoided. IV GP IIb/IIIa inhibitors have been shown to provide benefit in observational studies but not in 1 small RCT.433
Endotracheal intubation and mechanical ventilation with positive end-expiratory pressure is usually necessary in patients with respiratory failure. Placement of a temporary pacemaker is indicated for patients with bradycardia or high-degree atrioventricular heart block. A pulmonary artery catheter can provide information to dose and titrate inotropes and pressors. Further hemodynamic support is available with IABP counterpulsation or percutaneous LV assist devices, although no data support a reduction in mortality rates.434
Contrast medium injections should be minimized. Orthogonal angiograms of the left coronary artery and a left anterior oblique angiogram of the right coronary artery are usually sufficient to identify the infarct artery.435 Although most patients undergoing revascularization will receive a stent as part of the procedure, there are conflicting data on the impact of stenting over balloon angioplasty. Some studies reveal lower mortality rates,436–438 whereas others reveal no benefit439 or higher mortality rates.440 There are no data comparing the choice of BMS versus DES in cardiogenic shock; however, BMS are often used because compliance with long-term DAPT is often unclear in the emergency setting.
In patients with multivessel disease, revascularization of the noninfarct artery may be necessary to maximize myocardial perfusion. Alternatively, in patients with multivessel disease and particularly left main disease, emergency CABG as a primary reperfusion strategy may be preferred.50,441 Refractory cardiogenic shock unresponsive to revascularization may necessitate institution of more intensive cardiac support with a ventricular assist device or other hemodynamic support devices to allow for myocardial recovery or subsequent cardiac transplantation in suitable patients.
5.2.4. Revascularization Before Noncardiac Surgery: Recommendations
Class III: HARM
The 2007 and 2009 ACC/AHA Guidelines on Perioperative Cardiovascular Evaluation and Care for Noncardiac Surgery gave detailed recommendations for the evaluation of patients undergoing noncardiac surgery.444 Patients with evidence of ACS should receive standard therapy, including early revascularization, to minimize the risk of adverse events. Patients with known significant left main or 3-vessel CAD who would otherwise benefit from revascularization in terms of survival or symptomatic relief also generally undergo revascularization before elective noncardiac surgery.
Two RCTs449,450 found no benefit with routine preoperative revascularization before noncardiac surgery. Noncardiac surgery early after coronary stenting, particularly in the first 4 weeks, is associated with a high risk of stent thrombosis and death.444,446,448 When emergency surgery is necessary, the patient should proceed to surgery without prior PCI. When surgery is required within 30 days and coronary revascularization is required before surgery, many clinicians perform balloon angioplasty alone to avoid the need for DAPT. In situations where preoperative revascularization is required and surgery can be deferred for at least 30 days, many clinicians use BMS and discontinue DAPT after 30 days. If surgery is elective and can be deferred for 1 year, most clinicians would consider DES to reduce the long-term risk of restenosis. A dilemma occurs when a patient has undergone PCI and then unexpectedly requires noncardiac surgery. Many patients can undergo surgery on DAPT, where the risk-benefit ratio will favor continued dual antiplatelet inhibition. If it is necessary to hold P2Y12 inhibitor therapy, most clinicians will still continue aspirin uninterrupted during the perioperative period if the bleeding risk is not prohibitive. When the risk of delaying surgery or performing surgery while the patient is on DAPT exceeds the risk of stent thrombosis from stopping DAPT, the P2Y12 inhibitor is stopped before surgery and resumed as soon as possible afterward. No P2Y12 inhibitor “bridging” strategy (eg, GP IIb/IIIa inhibitor, antithrombin therapy) has been validated.
5.3. Coronary Stents: Recommendations
Class III: HARM
Coronary stent implantation is commonly performed during PCI to prevent recoil, abrupt closure, and late restenosis.463,464 BMS are composed of either stainless steel or cobalt chromium alloys. Because the risk of stent thrombosis is greatest within the first 30 days after implantation, the use of DAPT is required for 30 days after implantation of BMS.208
In the United States, 4 types of DES are currently approved: sirolimus-eluting stents, paclitaxel-eluting stents, zotarolimus-eluting stents, and everolimus-eluting stents. DES vary according to stent scaffold material and design, drug content, and the polymer used for drug elution; however, several common clinical features are present. First, sirolimus-eluting stents, paclitaxel-eluting stents, and zotarolimus-eluting stents have been demonstrated in RCTs to be associated with a reduced need for repeat revascularization and no increase in death or MI compared with BMS at 4 years' follow-up.465 Everolimus-eluting stents have been demonstrated in RCTs to be associated with a lower need for repeat revascularization than paclitaxel-eluting stents, and, by inference, a lower risk for repeat revascularization than BMS,466,467 with no increase in death or MI at 2-year follow-up.468 Second, each of these stents is presumed to be associated with delayed healing based on pathologic studies and longer periods of risk for thrombosis compared with BMS and require longer duration of DAPT.469 In the RCTs that led to the US Food and Drug Administration (FDA) approval of these stents, the recommended minimum duration of DAPT therapy was 3 to 6 months. Recently, the consensus of clinical practice has been 12 months of DAPT following DES implantation to avoid late (after 30 days) thrombosis,208 based on observational studies of paclitaxel-eluting stents and sirolimus-eluting stents that indicate lower risk of late stent thrombosis with >6 months of therapy.212 Extending DAPT beyond 1 year is considered reasonable by some practitioners based on observational data analysis,212 but RCTs to determine whether longer DAPT is associated with reduction in stent thrombosis risk have not been completed. Finally, DES therapy is more expensive than BMS. Cost-effectiveness analysis has shown a reduction in total cost associated with DES because of avoidance of repeat procedures, yet it may be reasonable to consider use of BMS in patient subsets in which the risk of restenosis is low.470
This risk-benefit profile is most favorable for DES over BMS when the risk of restenosis with BMS is high (Table 11). Pooled and meta-analyses have demonstrated that in patients with diabetes, use of DES decreases the risk of restenosis compared with BMS.471,472 DES may be more appealing for unprotected left main PCI, given the rate and clinical consequences of restenosis in this location.473–475 The risk of stent thrombosis is higher in populations or lesion types excluded from RCTs of DES (eg, STEMI, smaller arteries [<2.5 mm diameter], longer lesions, bifurcations).210,465 Importantly, these features also predict both stent thrombosis476 and restenosis in BMS.477 The greatest risk of stent thrombosis is within the first year, ranging from 0.7% to 2.0%, depending on patient and lesion complexity. Late stent thrombosis risk after 1 year with DES is observed at a rate of 0.2% to 0.4% per year.210,478
|DES Generally Preferred Over BMS (Efficacy Considerations)||BMS Preferred Over DES (Safety Considerations)|
Compared with balloon angioplasty, routine BMS implantation during primary PCI decreases risk for target-vessel revascularization and possibly reduces MI rates but does not reduce mortality rates.479 More recent primary PCI studies and meta-analyses have demonstrated lower restenosis rates without increased risk of adverse stent outcome with DES compared with BMS. Although stent thrombosis rates in trials of STEMI are higher than in trials of elective PCI, the rates of stent thrombosis are not higher with DES compared with BMS in STEMI.453,456–459
The greatest risk for DES thrombosis is early discontinuation of DAPT.208,460–462 It is therefore important to determine that the patient will likely be able to tolerate and comply with DAPT before implantation of DES. Therefore, DES should not be used in the presence of financial barriers to continuing prolonged DAPT, social barriers that may limit patient compliance, or medical issues involving bleeding risks or the need for invasive or surgical procedures in the following year that would interrupt antiplatelet therapy. The need for use of long-term warfarin and the associated increased risk of bleeding with long-term “triple therapy” is also a consideration in deciding on DES versus BMS.480
Patients implanted with most contemporary coronary stents can undergo magnetic resonance imaging (MRI) examination any time after implantation.481,482 The effect of the MRI examination on heating of the drug or polymer coating used in DES is unknown. There is no indication for antibiotic prophylaxis before dental or invasive procedures in patients with coronary stents.483
5.4. Adjunctive Diagnostic Devices
5.4.1. FFR: Recommendation
See Online Data Supplement 23 for additional data regarding FFR.
The limitations of coronary angiography for determination of lesion severity have been well described. Angiography may under- or overestimate lesion stenosis. Various physiologic measurements can be made in the catheterization laboratory, including coronary flow reserve and FFR. The correlation of ischemia on stress testing with FFR values of <0.75 has been established in numerous comparative studies with high sensitivity (88%), specificity (100%), positive predictive value (100%), and overall accuracy (93%).487 The 5-year outcomes for patients with medical therapy based on an FFR >0.75 were superior compared with PCI in the DEFER (Deferral Versus Performance of Balloon Angioplasty in Patients Without Documented Ischemia) study.485 The FAME (Fractional Flow Reserve Versus Angiography for Multivessel Evaluation) study identified the benefit for deferring PCI in patients with multivessel disease and lesion FFR >0.80, with reduced rates of cardiac events at both 1 and 2 years.97,486 Whereas both FFR and IVUS have been used for assessment of intermediate angiographic stenosis with favorable outcomes, FFR may reduce the need for revascularization when compared with IVUS.488 Although IVUS is often considered in the assessment of equivocal left main stenosis, FFR may be similarly effective.484
5.4.2. IVUS: Recommendations
Class III: NO BENEFIT
IVUS provides a unique coronary artery assessment of lesion characteristics, minimal and maximal lumen diameters, cross-sectional area, and plaque area. Diagnostic uses for IVUS include the assessment of angiographic indeterminant coronary artery stenoses, determination of the mechanism of stent restenosis or thrombosis, and postcardiac transplantation surveillance of CAD.488,490–492,499 For left main coronary artery stenoses, a minimal lumen diameter of <2.8 mm or a minimal lumen area of <6 mm2 suggests a physiologically significant lesion for which patients may benefit from revascularization. A minimal lumen area >7.5 mm2 suggests that revascularization may be safely deferred.490 A minimal lumen area between 6 and 7.5 mm2 requires further physiological assessment, such as measurement of FFR.487,500 For non–left main stenoses, minimal lumen diameter >2.0 mm and minimal lumen area >4.0 mm2 correlate with low event rates.489 However, in smaller-diameter arteries (minimal lumen area <3.0 mm2), measurement of FFR may more accurately reflect a significant stenosis.488 Studies correlating IVUS measures with ischemia have not specified the size of coronary arteries for which such correlations are valid.488,489,497
IVUS assessment after stent thrombosis may serve to identify stent underexpansion or malapposition.499 IVUS is superior to angiography in the early detection of the diffuse, immune-mediated, cardiac allograft vasculopathy; recommendations about the use of IVUS for this purpose were published in 2010 by the International Society of Heart and Lung Transplantation.492 Whereas IVUS has been an important research tool in interventional cardiology, most clinical studies of IVUS have not been able to demonstrate that its routine use results in a reduction of MACE or restenosis rates.498,501,502 IVUS has been inappropriately used in clinical practice to justify implanting stents in mildly diseased segments that may require no intervention.503
5.4.3. Optical Coherence Tomography
Compared with IVUS, optical coherence tomography has greater resolution (10 to 20 micronmeter axially) but more limited depth of imaging (1 to 1.5 mm).504,505 Unlike IVUS, optical coherence tomography requires that the artery be perfused with saline solution or crystalloid during image acquisition and therefore does not permit imaging of ostial lesions. Clinical studies have shown low optical coherence tomography complication rates,506,507 similar to those of IVUS.508 The excellent resolution of optical coherence tomography permits detailed in vivo 2-dimensional imaging of plaque morphological characteristics (eg, calcification, lipid, thrombus, fibrous cap thickness, and plaque ulceration or rupture)508–510 and evaluation of the arterial response to stent implantation (eg, stent strut neointimal thickness and apposition)511–513 and may be of value in clinical research. The appropriate role for optical coherence tomography in routine clinical decision making has not been established.
5.5. Adjunctive Therapeutic Devices
5.5.1. Coronary Atherectomy: Recommendations
Class III: NO BENEFIT
Rotational atherectomy in RCTs was associated with higher rates of MACE at 30 days and no reduction in restenosis. It has a limited role in facilitating the dilation or stenting of lesions that cannot be crossed or expanded with PCI.520,521 Devices for directional coronary atherectomy are no longer marketed in the United States.
5.5.2. Thrombectomy: Recommendation
The benefit of thrombectomy in patients with STEMI appears to be dependent on the type of thrombectomy technique used.522–526 No clinical benefit for routine rheolytic thrombectomy (AngioJet device, MEDRAD Interventional, Minneapolis, MN and Pittsburgh, PA) has been demonstrated in primary PCI.524–526 Two RCTs522,523 and a meta-analysis524 support the use of manual aspiration thrombectomy during primary PCI to improve microvascular reperfusion and decrease MACE. It is not known whether a strategy of selective thrombus aspiration in patients with a large thrombus burden might be equivalent to routine thrombus aspiration.
5.5.3. Laser Angioplasty: Recommendations
Class III: NO BENEFIT
RCTs of laser angioplasty have not demonstrated improved clinical or angiographic PCI outcomes, although some practitioners think that laser angioplasty may be of use in the treatment of lesions that are difficult to dilate with balloon angioplasty.527
5.5.4. Cutting Balloon Angioplasty: Recommendations
Class III: NO BENEFIT
Although some small, single-center trials have suggested that cutting balloon angioplasty was more efficacious than balloon angioplasty, it was not found to be safer or more effective in several large trials.516,529,531 When balloon dilation is required for in-stent restenosis, however, cutting balloons are less likely to slip and may offer a technical advantage over conventional balloons.529 Scoring balloons have been used by some cardiologists as an alternative to cutting balloons, but no RCTs have been reported.531
5.5.5. Embolic Protection Devices: Recommendation
The incidence of MACE doubles in SVG PCI compared with native-artery PCI.536 A distal balloon occlusion EPD decreased the 30-day composite outcome of death, MI, emergency CABG, or target-lesion revascularization (9.6% versus 16.5%) in the only RCT.532 Subsequent noninferiority comparisons have demonstrated similar benefit with proximal occlusion and distal filter EPDs, with benefit limited to reduction in periprocedural MI534,535 (Section 5.10). Distal EPDs do not improve survival or reinfarction rates in patients undergoing native-artery PCI.524,537
5.6. Percutaneous Hemodynamic Support Devices: Recommendation
IABP counterpulsation is frequently used as an adjunct to PCI in hemodynamically unstable patients.538,539 In single-center series, the routine prophylactic use of IABP during PCI in high-risk patients was associated with lower mortality and fewer major complications compared with rescue use of IABP.540,541 In the only RCT in high-risk PCI patients (BCIS-1 [Balloon Pump-Assisted Coronary Intervention Study]),542 there was no difference in the primary composite outcome between routine and provisional use of IABP. There were also no differences in major secondary endpoints except major procedural complications (eg, prolonged hypotension, ventricular tachycardia/fibrillation, cardiopulmonary arrest), which were lower in the routine IABP group. Bleeding and access site complication rates tended to be higher in the routine IABP group. The “bailout” rate of IABP insertion in the provisional IABP group was 12%, mostly for procedural hypotension.542 A meta-analysis of IABP therapy in patients with STEMI did not show improved outcomes with the use of IABP.434
The Impella Recover LP 2.5 System (Abiomed, Aachen, Germany/Danvers, Massachusetts) is a 12.5 Fr catheter that is inserted percutaneously through a 13 Fr femoral artery sheath and placed across the aortic valve into the left ventricle, through which a transaxial blood pump provides flows of up to 2.5 L/min. This has been used in patients with cardiogenic shock543,544 as well as elective PCI.545 The hemodynamic effects of the Impella 2.5 have been studied in high-risk PCI patients, demonstrating beneficial LV unloading effect (decreased end-diastolic pressure and wall stress) with no change in global or systolic LV function.546 The PROTECT I (A Prospective Feasibility Trial Investigating the Use of the IMPELLA Recover LP 2.5 System in Patients Undergoing High-Risk PCI) trial in 20 patients undergoing high-risk PCI with the Impella 2.5 system concluded that this device was safe, easy to implant, and hemodynamically effective.547 The Europella Registry included 144 patients undergoing high-risk PCI and reported the safety, feasibility, and potential usefulness of the device and that RCTs were warranted.548 The randomized PROTECT II (A Prospective, Multicenter, Randomized Controlled Trial of the IMPELLA Recover LP 2.5 System Versus Intra Aortic Balloon Pump in Patients Undergoing Non Emergent High Risk PCI) trial, which was designed to demonstrate superiority of Impella over IABP in terms of 1-month adverse events, was halted for futility after interim analysis of study results.549
The TandemHeart (CardiacAssist, Inc, Pittsburgh, PA) is a left atrial to aorta catheter-based system that includes a centrifugal blood pump providing flows of up to 4 L/min. This device uses a 21 Fr cannula percutaneously inserted into the femoral vein for transseptal access of the left atrium with a 15 Fr catheter placed in the contralateral femoral artery and positioned above the aortic bifurcation. An extracorporeal pump then returns oxygenated blood from the left atrium to the arterial system, thereby unloading the left ventricle.550,551 The hemodynamic effects have been studied in patients undergoing high-risk PCI.552 Several small studies have addressed the clinical efficacy of the TandemHeart in high-risk patients undergoing PCI.551,553–556 In a single-center report of 68 patients undergoing high-risk PCI using either TandemHeart or Impella Recover 2.5, success rates (>90%) and vascular complications (7%) were similar.553
High-risk patients may include those undergoing unprotected left main or last-remaining-conduit PCI, those with severely depressed EF undergoing PCI of a vessel supplying a large territory, and/or those with cardiogenic shock. Patient risk, hemodynamic support, ease of application/removal, and operator and laboratory expertise are all factors involved in consideration of use of these devices. With devices that require large cannula insertion, the risk of vascular injury and related complications are important considerations regarding necessity and choice of device.
5.7. Interventional Pharmacotherapy
5.7.1. Procedural Sedation
The term conscious sedation is falling out of favor with the recognition that there is a spectrum of procedural sedation levels. Most patients undergoing PCI fall under the definition of either minimal sedation (anxiolysis) or moderate sedation (depressed consciousness with the ability to respond purposefully to verbal commands).557 Nonetheless, an underlying principle of procedural sedation is that the physician should be prepared to manage one level of sedation deeper than the level intended. Thus, cardiologists should be cognizant of the principles of managing deep sedation (depressed consciousness without easy arousal that may require assistance in maintaining airway patency or spontaneous ventilation).
A full review of procedural sedation is beyond the scope of this document, but practice guidelines for sedation and analgesia by nonanesthesiologists, along with The Joint Commission standards, provides a reasonable framework. These guidelines outline several general principles.558,559 Before the procedure the patient should be assessed for predictors of difficult intubation or a history of prior difficult intubation. The patient should be monitored by someone dedicated to observing the level and effects of sedation. Level of consciousness, respiratory rate, blood pressure, cardiac rhythm, and oxygen saturation by pulse oximetry should be monitored. Available equipment should include a high-flow oxygen source, suction, airway management equipment, a defibrillator, resuscitation drugs, and reversal agents appropriate for the drugs being used. A free-flowing IV line should be established. Supplemental oxygen is usually administered, even in the absence of preexisting hypoxia, to provide a margin of safety.
Agents used for sedation are best given in incremental doses, allowing adequate time for the development and assessment of peak effect. The most commonly used agents are listed in Appendix 4F.
5.7.2. Oral Antiplatelet Therapy: Recommendations
Class III: HARM
Aspirin reduces the frequency of ischemic complications after PCI. Although the minimum effective aspirin dosage in the setting of PCI has not been established, aspirin 325 mg given at least 2 hours, and preferably 24 hours, before PCI is recommended,302,303 after which aspirin 81 mg daily should be continued indefinitely.
Several investigations have explored various loading doses of clopidogrel before or during PCI. Compared with a 300-mg loading dose, doses of either 600 mg or 900 mg achieve greater degrees of platelet inhibition with fewer low responders.577 A meta-analysis of 7 studies that included 25,383 patients undergoing PCI demonstrated that intensified loading of clopidogrel with 600 mg reduces the rate of MACE without an increase in major bleeding compared with 300 mg.578 Another study suggested that a 600-mg loading dose of clopidogrel is associated with improvements in procedural angiographic endpoints and 1-year clinical outcomes in patients with STEMI who undergo primary PCI compared with a 300-mg dose.579 There is no benefit with increasing the loading dose to 900 mg compared with 600 mg.577 Clopidogrel 75 mg daily should be given for a minimum of 4 weeks after balloon angioplasty or BMS implantation (a minimum of 2 weeks if increased bleeding risk is present)580 and for at least 12 months after DES implantation (unless the risk of bleeding outweighs the anticipated benefit). Patients should be counseled on the need for and risks of DAPT before stent implantation, especially DES implantation, and alternative therapies pursued (BMS or balloon angioplasty) if they are unwilling or unable to comply with the recommended duration of DAPT.
The efficacy of clopidogrel pretreatment remains controversial. Although some studies have suggested that pretreatment with clopidogrel is associated with decreased platelet aggregation and a significantly lower incidence of periprocedural MI after elective PCI, others have suggested no benefit to pretreatment compared with administration of the drug in the catheterization laboratory.572,581,582
When prasugrel was compared with clopidogrel in patients with ACS in TRITON–TIMI 38 (Trial to Assess Improvement in Therapeutic Outcomes by Optimizing Platelet Inhibition with Prasugrel–Thrombolysis In Myocardial Infarction), prasugrel was associated with a significant 2.2% reduction in absolute risk and a 19% reduction in relative risk in the composite endpoint of cardiovascular death, nonfatal MI, or nonfatal stroke, and a significant increase in the rate of TIMI major hemorrhage (1.8% versus 2.4%).567 Prasugrel is contraindicated in patients with a history of transient ischemic attack or stroke. Patients weighing <60 kg have an increased risk of bleeding on the 10 mg daily maintenance dose. The package insert suggests that consideration should be given to lowering the maintenance dose to 5 mg daily, although the effectiveness and safety of the 5-mg dose has not been studied. Prasugrel is not recommended for patients >75 years of age because of the increased risk of fatal and intracranial bleeding and lack of benefit, except in patients with diabetes or a history of prior MI. Prasugrel should not be started in patients likely to undergo urgent CABG. Prasugrel has not been studied in elective PCI, and thus no recommendation can be made regarding its use in this clinical setting.
Ticagrelor reversibly binds the P2Y12 receptor. Unlike clopidogrel or prasugrel, ticagrelor is not a thienopyridine. It also does not require metabolic conversion to an active metabolite. Compared with clopidogrel in patients with ACS in the PLATO (Platelet Inhibition and Patient Outcomes) trial, ticagrelor was associated with a significant 1.9% reduction in absolute risk and a 16% reduction in relative risk in the primary composite endpoint of vascular death, nonfatal MI, or nonfatal stroke.568 Importantly, a significant reduction in vascular mortality and all-cause mortality was observed. Although CABG-related bleeding was not significantly increased with ticagrelor compared with clopidogrel, a significantly greater incidence of major bleeding was observed in patients not undergoing CABG. Ticagrelor was associated with higher rates of transient dyspnea and bradycardia compared with clopidogrel, although only a very small percentage of patients discontinued the study drug because of dyspnea. Based on post hoc analysis of the PLATO study, specifically the results in the US patient cohort, a black box warning states that maintenance doses of aspirin above 100 mg reduce the effectiveness of ticagrelor and should be avoided. After any initial dose, ticagrelor should be used with aspirin 75 mg to 100 mg per day.583 Given the twice-daily dosing and reversible nature of the drug, patient compliance may be a particularly important issue to consider and emphasize. Ticagrelor has not been studied in elective PCI or in patients who received fibrinolytic therapy; thus, no recommendations about its use in these clinical settings can be made.
5.7.3. IV Antiplatelet Therapy: Recommendations
Class III: NO BENEFIT
See Online Data Supplement 24 for additional data regarding IV antiplatelet therapy.
In the era before DAPT, trials of adequately dosed GP IIb/IIIa inhibitors in patients undergoing balloon angioplasty and coronary stent implantation demonstrated a reduction in the incidence of composite ischemic events with GP IIb/IIIa treatment, primarily through a reduction of enzymatically defined MI.613,615,618,620,621 Earlier RCTs of GP IIb/IIIa inhibitors were generally conducted in patients treated with UFH. In some trials, use of GP IIb/IIIa inhibitors are associated with some increased bleeding risk, and trials of these agents have generally excluded patients at high risk of bleeding (eg, coagulopathy).584,587–589,613–618,620–626 Thus, recommendations about use of GP IIb/IIIa inhibitors are best construed as applying to those patients not at high risk of bleeding complications. Abciximab, double-bolus eptifibatide (180 mcg/kg bolus followed 10 minutes later by a second 180 mcg/kg bolus), and high-bolus dose tirofiban (25 mcg/kg) all result in a high degree of platelet inhibition,627–629 have been demonstrated to reduce ischemic complications in patients undergoing PCI,608,609,613,615,618–621 and appear to lead to comparable angiographic and clinical outcomes.630,631
Trials of GP IIb/IIIa inhibitors in the setting of STEMI and primary PCI were conducted in the era before routine stenting and DAPT. The results of these and more recent trials, as well as several meta-analyses, have yielded mixed results.584–590 Therefore, it is reasonable to administer GP IIb/IIIa inhibitors in patients with STEMI undergoing PCI, although these agents cannot be definitively recommended as routine therapy. These agents might provide more benefit in selective use, such as in patients with large anterior MI and/or large thrombus burden. Trials of precatheterization laboratory (eg, ambulance or emergency room) administered GP IIb/IIIa inhibitors in patients with STEMI undergoing PCI, with or without fibrinolytic therapy, have generally shown no clinical benefit, and GP IIb/IIIa inhibitor use in this setting may be associated with an increased risk of bleeding.605–610,612 Studies of intracoronary GP IIb/IIIa inhibitor administration (predominantly using abciximab) consist of several small RCTs, retrospective analyses, retrospective and prospective registries, cohort analyses, and case reports. Although most of these published studies have reported some benefit of intracoronary administration in terms of acute angiographic parameters, infarct size, left ventricle myocardial salvage, and composite clinical endpoints, several other studies have not detected any benefit with intracoronary administration.589,591–604
Trials of GP IIb/IIIa inhibitors in patients with UA/NSTEMI undergoing PCI demonstrated reduced ischemic outcomes, particularly in those with high-risk features such as positive biomarkers. Most trials were conducted in a prior PCI era and without P2Y12 inhibitor pretreatment,613,615,618,632,633 although several trials have also demonstrated benefit in patients with high-risk features pretreated with clopidogrel.616,619 In most older studies of stable patients undergoing balloon angioplasty or coronary stenting, treatment with GP IIb/IIIa inhibitors resulted in a reduction of composite ischemic events, primarily enzymatically defined MI.613–618,620,621,634,635 More contemporary trials of patients pretreated with a thienopyridine have not demonstrated any benefit with GP IIb/IIIa inhibitor therapy in patients with stable symptoms undergoing elective PCI.619,622–624
5.7.4. Anticoagulant Therapy
22.214.171.124. Use of Parenteral Anticoagulants During PCI: Recommendation
Anticoagulant therapy prevents thrombus formation at the site of arterial injury, on the coronary guidewire, and in the catheters used for PCI.8 With rare exceptions,636 all PCI studies have used some form of anticoagulant. It is the consensus of the writing committee that PCI be performed with the use of some form of anticoagulant therapy. Suggested dosing regimens of parenteral agents used in PCI are given in Table 12. Recommendations for antiplatelet and antithrombin pharmacotherapy in PCI are given in Table 13.
|Drug||Patient Has Received Prior Anticoagulant Therapy||Patient Has Not Received Prior Anticoagulant Therapy|
|Enoxaparin||0.5 to 0.75 mg/kg IV bolus|
|Bivalirudin||For patients who have received UFH, wait 30 min, then give 0.75 mg/kg IV bolus, then 1.75 mg/kg per h IV infusion.||0.75 mg/kg bolus, 1.75 mg/kg per h IV infusion|
|Fondaparinux||For prior treatment with fondaparinux, administer additional IV treatment with an anticoagulant possessing anti-IIa activity, taking into account whether GPI receptor antagonists have been administered.||N/A|
|Argatroban||200 mcg/kg IV bolus, then 15 mcg/kg per min IV infusion||350 mcg/kg bolus, then 15 mcg/kg per min IV infusion|
126.96.36.199. UFH: Recommendation
As the only anticoagulant available for PCI for many years, UFH became the standard of care by default.8 The dose of UFH for PCI has been based on empiricism and experience from RCTs. Suggested UFH dosing regimens are given in Table 12. When UFH is used during PCI, most cardiologists assess the degree of anticoagulation by measuring the activated clotting time. Although measurements are useful to show that an anti-IIa anticoagulant has been given, the value of the activated clotting time in current practice has been questioned. Although studies in the balloon angioplasty era did demonstrate a relationship between activated clotting time levels and ischemic complications,653–655 more recent analyses from the coronary stent era have not found a clear relationship between activated clotting time and outcomes.349,656,657 There may, however, be a modest relation between bleeding and activated clotting time levels.349,657 In addition, not only are there differences between activated clotting time levels measured by Hemochron and HemoTec devices, but both devices have less than optimal precision.658 Thus, although traditional target activated clotting time levels are included in this document, the utility of measured activated clotting time levels in current practice should be considered uncertain.
Most cardiologists remove femoral sheaths when the activated clotting time falls to <150 to 180 seconds or when the activated partial thromboplastin time falls to <50 seconds. Full-dose anticoagulation is no longer used after successful PCI procedures. Almost all large clinical trials have enrolled patients who underwent transfemoral PCI, but recent small studies assessing the transradial approach have used similar doses of UFH659 and similar activated clotting time target levels.660
188.8.131.52. Enoxaparin: Recommendations
Class III: HARM
Trials of enoxaparin relevant to PCI include both studies in which patients with UA/NSTEMI were started on upstream subcutaneous enoxaparin therapy that was continued up to the time of PCI and trials in which patients who had received no prior antithrombin therapy were treated with IV enoxaparin at the time of PCI.646–650,661–663,666 In the SYNERGY (Superior Yield of the New strategy of Enoxaparin, Revascularization and Glycoprotein IIb/IIIa Inhibitors) trial, there was an increased incidence of bleeding in those treated with upstream enoxaparin, later attributed at least in part to the fact that some patients being treated with enoxaparin were also administered UFH at the time of PCI (so-called “stacking”).649,665 Almost all patients undergoing elective PCI who are administered enoxaparin (0.5 mg/kg IV) will have a peak anti-Xa level >0.5 IU/mL.647 Most clinical studies have used a regimen of 0.5 to 0.75 mg IV.667 Several studies have used this regimen in elective patients and those with STEMI.646 Patients who have received multiple doses of subcutaneously administered enoxaparin who undergo PCI within 8 hours of the last subcutaneous dose generally have adequate degrees of anticoagulation to undergo PCI, but the degree of anticoagulation may diminish in the 8- to 12-hour period after the last subcutaneous dose. In such patients, as well as in patients who have received only 1 subcutaneous dose of enoxaparin, the addition of enoxaparin (0.3 mg/kg IV) at the time of PCI provides an additional degree of anticoagulation and has become standard practice.648,661–664 Patients who undergo PCI >12 hours after the last subcutaneous dose are usually treated with full-dose de novo anticoagulation using an established regimen (eg, full-dose UFH or bivalirudin).
184.108.40.206. Bivalirudin and Argatroban: Recommendations
Bivalirudin is being increasingly used in clinical practice670 as evidence emerges from clinical trials across the spectrum of CAD.638–644 In individual trials and meta-analyses, the use of bivalirudin has been associated with reduced bleeding compared with UFH plus a GP IIb/IIIa inhibitor, although concerns about ischemic events have emerged in individual studies.625,637–645 Longer-term follow-up of the major bivalirudin trials, however, suggests that small or nominal increases in ischemic events have not translated into long-term consequences and that treatment at or before the time of PCI with clopidogrel may mitigate any increased early ischemic risk.637–645 Thus, a treatment strategy of bivalirudin compared with heparin (or enoxaparin) plus GP IIb/IIIa inhibitor appears to lower the risk of bleeding complications. The lower bleeding rates associated with bivalirudin (compared with UFH plus a GP IIb/IIIa inhibitor) are mitigated when used concomitantly with a GP IIb/IIIa inhibitor.639 A strategy of use of provisional GP IIb/IIIa inhibitor in patients treated with bivalirudin is widely accepted.639,639,644
In patients with heparin-induced thrombocytopenia,671,672 a direct-thrombin inhibitor (argatroban) has been approved as an alternative parenteral anticoagulant to be used during PCI.668 The use of bivalirudin for heparin-induced thrombocytopenia has been reported as well.669
220.127.116.11. Fondaparinux: Recommendation
Class III: HARM
Fondaparinux, a pentasaccharide, is an indirect factor Xa inhibitor but has no effect on thrombin. On the basis of reports of catheter thrombosis when fondaparinux is used alone during primary PCI,651,652 the writing committee recommends that an anticoagulant with anti-IIa activity be used in patients undergoing PCI.651,652 One study suggested that clinical outcomes were better when fondaparinux was replaced during PCI by a standard dose of UFH (85 U/kg, 60 U/kg with GP IIb/IIIa inhibitors) rather than by a low dose (50 U/kg).673
5.7.5. No-Reflow Pharmacological Therapies: Recommendation
See Online Data Supplement 25 for additional data regarding no-reflow therapies.
No-reflow is a broad term used to describe 2 distinct entities. The first is “interventional no-reflow” attributed to vasospasm and downstream embolization of debris dislodged during PCI, usually in the setting of atherectomy, thrombus, or degenerated SVGs. The second entity is suboptimal reperfusion of an infarct artery, attributed to endothelial injury in addition to embolization and vasospasm. Angiographic no-reflow is the most obvious sequela of the same pathophysiology that produces abnormal TIMI frame counts and TIMI blush scores, so these measures are often used interchangeably. The principal clinical sequela of no-reflow is myonecrosis. Efforts to prevent no-reflow overlap with strategies to reduce MI size and prevent periprocedural MI.
In the setting of MI, several drugs have been shown to reduce the incidence of no-reflow. Evidence for a beneficial effect on no-reflow exists for abciximab, adenosine, nicorandil, and nitroprusside.674,675,680,682,683,685,687,688,690 However, their adoption into clinical practice has depended on their effect on hard clinical endpoints such as infarct size and mortality. These benefits, and consequentially the use of these agents, have been limited.
For interventional no-reflow, several therapies have proven effective after no-reflow has started. These include adenosine, calcium channel blockers, and nitroprusside.676,678,679,681,684,686,689,691 There are fewer data to support the use of epinephrine.692 No-reflow after rotational atherectomy was less common with nicorandil compared with verapamil infusions in 3 studies,693–695 and an infusion of nicorandil/adenosine during rotational atherectomy prevented no-reflow in 98% of patients.677 Trials of pre-PCI intracoronary verapamil, nicardipine, and adenosine have reported them to be safe but have not demonstrated reductions in post-PCI no-reflow.696–698 Mechanical devices to prevent interventional and myocardial infarct reperfusion no-reflow are also covered in Section 5.5.5.
5.8. PCI in Specific Anatomic Situations
5.8.1. CTOs: Recommendation
See Online Data Supplements 26 to 28 for additional data regarding CTOs.
Approximately one third of patients with suspected CAD who undergo coronary angiography have ≥1 CTO (defined as occlusion of a duration >3 months).704 Although stress-induced ischemia can be elicited in the majority of patients with CTO despite the presence of collaterals,706,707 only 8% to 15% of these patients undergo PCI.708,709 The disparity between the frequency of CTOs and percutaneous treatment underscores not only the technical and procedural complexities of this lesion subtype but also the clinical uncertainties regarding which patients benefit from CTO revascularization. Studies suggest that patients who undergo successful, rather than failed, recanalization of CTOs fare better in terms of symptom status and need for CABG,699 as well as LV function.710 However, the impact of successful CTO recanalization on long-term survival remains unsettled.701,711,712 The decision to try PCI for a CTO (versus continued medical therapy or surgical revascularization) requires an individualized risk-benefit analysis encompassing clinical, angio-graphic, and technical considerations. Consultation with a cardiothoracic surgeon and use of the Heart Team approach in cases of CTO in which a large territory is subtended and/or multivessel CAD is present are frequently done.
From a technical perspective, successful recanalization of CTOs has steadily increased over the years because of adoption of dedicated wires, novel techniques, and increased operator experience.702 In patients who undergo successful CTO recanalization, use of DES significantly reduces the need for repeated target-vessel revascularization, compared with BMS and balloon angioplasty, without compromising safety.703,713–719
5.8.2. SVGs: Recommendations
Class III: NO BENEFIT
Class III: HARM
See Online Data Supplement 29 for additional data regarding SVG.
Adverse cardiac event rates are doubled after SVG PCI compared with native-artery PCI.536 A distal balloon occlusion EPD decreased the 30-day composite outcome of death, MI, emergency CABG, or target-lesion revascularization (9.6% versus 16.5%) in the only RCT comparing embolic protection with no embolic protection.532 Subsequent noninferiority comparisons have demonstrated similar benefit with proximal occlusion and distal filter EPDs, with benefit limited to reduction in periprocedural MI.534,535 PCI in chronic SVG occlusion is associated with low success rates, high complication rates, and poor long-term patency rates.722,723 Restenosis and target-vessel revascularization rates are lower with DES compared with BMS, although mortality and stent thrombosis rates are similar.725 The use of covered stents is limited to the treatment of the uncommon complication of SVG perforation. Balloon angioplasty for distal SVG anastomotic stenoses has low restenosis rates,724 so stenting is commonly reserved at this location for suboptimal balloon angioplasty results or restenosis. Routine GP IIb/IIIa inhibitor therapy has not proven beneficial in SVG PCI.720 Fibrinolytic therapy is no longer used for thrombus-containing lesions, but rheolytic or manual aspiration thrombectomy is sometimes employed.
5.8.3. Bifurcation Lesions: Recommendations
Side-branch occlusion or severe stenosis after stenting the main artery in coronary bifurcation PCI occurs in 8% to 80% of unselected patients.732,734 The frequency of side-branch occlusion is related to complex bifurcation morphology (severe and/or long side-branch ostial stenosis, large plaque burden in the side-branch ostium, and/or unfavorable side-branch angulation).732,735,736 Side-branch occlusion after PCI is associated with Q-wave and non–Q-wave MI.734,735 Therefore, preservation of physiologic flow in the side branch after PCI is important.736 There are 2 bifurcation PCI strategies: provisional stenting (stenting the main vessel with additional balloon angioplasty or stenting of the side branch only in the case of an unsatisfactory result) and elective double stenting of the main vessel and the side branch. When there is an unsatisfactory result in the side branch from the provisional stent in the main branch, sometimes balloon angioplasty alone in the side branch will improve the result and stenting the side branch is not necessary. Some experts have suggested that using the side-branch balloon alone will distort the main branch stent and thus this always needs to be a kissing balloon inflation.
In patients with low-risk bifurcation lesions (minimal or moderate ostial side-branch disease [<50% diameter stenosis] of focal length [5 to 6 mm]), provisional stenting yields similar clinical outcome to elective double stenting, with lower incidence of periprocedural biomarker elevation.726–729 Conversely, in patients with high-risk bifurcations, elective double stenting is associated with a trend toward higher angiographic success rates, lower in-hospital MACE, and better long-term patency of the side branch compared with provisional stenting.193 Culotte, Crush, and T-stent techniques have been studied in RCTs.726–729,737 Use of DES yields better outcomes than BMS,738 and sirolimus-eluting stents yield better outcomes than paclitaxel-eluting stents.739–742 Clinical evidence supports the use of final kissing balloon inflation after elective double stenting.743
5.8.4. Aorto-Ostial Stenoses: Recommendations
Aorto-ostial stenoses of native coronary arteries (left main coronary artery and right coronary artery) are most commonly caused by atherosclerosis, but they can also occur in patients with congenital malformations, radiation exposure, vasculitides, and aortic valve replacement. The angiographic diagnosis of aorto-ostial disease is not always straightforward, especially in the ostial left main coronary artery, where eccentricity and angulation can be mistaken for stenosis.490,748 Aorto-ostial disease can be evaluated with IVUS744,745; FFR (with IV adenosine) has also been used.484,749 The treatment of aorto-ostial stenoses with balloon angioplasty has been associated with lower procedural success rates, more frequent in-hospital complications, and a greater likelihood of late restenosis.750 Although atherectomy devices (directional atherectomy, rotational atherectomy, and excimer laser angioplasty) have improved acute angiographic results over balloon angioplasty, restenosis has remained a limitation.751 In patients with aorto-ostial stenoses undergoing PCI, use of DES has been shown to reduce restenosis compared with BMS.176,746,752
5.8.5. Calcified Lesions: Recommendation
The presence of coronary calcification is a marker for significant CAD and increased long-term mortality.753 Calcified coronary lesions are not a homogenous entity, and their response to PCI varies according to severity of calcification. Severely calcified lesions respond poorly to balloon angioplasty,230,754 and when stents are implanted in such lesions, an incomplete and asymmetrical stent expansion occurs in the majority of cases.755 Attempts to remedy the underexpanded stents with aggressive high-pressure balloon dilatation may result in coronary artery rupture.756 All the published prospective RCTs that evaluated the various catheter-based coronary interventional devices excluded patients with severely calcified lesions. Therefore, the evidence base for best PCI practices in patients with severely calcified lesions comes from nonrandomized single-arm studies. Among the various adjunct devices that are used to facilitate PCI in severely calcified lesions, only rotational atherectomy has been shown to have potential utility.514,757 Although rotational atherectomy increases the chances of angiographic success in severely calcified lesions, its use as a stand-alone device has not led to a reduction in restenosis.520,521,758 Several retrospective studies have shown that in patients with severely calcified lesions, the use of rotational atherectomy before implantation of BMS514 or DES515 is safe. Intermediate-term patency is more favorable with DES than BMS.759
5.9. PCI in Specific Patient Populations
Several specific patient subsets with higher risks for PCI, and at times higher absolute clinical benefit, have traditionally been underrepresented in RCTs and are described below.
The elderly constitute a growing proportion of patients considered for PCI.760 In 1 series examining trends over a 25-year period, the proportion of patients undergoing PCI who were 75 to 84 years of age doubled, and those >85 years of age increased 5-fold.761 Age is one of the strongest predictors of mortality after PCI,762 and elderly patients present with a substantially higher clinical risk profile760 Nonetheless, the angiographic success rates and clinical benefits of PCI in elderly patients are similar to younger patients.763 In fact, the absolute benefit is typically greater because of higher absolute risk of adverse outcomes in these patients.764 However, increased risks of complications such as major bleeding and stroke mandate careful consideration of the benefits and risks of PCI in elderly patients.373
Patients with diabetes represent approximately one third of patients undergoing PCI in the United States. Restenosis, which had been a major limitation of PCI, is significantly reduced in patients with diabetes treated with DES compared with BMS.471 However, there are no definitive data from RCTs supporting different clinical outcomes for different types of DES,765 with a recent meta-analysis of 35 RCTs involving 3852 patients with diabetes unable to find major differences between patients receiving sirolimuseluting stents or paclitaxel-eluting stents.472 Numerous analyses and clinical studies have evaluated how the presence of diabetes may impact the clinical outcome of patients undergoing PCI and decisions about PCI or CABG.14,116,163,164,186 These studies and the approach to revascularization decisions in diabetes are addressed in Section 4.
Diabetes is an important risk factor for the development of contrast-induced AKI. Strategies to reduce the risk of contrast-induced AKI in patients with diabetes are discussed in Section 4.4.
Cardiovascular disease is the leading cause of death in women in the United States and Europe,766 and an estimated 35% of PCIs in the United States are performed in women.767,768 Women undergoing PCI usually have more risk factors (including hypertension, advanced age, elevated cholesterol, and more significant and diffuse CAD) compared with men.769 Women with STEMI are also less likely to receive early medical treatments and experience longer delays to reperfusion therapy.770,771 In subgroup analyses of clinical trials, use of DES appears to be similarly efficacious in women and men.772
5.9.4. CKD: Recommendation
CKD is an independent risk factor for the development and progression of CAD,773,774 and is also associated with worse prognosis after MI or PCI.369,775 A glomerular filtration rate of <60 mL/min per 1.73 m2 of body surface area should be considered abnormal. Patients with CKD undergoing PCI have a higher risk of complications, including bleeding,776 AKI, and death,236,777 but CKD is not a strong predictor of restenosis after BMS or DES.778 Strategies to reduce the risk of contrast-induced AKI in patients with CKD are discussed in Section 4.4. Platelet dysfunction and overdosing of antiplatelet and antithrombin drugs350 in patients with CKD contribute to the increased risk of bleeding. The Cockcroft-Gault formula is commonly used as a surrogate marker for estimating creatinine clearance, which in turn estimates glomerular filtration rate.298,299,779,780 Medications that require dosage adjustments in patients with CKD include eptifibatide, tirofiban, bivalirudin, enoxaparin, and fondaparinux.781
5.9.5. Cardiac Allografts
Cardiac allograft vasculopathy is a major cause of death in cardiac transplant recipients after their first year of survival.782 In general, revascularization for cardiac allograft vasculopathy with PCI is only palliative, with no evidence supporting benefit in regard to long-term survival or avoidance of retransplantation. The restenosis rate after PCI in patients with cardiac allograft vasculopathy is high, although stent implantation reduces early and midterm restenosis compared with balloon angioplasty. DES have been shown to have a tendency to lower restenosis rates compared with BMS.783,784 Thus, many clinicians perform stenting with DES or BMS in cardiac transplant patients with discrete lesions who have an abnormal stress test or symptoms suggestive of myocardial ischemia.
5.10. Periprocedural MI Assessment: Recommendations
Major events leading to ischemia or MI after PCI include acute closure, embolization and no-reflow, side-branch occlusion, and acute stent thrombosis. Issues surrounding the routine assessment of cardiac biomarkers after PCI are complex, especially given that the definition of PCI-related MI has evolved over the years and most events are asymptomatic. The most recent consensus definition of MI considers troponin elevations of 3 times the upper limit of normal as a PCI-related MI in patients with normal baseline levels; this is further classified as a type 4a MI.240 This definition is supported by studies with delayed-enhancement MRI confirming that there is irreversible injury in the myocardium associated with biomarker elevations and that the size of this injury correlates with the degree of elevation.785 Furthermore, a meta-analysis of 15 observational studies found that troponin elevations at any level were linked with worse in-hospital and long-term outcomes; elevations >3 times the upper limit of normal predicted even worse outcomes.242 Other observational data, however, have raised concerns about whether the relationship is causal.786,787 A recent study found creatinine kinase-MB to correlate better with MRI-detected MI than troponin level.788 Definitions of PCI-related MI are being reevaluated by the Task Force for the Redefinition of Myocardial Infarction. Although there may be value for individual operators and hospitals to routinely measure cardiac biomarkers to track rates of PCI-related MI, at present there are not compelling data to recommend this for all PCI procedures.
5.11. Vascular Closure Devices: Recommendations
Class III: NO BENEFIT
See Online Data Supplement 30 for additional data regarding vascular closure devices.
Vascular (arteriotomy) closure devices have been extensively reviewed,790 most recently in a 2010 AHA scientific statement,257 which issued several formal recommendations. The results of 4 meta-analyses have found that vascular closure devices decrease time to hemostasis compared with manual compression but do not decrease vascular complications, bleeding complications, or the need for blood transfusions.256,789,791,793 Future studies of vascular closure devices need to be randomized, include “high-risk” patients and “high-risk” anatomy, use blinded endpoint adjudication as much as possible, use well-defined and comprehensive complication endpoints, and be adequately powered to detect clinically important endpoints, particularly bleeding and vascular complications.
6. Postprocedural Considerations
Postprocedural considerations in patients undergoing PCI are discussed below and summarized in Table 14. Some recommendations and text regarding DAPT in Section 5.7.2 are intentionally repeated in this section for reader ease of use.
6.1. Postprocedural Antiplatelet Therapy: Recommendations
Continued treatment with the combination of aspirin and a P2Y12 inhibitor antagonist after PCI appears to reduce MACE.570,572 On the basis of RCT protocols, secondary prevention measures, and expert consensus opinion, aspirin 81 mg daily should be given indefinitely after PCI.
Likewise, P2Y12 inhibitors should be given for a minimum of 1 month after BMS (minimum 2 weeks for patients at significant increased risk of bleeding)580 and for 12 months after DES and ideally in all patients who are not at high risk of bleeding.
The 2009 STEMI/PCI guidelines update10 listed the recommendation “if the risk of morbidity because of bleeding outweighs the anticipated benefit afforded by thienopyridine therapy, earlier discontinuation should be considered” as a Class I recommendation, although the language used, in part, was consistent with a Class IIa recommendation. To clarify the intent of the recommendation, as well as to acknowledge the inherent difficulties in weighing bleeding and stent thrombosis risks, the recommendation is designated a Class IIa recommendation, using the phrase “earlier discontinuation is reasonable.” Recommendations regarding P2Y12 inhibitor discontinuation before elective or urgent CABG are provided in the “2011 ACCF/AHA Guideline for Coronary Artery Bypass Graft Surgery.”824
6.1.1. PPIs and Antiplatelet Therapy: Recommendations
Class III: NO BENEFIT
See Online Data Supplement 31 for additional data regarding the clopidogrel–PPI interaction.
PPIs are often prescribed prophylactically when clopidogrel is started to prevent GI complications such as ulceration and bleeding due to DAPT.825 There is pharmacodynamic evidence that omeprazole interferes with clopidogrel metabolism,826,827 but there is no clear evidence implicating other PPIs. However, even with omeprazole, there are no convincing data supporting an important clinical drug–drug interaction.826 The FDA communication about an ongoing safety review of clopidogrel advises that healthcare providers avoid the use of clopidogrel in patients with impaired CYP2C19 function due to known genetic variation or drugs that inhibit CYP2C19 activity. The FDA notes that there is no evidence that other drugs that reduce stomach acid, such as histamine-2 receptor antagonists (except cimetidine) or antacids, interfere with clopidogrel responsiveness. The COGENT (Clopidogrel and the Optimization of Gastrointestinal Events) trial randomized patients with DAPT to clopidogrel and omeprazole or clopidogrel and placebo, and while there was no difference in cardiovascular events between the 2 groups, GI events were halved in those randomized to omeprazole.828 It is reasonable to carefully evaluate the indication for PPI therapy in patients treated with clopidogrel, based on the presence or absence of the risk factors discussed above.794 The need for GI protection increases with the number of risk factors for bleeding. Prior upper GI bleeding is the strongest and most consistent risk factor for GI bleeding on antiplatelet therapy. Patients with ACS and prior upper GI bleeding are at substantial cardiovascular risk, so DAPT with concomitant use of a PPI may provide the optimal balance of risk and benefit. It should be noted that PPIs, by decreasing adverse GI effects related to clopidogrel, might decrease patients' discontinuation of clopidogrel. In patients in whom there is a clear indication for PPI therapy, some clinicians may choose to use a PPI other than omeprazole.
6.1.2. Clopidogrel Genetic Testing: Recommendations
Class III: NO BENEFIT
On March 12, 2010, the FDA approved a new label for clopidogrel with a “boxed warning” about the diminished effectiveness of clopidogrel in patients with impaired ability to convert the drug into its active metabolite.829 Patients with decreased CYP2C19 function because of genetic polymorphisms metabolize clopidogrel poorly and have higher rates of cardiovascular events after ACS and PCI than patients with normal CYP2C19 function. The warning also notes that tests are available to identify patients with genetic polymorphisms and that alternative treatment strategies should be considered for patients who are poor metabolizers. The clopidogrel boxed warning leaves the issue of whether to perform CYP2C19 testing up to the individual physician. It does not specifically require genetic testing or other changes in evaluation or treatment and does not imply that there are solid evidence-based reasons for such actions. Rather, it serves to inform clinicians of genetic variations in response to clopidogrel and to emphasize that clinicians should use this knowledge to make decisions about how to treat individual patients. At the present time, the evidence base is insufficient to recommend routine genetic testing in patients undergoing PCI. There may be a potential role for genetic testing for patients undergoing elective high-risk PCI procedures (eg, unprotected left main, bifurcating left main, or last patent coronary artery).
6.1.3. Platelet Function Testing: Recommendations
Class III: NO BENEFIT
Platelet function testing to tailor antiplatelet therapy has received considerable interest. The GRAVITAS (Gauging Responsiveness With A VerifyNow Assay-Impact On Thrombosis And Safety) trial and several other ongoing trials test the concept that tailoring antiplatelet therapy based on platelet responsiveness assessed in an ex vivo P2Y12 assay will improve cardiovascular outcomes.830 In GRAVITAS, treatment with high-dose clopidogrel for 6 months in patients with high platelet reactivity on standard-dose clopidogrel was not beneficial. At the present time, the evidence base is insufficient to recommend routine platelet function testing. The results of 2 ongoing trials (DANTE [Dual Antiplatelet Therapy Tailored on the Extent of Platelet Inhibition] and ARCTIC [Double Randomization of a Monitoring Adjusted Antiplatelet Treatment Versus a Common Antiplatelet Treatment for DES Implantation, and Interruption Versus Continuation of Double Antiplatelet Therapy, One Year After Stenting]) will provide further information on the issue (www.clinicaltrials.gov).
6.2. Stent Thrombosis
The majority of stent thrombosis occurs early (0 to 30 days after PCI). In broad clinical practice, the expected rate of early stent thrombosis is <1%, and beyond 30 days it is 0.2% to 0.6% per year.210,831 Acute stent thrombosis often presents as STEMI, and emergency revascularization is indicated. Acute stent thrombosis is associated with mortality rates of 20% to 45%.832 Survivors are also at risk of recurrent stent thrombosis.833
Mechanical and pharmacological factors are the most frequent cause of acute stent thrombosis. After the usual measures to restore flow in the infarct-related artery, it is important to consider the etiology of stent thrombosis as it pertains to further therapy and avoidance of recurrence. IVUS may identify factors such as an undersized stent, incomplete stent apposition, residual stenosis, or dissection and can guide subsequent treatment. The most common cause of acute stent thrombosis is nonadherence to DAPT; however, resistance to aspirin or thienopyridines and prothrombotic states such as congenital or acquired thrombophilic states (malignancy) are additional risk factors.834,835
Given the poor prognosis of stent thrombosis and the uncertainties surrounding treatment, the importance of prevention must be emphasized. This includes ensuring compliance with DAPT and adequate stent sizing and expansion.836
6.3. Restenosis: Recommendations
6.3.1. Background and Incidence
After balloon angioplasty, mechanisms contributing to restenosis include smooth muscle cell migration and proliferation, platelet deposition, thrombus formation, elastic recoil, and negative arterial remodeling. Stents block elastic recoil and negative remodeling, and the predominant mechanism for restenosis after stent implantation is neointimal hyperplasia. Restenosis rates vary, depending on whether angiographic restenosis (defined as >50% diameter stenosis at follow-up angiography) or clinical restenosis (symptomatic and requiring target-lesion revascularization or target-vessel revascularization) is measured, as well as on patient characteristics, coronary anatomy considerations, and device type (balloon angioplasty, BMS, or DES). The incidence of angiographic restenosis rates for uncomplicated lesions treated in RCTs ranges from 32% to 42% after balloon angioplasty463,464 and from 16% to 32% after BMS,463,464 and is generally <10% after DES.454,841 Less than half of patients with angiographic restenosis present with symptomatic, clinically relevant restenosis at 1-year follow-up, and a pooled analysis of 6186 patients from 6 trials of BMS showed target-lesion revascularization was performed in 12% and target-vessel revascularization in 14% at 1 year.842,843 Patients with clinical restenosis typically present with recurrent exertional angina, but 5% to 10% of patients present with acute MI and 25% with UA.844,845
Factors associated with an increased risk of restenosis in various models include clinical setting (STEMI, ACS, daily angina), patient characteristics (diabetes, age <55 to 60 years, prior PCI, male sex, multivessel CAD), lesion location (unprotected left main, SVG), and procedural characteristics (minimum stent diameter ≤2.5 mm, total stent length ≥40 mm).778,846
PCI strategies for treating restenosis after balloon angioplasty, BMS, and DES are reviewed in the following sections. In addition to repeat PCI, intensified medical therapy or CABG are often also reasonable strategies, dependent on initial treatment (eg, balloon angioplasty, BMS), pattern of restenosis, likelihood of recurrent restenosis, ability to intensify medical therapy, suitability for CABG, and patient preference. Repeat PCI with BMS or DES is not appropriate if the patient is not able to comply with and tolerate DAPT.
6.3.2. Restenosis After Balloon Angioplasty
For clinical restenosis after balloon angioplasty, stent implantation is superior to repeat balloon angioplasty or atheroablation devices. The REST (REstenosis STent) study showed that target-lesion revascularization rates were 10% for stent-treated patients and 27% for balloon-treated patients (P=0.001).837
6.3.3. Restenosis After BMS
In-stent restenosis is classified according to these angio-graphic characteristics: Pattern I includes focal lesions ≤10 mm in length; Pattern II is in-stent restenosis >10 mm within the stent; Pattern III includes in-stent restenosis >10 mm extending outside the stent; and Pattern IV is totally occluded in-stent restenosis.847 Treatment of in-stent restenosis with balloon angioplasty, repeat BMS, or atheroablation devices for Patterns I to IV resulted in 1-year target-lesion revascularization rates of 19%, 35%, 50%, and 83%, respectively. For clinical restenosis after BMS, repeat stenting with DES is preferred. Studies have demonstrated lower recurrent restenosis rates with DES compared with BMS or vascular brachytherapy.495,838–840
6.3.4. Restenosis After DES
Clinical restenosis after placement of DES is becoming increasingly common due to the large numbers of patients who have been treated with DES. The predominant angio-graphic pattern for DES in-stent restenosis is focal (≤10 mm in length). Several biologic, mechanical, and technical factors may contribute to DES in-stent restenosis, including drug resistance, hypersensitivity, stent underexpansion, stent strut fracture, nonuniform stent strut coverage, gap in stent coverage, and residual uncovered atherosclerotic lesion. IVUS might be considered to determine the cause for in-stent restenosis and help guide treatment strategy. Interventionists may treat focal DES restenosis with balloon angioplasty and treat nonfocal DES restenosis with BMS, CABG, or repeat DES with the same or an alternative antiproliferative drug.848,849 Small, observational cohort studies have demonstrated angiographic restenosis rates of 25% to 30% with repeat DES either with the same or an alternative drug.495,850,850 There are no RCTs, and the most appropriate treatment of restenosis of DES remains unknown.
6.4. Clinical Follow-Up
At the time of discharge, patients are instructed to contact their physician or seek immediate medical attention if symptoms recur. Most physicians will give the patient instructions on return to work and timing of return to full activities. The importance of strict compliance with aspirin and P2Y12 inhibitor therapy is ideally emphasized to the patient at the time of discharge and during follow-up visits.
Secondary prevention measures after PCI are an essential part of long-term therapy, reducing both future morbidity and mortality associated with CAD, and are discussed in Section 6.5. A follow-up visit after PCI is usually scheduled to assess the patient's clinical status, the patient's compliance with secondary prevention therapies, and the success of secondary prevention measures (eg, blood pressure control, low-density lipoprotein levels, smoking cessation). Routine, periodic stress testing of asymptomatic patients is not considered part of standard patient follow-up.
6.4.1. Exercise Testing: Recommendations
Class III: NO BENEFIT
Treadmill exercise testing before cardiac rehabilitation provides information about peak exercise capacity and heart rate, helping to stratify patients for the level of supervision during training, and seems reasonable for this purpose851; nuclear imaging to assess ischemia in this context usually adds little.
The role of exercise testing to evaluate restenosis is much less certain. Although the presence of symptoms may not be a reliable means of detecting restenosis, there is no evidence that the detection of silent restenosis leads to improved outcome.852,853 Routine testing of all patients after PCI will also lead to many false-positive tests, particularly in the era of DES. As restenosis rates decline from 30% to 10%, the false-positive rate of stress imaging increases from 37% to 77%.854 A recent analysis of a national health insurance claims database and accompanying editorial find that stress testing after PCI is likely overused and rarely leads to repeat revascularization.855,856 In summary, there is no proven benefit or indication for routine periodic stress testing in patients after PCI, and, thus, it is not indicated.8,851 In cases in which there is a clear clinical indication for stress testing in a patient after PCI, exercise ECG alone is an insensitive predictor of restenosis857,858; therefore, stress imaging is the preferred stress test.8 In cases of recurrent angina after PCI in which the pretest likelihood of restenosis is high and repeat revascularization based on symptoms is likely indicated, most practitioners will proceed directly to cardiac catheterization rather than first obtain stress imaging.
6.4.2. Activity and Return to Work
The timing of return to physical activity depends on the presenting condition as well as previous functional status. For STEMI, for example, daily walking is encouraged immediately, and driving can begin within 1 week after uncomplicated MI if allowed by local motor vehicle laws.859 Sexual activity usually can be resumed within days, provided exercise tolerance is adequate, normally assessed by the ability to climb a fiight of stairs.859 Similar recommendations have been issued for UA/NSTEMI.860 Patients with UA who have undergone successful revascularization and are otherwise doing well may return to physical activity on an accelerated schedule, usually within a few days.860
Return to work is more complex. Return to work rates after MI range from 63% to 94% and are confounded by factors such as job satisfaction, financial stability, and company policies.861 The physical demands and degree of stress of a particular job require that recommendations be individualized. In the PAMI-2 (Primary Angioplasty in Myocardial Infarction) trial, patients were encouraged to return to work 2 weeks after primary PCI for STEMI, and no adverse events were reported.862 In the RITA (Randomized Intervention Treatment of Angina) trial, revascularization with PCI led to earlier return to work compared with CABG, and subsequent employment rates were associated with relief of angina.105 Many practitioners use graded exercise treadmill testing to determine the safety of activity and return to work by measuring the metabolic equivalent of task (MET) level achieved and comparing that level to energy levels required to perform different activities.863
6.4.3. Cardiac Rehabilitation: Recommendation
Participation in cardiac rehabilitation is associated with significant reductions in all-cause mortality (OR: 0.80, 95% CI: 0.68 to 0.93) and cardiac mortality.796,797 Reports from community-based surveys, which in general enroll older and higher-risk patients than clinical trials, have confirmed that participation in comprehensive rehabilitation is independently associated with a reduction in recurrent MI and reduced mortality.799 Cardiac rehabilitation is also associated with improvements in exercise tolerance, cardiac symptoms, lipid levels, cigarette smoking cessation rates (in conjunction with a smoking cessation program), stress levels, improved medical regimen compliance, and improved psychosocial well-being.800 Cardiac rehabilitation is cost-effective as well.864 Physician referral may be the most powerful predictor of patient participation in a cardiac rehabilitation program.865
6.5. Secondary Prevention
The treatment of the patient does not end with PCI; secondary prevention measures are a critical component of patient management. Important secondary prevention measures were presented in detail in the “2006 AHA/ACC Guidelines for Secondary Prevention for Patients With Coronary and Other Atherosclerotic Vascular Disease”562 and have recently been updated in the “AHA/ACCF Secondary Prevention and Risk Reduction Therapy for Patients With Coronary and Other Atherosclerotic Vascular Disease: 2011 Update.”805 The reader is referred to this document for detailed discussions of secondary prevention. Among the important recommendations are the following:
Lipid management with lifestyle modification (Class I; Level of Evidence: B)805–807 and statin therapy are recommended. (Level of Evidence: A)344,806,808–810,810a An adequate statin dose should be employed which reduces low-density lipoprotein cholesterol to <100 mg/dL AND achieves at least a 30% lowering of low-density lipoprotein cholesterol. (Class I; Level of Evidence: C)806–810,810a It is reasonable to treat patients with statin therapy which lowers low-density lipoprotein cholesterol to <70 mg/dL in very high risk* patients. (Class IIa; Level of Evidence: C)345,808–810,810a,811,812 Patients who have triglycerides ≥200 mg/dL should be treated with statins to lower non–high-density lipoprotein cholesterol to <130 mg/dL. (Class I; Level of Evidence: B)344,809,810,866 In patients who are very high risk* and have triglycerides ≥200 mg/dL, a non–high-density lipoprotein cholesterol goal of <100 mg/dL is reasonable. (Class IIa; Level of Evidence: C)344,809,810,866
Blood pressure control with lifestyle modification (Class I; Level of Evidence: B)813–817 and pharmacotherapy (Class I; Level of Evidence: A),805,813,818,819 with the goal of blood pressure <140/90 mm Hg.
Diabetes management (eg, lifestyle modification and pharmacotherapy), coordinated with the patient's primary care physician and/or endocrinologist. (Class I; Level of Evidence: C)805
7. Quality and Performance Considerations
7.1. Quality and Performance: Recommendations
PCI quality and performance considerations are defined by attributes related to structure, processes, and risk-adjusted outcomes. Structural attributes include elements such as equipment, supplies, staffing, institutional and operator-level volumes, and the availability of electronic medical records. Processes include strategies for the appropriate patient, protocols for pre- and postprocedural care, appropriate procedural execution and management of complications, and participation in databases and registries for benchmarking performance of the program and individual operator. Risk-adjusted outcomes are the end result of these structures and processes of care, and when available are more reliable measures of quality than the institutional and individual operator volumes discussed in Section 7.4.
PCI process and outcomes assessments can be used for internal quality-improvement efforts and public reporting. Public reporting of institutional risk-adjusted outcomes is becoming more common. Although operator-level outcomes can be assessed and risk adjusted, the results are much less reliable due to lack of statistical power resulting from lower volumes. Any public reporting must use statistical methods that meet the high criteria established by the AHA Work Group.867
The cognitive knowledge and technical skill required to perform PCI continue to grow. Details on the training required for interventional cardiology are found in the most recent ACCF Core Cardiology Training Statement.868
7.3. Certification and Maintenance of Certification: Recommendation
The American Board of Internal Medicine established interventional cardiology board certification in 1999 as an “added qualification” to the cardiovascular disease board certification. Since 1990 all certificates from the American Board of Internal Medicine are time limited for a 10-year period and require all diplomats to participate in maintenance of certification to maintain their board-certified status. Maintenance of certification in interventional cardiology requires physicians to document a minimum of 150 interventional cases over the 2 years before expiration of the current certification, complete self-assessment modules of their medical knowledge, participate in practice-based quality-improvement activities, and pass a secure, knowledge-based examination.869–871 For those who cannot meet the case volume requirement, an alternative option is to submit a log of 25 consecutive cases including patient characteristics and procedural outcomes. The maintenance of certification process is likely to change, as the American Board of Internal Medicine intends to evolve maintenance of certification from an episodic event that occurs once every 10 years to a more continuous process of continuous professional development.
7.4. Operator and Institutional Competency and Volume: Recommendations
Class III: NO BENEFIT
Older observational evidence supported a volume-outcome relationship in PCI at both the institutional and operator level.873 However, this relationship is complicated and may be inconsistent across low-volume institutions or operators. More recent data on primary PCI suggest that operator experience may modify the volume-outcome relationship at the institutional level.876,878 Risk-adjusted outcomes remain preferable to institutional and individual operator volumes as quality measures.
Operator and hospital volume recommendations have been carried over from the 2005 PCI guideline. However, the writing committee recognizes that these volume recommendations are controversial. In addition, after extensive review of all relevant data, the writing committee believes that the LOE in support of all the above recommendations is best categorized as LOE C rather than LOE B as it has been in prior guidelines for some recommendations. We encourage the ACCF/AHA/ACP Clinical Competence and Training writing group for PCI and other expert writing groups to review this issue so that new recommendations can be considered by the next PCI guideline writing committee.
7.5. Participation in ACC NCDR or National Quality Database
Assessment of PCI quality and outcomes is important both at the level of the entire program and at the level of the individual physician. This requires collection of clinical and procedural data for PCI that allows regular comparison of risk-adjusted outcomes and complications with national benchmarks. The ACC NCDR CathPCI Registry is an example of a national registry to fulfill the goals of assessing and benchmarking quality and outcomes.
8. Future Challenges
Although this latest guideline reflects significant advancements in the field of PCI, there remain future challenges to the formulation and updating of guidelines for PCI. The proliferation of studies comparing the many newer drugs and devices with older therapies (or other newer therapies), often using different or novel study endpoints, endpoint definitions, and noninferiority designs, pose increasing challenges to objectively evaluating newer therapies and generating recommendations for their use. Numerous potential advances in the field of PCI, including intracoronary stem cell infusions for chronic and acute ischemic heart disease, designer drugs, novel intracoronary imaging technologies such as optical coherence tomography and virtual histology, new stent composition and designs (eg, drug-eluting, biodegradable, bifurcation), and drug-eluting balloons were considered for formal evaluation by the current writing committee, but it was thought that there were insufficient data at present to formulate any formal recommendations on these topics. These and other emerging technologies and treatments will need to be addressed in future PCI guidelines.
Finally, with this proliferation of new technology, the amount of data generated in the evaluation of these potential therapeutic advances will grow dramatically, adding significant challenges to future guideline generations. Of note, the Web site www.clinicaltrials.gov currently lists several hundred PCI-related clinical trials.
American College of Cardiology Foundation
David R. Holmes, Jr, MD, FACC, President
John C. Lewin, MD, Chief Executive Officer
Janet Wright, MD, FACC, Senior Vice President, Science and Quality
Charlene May, Senior Director, Science and Clinical Policy
Erin A. Barrett, MPS, Senior Specialist, Science and Clinical Policy
American College of Cardiology Foundation/American Heart Association
Lisa Bradfield, CAE, Director, Science and Clinical Policy
Sue Keller, BSN, MPH, Senior Specialist, Evidence-Based Medicine
Jesse M. Welsh, Specialist, Science and Clinical Policy
Debjani Mukherjee, MPH, Associate Director, Evidence-Based Medicine
American Heart Association
Ralph L. Sacco, MS, MD, FAAN, FAHA, President
Nancy Brown, Chief Executive Officer
Rose Marie Robertson, MD, FAHA, Chief Science Officer
Gayle R. Whitman, PhD, RN, FAHA, FAAN, Senior Vice President, Office of Science Operations
Mark D. Stewart, MPH, Science and Medicine Advisor, Office of Science and Medicine
- 1. ACCF/AHA Task Force on Practice Guidelines.
Methodologies and Policies from the ACCF/AHA Task Force on Practice Guideline. Available at: http://assets.cardiosource.com/Methodology_Manual_for_ACC_AHA_Writing_Committees.pdf and http://circ.ahajournals.org/site/manual/index.xhtml.
Accessed July 1, 2011. Google Scholar
- 2. Institute of Medicine. Clinical Practice Guidelines We Can Trust. Washington, DC: The National Academies Press, 2011. Google Scholar
- 3. Institute of Medicine. Finding What Works in Health Care: Standards for Systematic Reviews. Washington, DC: The National Academies Press, 2011. Google Scholar
Williams DO, Gruntzig A, Kent KM,. Guidelines for the performance of percutaneous transluminal coronary angioplasty. Circulation. 1982; 66: 693– 4. LinkGoogle Scholar
- 5. Guidelines for percutaneous transluminal coronary angioplasty. A report of the American College of Cardiology/American Heart Association Task Force on Assessment of Diagnostic and Therapeutic Cardiovascular Procedures (Subcommittee on Percutaneous Transluminal Coronary Angioplasty). Circulation. 1988; 78: 486– 502. CrossrefMedlineGoogle Scholar
Ryan TJ, Bauman WB, Kennedy JW,. Guidelines for percutaneous transluminal coronary angioplasty. A report of the American Heart Association/American College of Cardiology Task Force on Assessment of Diagnostic and Therapeutic Cardiovascular Procedures (Committee on Percutaneous Transluminal Coronary Angioplasty). Circulation. 1993; 88: 2987– 3007. CrossrefMedlineGoogle Scholar
Smith SC, Dove JT, Jacobs AK,. ACC/AHA guidelines of percutaneous coronary intervention (revision of the 1993 PTCA guidelines)—Executive Summary. A report of the American College of Cardiology/American Heart Association Task Force on practice guidelines (Committee to revise the 1993 guidelines for percutaneous transluminal coronary angioplasty). Circulation. 2001; 103: 3019– 41. CrossrefMedlineGoogle Scholar
Smith SC, Feldman TE, Hirshfeld JW,. ACC/AHA/SCAI 2005 guideline update for percutaneous coronary intervention: A report of the American College of Cardiology/American Heart Association Task Force on practice guidelines (ACC/AHA/SCAI Writing Committee to Update the 2001 Guidelines for Percutaneous Coronary Intervention). Circulation. 2006; 113: e166– 286. MedlineGoogle Scholar
King SBI, Smith SC, Hirshfeld JW,. 2007 focused update of the ACC/AHA/SCAI 2005 guideline update for percutaneous coronary intervention: A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines [published correction appears in Circulation 2008;117:e161]. Circulation. 2008; 117: 261– 95. LinkGoogle Scholar
Kushner FG, Hand M, Smith SC,. 2009 focused updates: ACC/AHA guidelines for the management of patients with ST-elevation myocardial infarction (updating the 2004 guideline and 2007 focused update) and ACC/AHA/SCAI guidelines on percutaneous coronary intervention (updating the 2005 guideline and 2007 focused update): A Report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines [published correction appears in Circulation 2010;121:e257]. Circulation. 2009; 120: 2271– 306. LinkGoogle Scholar
Beller GA, Ragosta M. Decision making in multivessel coronary disease: the need for physiological lesion assessment. J Am Coll Cardiol Intv. 2010; 3: 315– 7. CrossrefGoogle Scholar
Tonino PA, Fearon WF, De Bruyne B,. Angiographic versus functional severity of coronary artery stenoses in the FAME study fractional flow reserve versus angiography in multivessel evaluation. J Am Coll Cardiol. 2010; 55: 2816– 21. CrossrefMedlineGoogle Scholar
Morice MC, Serruys PW, Kappetein AP,. Outcomes in patients with de novo left main disease treated with either percutaneous coronary intervention using paclitaxel-eluting stents or coronary artery bypass graft treatment in the Synergy between Percutaneous Coronary Intervention with TAXUS and Cardiac Surgery (SYNTAX) trial. Circulation. 2010; 121: 2645– 53. LinkGoogle Scholar
Serruys PW, Morice MC, Kappetein AP,. Percutaneous coronary intervention versus coronary-artery bypass grafting for severe coronary artery disease. N Engl J Med. 2009; 360: 961– 72. CrossrefMedlineGoogle Scholar
Feit F, Brooks MM, Sopko G,., BARI Investigators. Long-term clinical outcome in the Bypass Angioplasty Revascularization Investigation Registry: comparison with the randomized trial. Circulation. 2000; 101: 2795– 802. LinkGoogle Scholar
King SBI, Barnhart HX, Kosinski AS,., Emory Angioplasty versus Surgery Trial Investigators. Angioplasty or surgery for multi-vessel coronary artery disease: comparison of eligible registry and randomized patients in the EAST trial and influence of treatment selection on outcomes. Am J Cardiol. 1997; 79: 1453– 9. CrossrefMedlineGoogle Scholar
Chakravarty T, Buch MH, Naik H,. Predictive accuracy of SYNTAX score for predicting long-term outcomes of unprotected left main coronary artery revascularization. Am J Cardiol. 2011; 107: 360– 6. CrossrefMedlineGoogle Scholar
Grover FL, Shroyer AL, Hammermeister K,. A decade's experience with quality improvement in cardiac surgery using the Veterans Affairs and Society of Thoracic Surgeons national databases. Ann Surg. 2001; 234: 464– 72. CrossrefMedlineGoogle Scholar
Kim YH, Park DW, Kim WJ,. Validation of SYNTAX (Synergy between PCI with TAXUS and Cardiac Surgery) score for prediction of outcomes after unprotected left main coronary revascularization. J Am Coll Cardiol Intv. 2010; 3: 612– 23. CrossrefGoogle Scholar
Shahian DM, O'Brien SM, Filardo G,. The Society of Thoracic Surgeons 2008 cardiac surgery risk models: part 1—coronary artery bypass grafting surgery. Ann Thorac Surg. 2009; 881 Suppl: S2– 22. CrossrefMedlineGoogle Scholar
Shahian DM, O'Brien SM, Normand SL,. Association of hospital coronary artery bypass volume with processes of care, mortality, morbidity, and the Society of Thoracic Surgeons composite quality score. J Thorac Cardiovasc Surg. 2010; 139: 273– 82. CrossrefMedlineGoogle Scholar
Welke KF, Peterson ED, Vaughan-Sarrazin MS,. Comparison of cardiac surgery volumes and mortality rates between the Society of Thoracic Surgeons and Medicare databases from 1993 through 2001. Ann Thorac Surg. 2007; 84: 1538– 46. CrossrefMedlineGoogle Scholar
Buszman PE, Kiesz SR, Bochenek A,. Acute and late outcomes of unprotected left main stenting in comparison with surgical revascularization. J Am Coll Cardiol. 2008; 51: 538– 45. CrossrefMedlineGoogle Scholar
Caracciolo EA, Davis KB, Sopko G,. Comparison of surgical and medical group survival in patients with left main coronary artery disease. Long-term CASS experience. Circulation. 1995; 91: 2325– 34. CrossrefMedlineGoogle Scholar
Chaitman BR, Fisher LD, Bourassa MG,. Effect of coronary bypass surgery on survival patterns in subsets of patients with left main coronary artery disease. Report of the Collaborative Study in Coronary Artery Surgery (CASS). Am J Cardiol. 1981; 48: 765– 77. CrossrefMedlineGoogle Scholar
Dzavik V, Ghali WA, Norris C,. Long-term survival in 11 661 patients with multivessel coronary artery disease in the era of stenting: a report from the Alberta Provincial Project for Outcome Assessment in Coronary Heart Disease (APPROACH) Investigators. Am Heart J. 2001; 142: 119– 26. CrossrefMedlineGoogle Scholar
Takaro T, Hultgren HN, Lipton MJ,. The VA cooperative randomized study of surgery for coronary arterial occlusive disease II. Subgroup with significant left main lesions. Circulation. 1976; 54: III107– 17. MedlineGoogle Scholar
Takaro T, Peduzzi P, Detre KM,. Survival in subgroups of patients with left main coronary artery disease. Veterans Administration Cooperative Study of Surgery for Coronary Arterial Occlusive Disease. Circulation. 1982; 66: 14– 22. CrossrefMedlineGoogle Scholar
Taylor HA, Deumite NJ, Chaitman BR,. Asymptomatic left main coronary artery disease in the Coronary Artery Surgery Study (CASS) registry. Circulation. 1989; 79: 1171– 9. CrossrefMedlineGoogle Scholar
Yusuf S, Zucker D, Peduzzi P,. Effect of coronary artery bypass graft surgery on survival: overview of 10-year results from randomised trials by the Coronary Artery Bypass Graft Surgery Trialists Collaboration. Lancet. 1994; 344: 563– 70. CrossrefMedlineGoogle Scholar
Capodanno D, Caggegi A, Miano M,. Global risk classification and Clinical SYNTAX (Synergy between Percutaneous Coronary Intervention with TAXUS and Cardiac Surgery) score in patients undergoing percutaneous or surgical left main revascularization. J Am Coll Cardiol Intv. 2011; 4: 287– 97. CrossrefGoogle Scholar
Hannan EL, Wu C, Walford G,. Drug-eluting stents vs coronary-artery bypass grafting in multivessel coronary disease. N Engl J Med. 2008; 358: 331– 41. CrossrefMedlineGoogle Scholar
Ellis SG, Tamai H, Nobuyoshi M,. Contemporary percutaneous treatment of unprotected left main coronary stenoses: initial results from a multicenter registry analysis 1994–1996. Circulation. 1997; 96: 3867– 72. CrossrefMedlineGoogle Scholar
Biondi-Zoccai GG, Lotrionte M, Moretti C,. A collaborative systematic review and meta-analysis on 1278 patients undergoing percutaneous drug-eluting stenting for unprotected left main coronary artery disease. Am Heart J. 2008; 155: 274– 83. CrossrefMedlineGoogle Scholar
Boudriot E, Thiele H, Walther T,. Randomized comparison of percutaneous coronary intervention with sirolimus-eluting stents versus coronary artery bypass grafting in unprotected left main stem stenosis. J Am Coll Cardiol. 2011; 57: 538– 45. CrossrefMedlineGoogle Scholar
Brener SJ, Galla JM, Bryant RI,. Comparison of percutaneous versus surgical revascularization of severe unprotected left main coronary stenosis in matched patients. Am J Cardiol. 2008; 101: 169– 72. CrossrefMedlineGoogle Scholar
Chieffo A, Magni V, Latib A,. 5-year outcomes following percutaneous coronary intervention with drug-eluting stent implantation versus coronary artery bypass graft for unprotected left main coronary artery lesions: the Milan experience. J Am Coll Cardiol Intv. 2010; 3: 595– 601. CrossrefGoogle Scholar
Chieffo A, Morici N, Maisano F,. Percutaneous treatment with drug-eluting stent implantation versus bypass surgery for unprotected left main stenosis: a single-center experience. Circulation. 2006; 113: 2542– 7. LinkGoogle Scholar
Lee MS, Kapoor N, Jamal F,. Comparison of coronary artery bypass surgery with percutaneous coronary intervention with drug-eluting stents for unprotected left main coronary artery disease. J Am Coll Cardiol. 2006; 47: 864– 70. CrossrefMedlineGoogle Scholar
Makikallio TH, Niemela M, Kervinen K,. Coronary angioplasty in drug eluting stent era for the treatment of unprotected left main stenosis compared to coronary artery bypass grafting. Ann Med. 2008; 40: 437– 43. CrossrefMedlineGoogle Scholar
Naik H, White AJ, Chakravarty T,. A meta-analysis of 3,773 patients treated with percutaneous coronary intervention or surgery for unprotected left main coronary artery stenosis. J Am Coll Cardiol Intv. 2009; 2: 739– 47. CrossrefGoogle Scholar
Palmerini T, Marzocchi A, Marrozzini C,. Comparison between coronary angioplasty and coronary artery bypass surgery for the treatment of unprotected left main coronary artery stenosis (the Bologna Registry). Am J Cardiol. 2006; 98: 54– 9. CrossrefMedlineGoogle Scholar
Park DW, Seung KB, Kim YH,. Long-term safety and efficacy of stenting versus coronary artery bypass grafting for unprotected left main coronary artery disease: 5-year results from the MAIN-COMPARE (Revascularization for Unprotected Left Main Coronary Artery Stenosis: Comparison of Percutaneous Coronary Angioplasty Versus Surgical Revascularization) registry. J Am Coll Cardiol. 2010; 56: 117– 24. MedlineGoogle Scholar
Rodes-Cabau J, Deblois J, Bertrand OF,. Nonrandomized comparison of coronary artery bypass surgery and percutaneous coronary intervention for the treatment of unprotected left main coronary artery disease in octogenarians. Circulation. 2008; 118: 2374– 81. LinkGoogle Scholar
Sanmartin M, Baz JA, Claro R,. Comparison of drug-eluting stents versus surgery for unprotected left main coronary artery disease. Am J Cardiol. 2007; 100: 970– 3. CrossrefMedlineGoogle Scholar
Kappetein AP, Mohr FW, Feldman TE,. Comparison of coronary bypass surgery with drug-eluting stenting for the treatment of left main and/or three-vessel disease: 3-year follow-up of the SYNTAX trial. Eur Heart J. 2011; 17: 2125– 34. CrossrefGoogle Scholar
Seung KB, Park DW, Kim YH,. Stents versus coronary-artery bypass grafting for left main coronary artery disease. N Engl J Med. 2008; 358: 1781– 92. CrossrefMedlineGoogle Scholar
White AJ, Kedia G, Mirocha JM,. Comparison of coronary artery bypass surgery and percutaneous drug-eluting stent implantation for treatment of left main coronary artery stenosis. J Am Coll Cardiol Intv. 2008; 1: 236– 45. CrossrefGoogle Scholar
Montalescot G, Brieger D, Eagle KA,. Unprotected left main revascularization in patients with acute coronary syndromes. Eur Heart J. 2009; 30: 2308– 17. CrossrefMedlineGoogle Scholar
Lee MS, Tseng CH, Barker CM,. Outcome after surgery and percutaneous intervention for cardiogenic shock and left main disease. Ann Thorac Surg. 2008; 86: 29– 34. CrossrefMedlineGoogle Scholar
Lee MS, Bokhoor P, Park SJ,. Unprotected left main coronary disease and ST-segment elevation myocardial infarction: a contemporary review and argument for percutaneous coronary intervention. J Am Coll Cardiol Intv. 2010; 3: 791– 5. CrossrefGoogle Scholar
Park SJ, Kim YH, Park DW,. Randomized Trial of Stents versus Bypass Surgery for Left Main Coronary Artery Disease. N Engl J Med. 2011; 364: 1718– 27. CrossrefMedlineGoogle Scholar
Jones RH, Kesler K, Phillips HR,. Long-term survival benefits of coronary artery bypass grafting and percutaneous transluminal angioplasty in patients with coronary artery disease. J Thorac Cardiovasc Surg. 1996; 111: 1013– 25. CrossrefMedlineGoogle Scholar
Myers WO, Schaff HV, Gersh BJ,. Improved survival of surgically treated patients with triple vessel coronary artery disease and severe angina pectoris. A report from the Coronary Artery Surgery Study (CASS) registry. J Thorac Cardiovasc Surg. 1989; 97: 487– 95. MedlineGoogle Scholar
Varnauskas E. Twelve-year follow-up of survival in the randomized European Coronary Surgery Study. N Engl J Med. 1988; 319: 332– 7. CrossrefMedlineGoogle Scholar
Smith PK, Califf RM, Tuttle RH,. Selection of surgical or percutaneous coronary intervention provides differential longevity benefit. Ann Thorac Surg. 2006; 82: 1420– 8. CrossrefMedlineGoogle Scholar
Borger van der Burg AE, Bax JJ, Boersma E,. Impact of percutaneous coronary intervention or coronary artery bypass grafting on outcome after nonfatal cardiac arrest outside the hospital. Am J Cardiol. 2003; 91: 785– 9. CrossrefMedlineGoogle Scholar
Every NR, Fahrenbruch CE, Hallstrom AP,. Influence of coronary bypass surgery on subsequent outcome of patients resuscitated from out of hospital cardiac arrest. J Am Coll Cardiol. 1992; 19: 1435– 9. CrossrefMedlineGoogle Scholar
Kaiser GA, Ghahramani A, Bolooki H,. Role of coronary artery surgery in patients surviving unexpected cardiac arrest. Surgery. 1975; 78: 749– 54. MedlineGoogle Scholar
Di Carli MF, Maddahi J, Rokhsar S,. Long-term survival of patients with coronary artery disease and left ventricular dysfunction: implications for the role of myocardial viability assessment in management decisions. J Thorac Cardiovasc Surg. 1998; 116: 997– 1004. CrossrefMedlineGoogle Scholar
Hachamovitch R, Hayes SW, Friedman JD,. Comparison of the short-term survival benefit associated with revascularization compared with medical therapy in patients with no prior coronary artery disease undergoing stress myocardial perfusion single photon emission computed tomography. Circulation. 2003; 107: 2900– 7. LinkGoogle Scholar
Sorajja P, Chareonthaitawee P, Rajagopalan N,. Improved survival in asymptomatic diabetic patients with high-risk SPECT imaging treated with coronary artery bypass grafting. Circulation. 2005; 112: I311– 6. MedlineGoogle Scholar
Davies RF, Goldberg AD, Forman S,. Asymptomatic Cardiac Ischemia Pilot (ACIP) study two-year follow-up: outcomes of patients randomized to initial strategies of medical therapy versus revascularization. Circulation. 1997; 95: 2037– 43. CrossrefMedlineGoogle Scholar
Alderman EL, Fisher LD, Litwin P,. Results of coronary artery surgery in patients with poor left ventricular function (CASS). Circulation. 1983; 68: 785– 95. CrossrefMedlineGoogle Scholar
O'Connor CM, Velazquez EJ, Gardner LH,. Comparison of coronary artery bypass grafting versus medical therapy on long-term outcome in patients with ischemic cardiomyopathy (a 25-year experience from the Duke Cardiovascular Disease Databank). Am J Cardiol. 2002; 90: 101– 7. CrossrefMedlineGoogle Scholar
Phillips HR, O'Connor CM, Rogers J. Revascularization for heart failure. Am Heart J. 2007; 153: 65– 73. CrossrefMedlineGoogle Scholar
Tarakji KG, Brunken R, McCarthy PM,. Myocardial viability testing and the effect of early intervention in patients with advanced left ventricular systolic dysfunction. Circulation. 2006; 113: 230– 7. LinkGoogle Scholar
Tsuyuki RT, Shrive FM, Galbraith PD,. Revascularization in patients with heart failure. CMAJ. 2006; 175: 361– 5. CrossrefMedlineGoogle Scholar
Cameron A, Davis KB, Green G,. Coronary bypass surgery with internal-thoracic-artery grafts—effects on survival over a 15-year period. N Engl J Med. 1996; 334: 216– 9. CrossrefMedlineGoogle Scholar
Loop FD, Lytle BW, Cosgrove DM,. Influence of the internal-mammary-artery graft on 10-year survival and other cardiac events. N Engl J Med. 1986; 314: 1– 6. CrossrefMedlineGoogle Scholar
Brener SJ, Lytle BW, Casserly IP,. Propensity analysis of long-term survival after surgical or percutaneous revascularization in patients with multivessel coronary artery disease and high-risk features. Circulation. 2004; 109: 2290– 5. LinkGoogle Scholar
Hannan EL, Racz MJ, Walford G,. Long-term outcomes of coronary-artery bypass grafting versus stent implantation. N Engl J Med. 2005; 352: 2174– 83. CrossrefMedlineGoogle Scholar
- 73. Deleted in proof. Google Scholar
- 74. The BARI Investigators. Influence of diabetes on 5-year mortality and morbidity in a randomized trial comparing CABG and PTCA in patients with multivessel disease: the Bypass Angioplasty Revascularization Investigation (BARI). Circulation. 1997; 96: 1761– 9. LinkGoogle Scholar
- 75. The BARI Investigators. The final 10-year follow-up results from the BARI randomized trial. J Am Coll Cardiol. 2007; 49: 1600– 6. CrossrefMedlineGoogle Scholar
Banning AP, Westaby S, Morice MC,. Diabetic and nondiabetic patients with left main and/or 3-vessel coronary artery disease: comparison of outcomes with cardiac surgery and paclitaxel-eluting stents. J Am Coll Cardiol. 2010; 55: 1067– 75. CrossrefMedlineGoogle Scholar
Hoffman SN, TenBrook JA, Wolf MP,. A meta-analysis of randomized controlled trials comparing coronary artery bypass graft with percutaneous transluminal coronary angioplasty: one- to eight-year outcomes. J Am Coll Cardiol. 2003; 41: 1293– 304. CrossrefMedlineGoogle Scholar
Hueb W, Lopes NH, Gersh BJ,. Five-year follow-up of the Medicine, Angioplasty, or Surgery Study (MASS II): a randomized controlled clinical trial of 3 therapeutic strategies for multivessel coronary artery disease. Circulation. 2007; 115: 1082– 9. LinkGoogle Scholar
Malenka DJ, Leavitt BJ, Hearne MJ,. Comparing long-term survival of patients with multivessel coronary disease after CABG or PCI: analysis of BARI-like patients in northern New England. Circulation. 2005; 112: I371– 6. MedlineGoogle Scholar
Niles NW, McGrath PD, Malenka D,. Northern New England Cardiovascular Disease Study Group. Survival of patients with diabetes and multivessel coronary artery disease after surgical or percutaneous coronary revascularization: results of a large regional prospective study. J Am Coll Cardiol. 2001; 37: 1008– 15. CrossrefMedlineGoogle Scholar
Weintraub WS, Stein B, Kosinski A,. Outcome of coronary bypass surgery versus coronary angioplasty in diabetic patients with multivessel coronary artery disease. J Am Coll Cardiol. 1998; 31: 10– 9. CrossrefMedlineGoogle Scholar
Boden WE, O'Rourke RA, Teo KK,. Optimal medical therapy with or without PCI for stable coronary disease. N Engl J Med. 2007; 356: 1503– 16. CrossrefMedlineGoogle Scholar
Bonow RO, Maurer G, Lee KL,. Myocardial viability and survival in ischemic left ventricular dysfunction. N Engl J Med. 2011; 364: 1617– 25. CrossrefMedlineGoogle Scholar
Velazquez EJ, Lee KL, Deja MA,. Coronary artery bypass surgery in patients with left ventricular dysfunction. N Engl J Med. 2011; 364: 1607– 16. CrossrefMedlineGoogle Scholar
Brener SJ, Lytle BW, Casserly IP,. Predictors of revascularization method and long-term outcome of percutaneous coronary intervention or repeat coronary bypass surgery in patients with multivessel coronary disease and previous coronary bypass surgery. Eur Heart J. 2006; 27: 413– 8. CrossrefMedlineGoogle Scholar
Gurfinkel EP, Perez de la Hoz R, Brito VM,. Invasive vs non-invasive treatment in acute coronary syndromes and prior bypass surgery. Int J Cardiol. 2007; 119: 65– 72. CrossrefMedlineGoogle Scholar
Lytle BW, Loop FD, Taylor PC,. The effect of coronary reoperation on the survival of patients with stenoses in saphenous vein bypass grafts to coronary arteries. J Thorac Cardiovasc Surg. 1993; 105: 605– 12. MedlineGoogle Scholar
Morrison DA, Sethi G, Sacks J,., Investigators of the Department of Veterans Affairs Cooperative Study #385, the Angina With Extremely Serious Operative Mortality Evaluation (AWESOME). Percutaneous coronary intervention versus coronary artery bypass graft surgery for patients with medically refractory myocardial ischemia and risk factors for adverse outcomes with bypass: a multicenter, randomized trial. J Am Coll Cardiol. 2001; 38: 143– 9. CrossrefMedlineGoogle Scholar
Pfautsch P, Frantz E, Ellmer A,. [Long-term outcome of therapy of recurrent myocardial ischemia after surgical revascularization]. Z Kardiol. 1999; 88: 489– 97. CrossrefMedlineGoogle Scholar
Sergeant P, Blackstone E, Meyns B,. First cardiological or cardiosurgical reintervention for ischemic heart disease after primary coronary artery bypass grafting. Eur J Cardiothorac Surg. 1998; 14: 480– 7. CrossrefMedlineGoogle Scholar
Stephan WJ, O'Keefe JH, Piehler JM,. Coronary angioplasty versus repeat coronary artery bypass grafting for patients with previous bypass surgery. J Am Coll Cardiol. 1996; 28: 1140– 6. CrossrefMedlineGoogle Scholar
Subramanian S, Sabik JFI, Houghtaling PL,. Decision-making for patients with patent left internal thoracic artery grafts to left anterior descending. Ann Thorac Surg. 2009; 87: 1392– 8. CrossrefMedlineGoogle Scholar
Weintraub WS, Jones EL, Morris DC,. Outcome of reoperative coronary bypass surgery versus coronary angioplasty after previous bypass surgery. Circulation. 1997; 95: 868– 77. CrossrefMedlineGoogle Scholar
Shaw LJ, Berman DS, Maron DJ,. Optimal medical therapy with or without percutaneous coronary intervention to reduce ischemic burden: results from the Clinical Outcomes Utilizing Revascularization and Aggressive Drug Evaluation (COURAGE) trial nuclear substudy. Circulation. 2008; 117: 1283– 91. LinkGoogle Scholar
Cashin WL, Sanmarco ME, Nessim SA,. Accelerated progression of atherosclerosis in coronary vessels with minimal lesions that are bypassed. N Engl J Med. 1984; 824– 8. CrossrefMedlineGoogle Scholar
Pijls NH, De Bruyne B, Peels K,. Measurement of fractional flow reserve to assess the functional severity of coronary-artery stenoses. N Engl J Med. 1996; 334: 1703– 8. CrossrefMedlineGoogle Scholar
Tonino PA, De Bruyne B, Pijls NH,. Fractional flow reserve versus angiography for guiding percutaneous coronary intervention. N Engl J Med. 2009; 360: 213– 24. CrossrefMedlineGoogle Scholar
Sawada S, Bapat A, Vaz D,. Incremental value of myocardial viability for prediction of long-term prognosis in surgically revascularized patients with left ventricular dysfunction. J Am Coll Cardiol. 2003; 42: 2099– 105. CrossrefMedlineGoogle Scholar
- 99. Trial of invasive versus medical therapy in elderly patients with chronic symptomatic coronary-artery disease (TIME): a randomised trial. Lancet. 2001; 358: 951– 7. CrossrefMedlineGoogle Scholar
Benzer W, Hofer S, Oldridge NB. Health-related quality of life in patients with coronary artery disease after different treatments for angina in routine clinical practice. Herz. 2003; 28: 421– 8. CrossrefMedlineGoogle Scholar
Bonaros N, Schachner T, Ohlinger A,. Assessment of health-related quality of life after coronary revascularization. Heart Surg Forum. 2005; 8: E380– 5. CrossrefMedlineGoogle Scholar
Bucher HC, Hengstler P, Schindler C,. Percutaneous transluminal coronary angioplasty versus medical treatment for non-acute coronary heart disease: meta-analysis of randomised controlled trials. BMJ. 2000; 321: 73– 7. CrossrefMedlineGoogle Scholar
Favarato ME, Hueb W, Boden WE,. Quality of life in patients with symptomatic multivessel coronary artery disease: a comparative post hoc analyses of medical, angioplasty or surgical strategies—MASS II trial. Int J Cardiol. 2007; 116: 364– 70. CrossrefMedlineGoogle Scholar
Hueb W, Lopes N, Gersh BJ,. Ten-year follow-up survival of the Medicine, Angioplasty, or Surgery Study (MASS II): a randomized controlled clinical trial of 3 therapeutic strategies for multivessel coronary artery disease. Circulation. 2010; 122: 949– 57. LinkGoogle Scholar
Pocock SJ, Henderson RA, Seed P,. Quality of life, employment status, and anginal symptoms after coronary angioplasty or bypass surgery. 3-year follow-up in the Randomized Intervention Treatment of Angina (RITA) Trial. Circulation. 1996; 94: 135– 42. CrossrefMedlineGoogle Scholar
Pocock SJ, Henderson RA, Clayton T,. Quality of life after coronary angioplasty or continued medical treatment for angina: three-year follow-up in the RITA-2 trial. Randomized Intervention Treatment of Angina. J Am Coll Cardiol. 2000; 35: 907– 14. CrossrefMedlineGoogle Scholar
Weintraub WS, Spertus JA, Kolm P,. Effect of PCI on quality of life in patients with stable coronary disease. N Engl J Med. 2008; 359: 677– 87. CrossrefMedlineGoogle Scholar
Wijeysundera HC, Nallamothu BK, Krumholz HM,. Meta-analysis: effects of percutaneous coronary intervention versus medical therapy on angina relief. Ann Intern Med. 2010; 152: 370– 9. CrossrefMedlineGoogle Scholar
Schofield PM, Sharples LD, Caine N,. Transmyocardial laser revascularisation in patients with refractory angina: a randomised controlled trial. Lancet. 1999; 353: 519– 24. CrossrefMedlineGoogle Scholar
Aaberge L, Nordstrand K, Dragsund M,. Transmyocardial revascularization with CO2 laser in patients with refractory angina pectoris. Clinical results from the Norwegian randomized trial. J Am Coll Cardiol. 2000; 35: 1170– 7. CrossrefMedlineGoogle Scholar
Burkhoff D, Schmidt S, Schulman SP,., ATLANTIC Investigators. Transmyocardial laser revascularisation compared with continued medical therapy for treatment of refractory angina pectoris: a prospective randomised trial. Angina Treatments-Lasers and Normal Therapies in Comparison. Lancet. 1999; 354: 885– 90. CrossrefMedlineGoogle Scholar
Allen KB, Dowling RD, DelRossi AJ,. Transmyocardial laser revascularization combined with coronary artery bypass grafting: a multicenter, blinded, prospective, randomized, controlled trial. J Thorac Cardiovasc Surg. 2000; 119: 540– 9. CrossrefMedlineGoogle Scholar
Stamou SC, Boyce SW, Cooke RH,. One-year outcome after combined coronary artery bypass grafting and transmyocardial laser revascularization for refractory angina pectoris. Am J Cardiol. 2002; 89: 1365– 8. CrossrefMedlineGoogle Scholar
- 114. The VA Coronary Artery Bypass Surgery Cooperative Study Group. Eighteen-year follow-up in the Veterans Affairs Cooperative Study of Coronary Artery Bypass Surgery for stable angina. Circulation. 1992; 86: 121– 30. LinkGoogle Scholar
Passamani E, Davis KB, Gillespie MJ,. A randomized trial of coronary artery bypass surgery. Survival of patients with a low ejection fraction. N Engl J Med. 1985; 312: 1665– 71. CrossrefMedlineGoogle Scholar
Frye RL, August P, Brooks MM,. A randomized trial of therapies for type 2 diabetes and coronary artery disease. N Engl J Med. 2009; 360: 2503– 15. CrossrefMedlineGoogle Scholar
Al Suwaidi J, Holmes DR, Salam AM,. Impact of coronary artery stents on mortality and nonfatal myocardial infarction: meta-analysis of randomized trials comparing a strategy of routine stenting with that of balloon angioplasty. Am Heart J. 2004; 147: 815– 22. CrossrefMedlineGoogle Scholar
Brophy JM, Belisle P, Joseph L. Evidence for use of coronary stents. A hierarchical bayesian meta-analysis. Ann Intern Med. 2003; 138: 777– 86. CrossrefMedlineGoogle Scholar
Trikalinos TA, Alsheikh-Ali AA, Tatsioni A,. Percutaneous coronary interventions for non-acute coronary artery disease: a quantitative 20-year synopsis and a network meta-analysis. Lancet. 2009; 373: 911– 8. CrossrefMedlineGoogle Scholar
Kastrati A, Mehilli J, Pache J,. Analysis of 14 trials comparing sirolimus-eluting stents with bare-metal stents. N Engl J Med. 2007; 356: 1030– 9. CrossrefMedlineGoogle Scholar
Cecil WT, Kasteridis P, Barnes JW,. A meta-analysis update: percutaneous coronary interventions. Am J Manag Care. 2008; 14: 521– 8. MedlineGoogle Scholar
Katritsis DG, Ioannidis JP. Percutaneous coronary intervention versus conservative therapy in nonacute coronary artery disease: a meta-analysis. Circulation. 2005; 111: 2906– 12. LinkGoogle Scholar
Schomig A, Mehilli J, de Waha A,. A meta-analysis of 17 randomized trials of a percutaneous coronary intervention-based strategy in patients with stable coronary artery disease. J Am Coll Cardiol. 2008; 52: 894– 904. CrossrefMedlineGoogle Scholar
Katritsis DG, Ioannidis JP. PCI for stable coronary disease. N Engl J Med. 2007; 357: 414– 5. CrossrefMedlineGoogle Scholar
Hambrecht R, Walther C, Mobius-Winkler S,. Percutaneous coronary angioplasty compared with exercise training in patients with stable coronary artery disease: a randomized trial. Circulation. 2004; 109: 1371– 8. LinkGoogle Scholar
Pitt B, Waters D, Brown WV,., Atorvastatin versus Revascularization Treatment Investigators. Aggressive lipid-lowering therapy compared with angioplasty in stable coronary artery disease. N Engl J Med. 1999; 341: 70– 6. CrossrefMedlineGoogle Scholar
- 127. Deleted in proof. Google Scholar
- 128. The RITA Investigators. Coronary angioplasty versus coronary artery bypass surgery: the Randomized Intervention Treatment of Angina (RITA) trial. Lancet. 1993; 341: 573– 80. CrossrefMedlineGoogle Scholar
- 129. CABRI Trial Participants. First-year results of CABRI (Coronary Angioplasty versus Bypass Revascularisation Investigation). Lancet. 1995; 346: 1179– 84. CrossrefMedlineGoogle Scholar
- 130. The Bypass Angioplasty Revascularization Investigation (BARI) Investigators. Comparison of coronary bypass surgery with angioplasty in patients with multivessel disease. N Engl J Med. 1996; 335: 217– 25. CrossrefMedlineGoogle Scholar
- 131. Writing Group for the Bypass Angioplasty Revascularization Investigation (BARI) Investigators. Five-year clinical and functional outcome comparing bypass surgery and angioplasty in patients with multivessel coronary disease. A multicenter randomized trial. JAMA. 1997; 277: 715– 21. CrossrefMedlineGoogle Scholar
Carrie D, Elbaz M, Puel J,. Five-year outcome after coronary angioplasty versus bypass surgery in multivessel coronary artery disease: results from the French Monocentric Study. Circulation. 1997; 96: II6. Google Scholar
Goy JJ, Eeckhout E, Burnand B,. Coronary angioplasty versus left internal mammary artery grafting for isolated proximal left anterior descending artery stenosis. Lancet. 1994; 343: 1449– 53. CrossrefMedlineGoogle Scholar
Goy JJ, Eeckhout E, Moret C,. Five-year outcome in patients with isolated proximal left anterior descending coronary artery stenosis treated by angioplasty or left internal mammary artery grafting. A prospective trial. Circulation. 1999; 99: 3255– 9. CrossrefMedlineGoogle Scholar
Hamm CW, Reimers J, Ischinger T,. A randomized study of coronary angioplasty compared with bypass surgery in patients with symptomatic multivessel coronary disease. German Angioplasty Bypass Surgery Investigation (GABI). N Engl J Med. 1994; 331: 1037– 43. CrossrefMedlineGoogle Scholar
Henderson RA, Pocock SJ, Sharp SJ,. Long-term results of RITA-1 trial: clinical and cost comparisons of coronary angioplasty and coronary-artery bypass grafting. Randomised Intervention Treatment of Angina. Lancet. 1998; 352: 1419– 25. CrossrefMedlineGoogle Scholar
Hueb WA, Soares PR, Almeida De Oliveira S,. Five-year follow-up of the medicine, angioplasty, or surgery study (MASS): a prospective, randomized trial of medical therapy, balloon angioplasty, or bypass surgery for single proximal left anterior descending coronary artery stenosis. Circulation. 1999; 100: II107– 13. CrossrefMedlineGoogle Scholar
King SBI, Lembo NJ, Weintraub WS,. A randomized trial comparing coronary angioplasty with coronary bypass surgery. Emory Angioplasty versus Surgery Trial (EAST). N Engl J Med. 1994; 331: 1044– 50. CrossrefMedlineGoogle Scholar
King SBI, Kosinski AS, Guyton RA,. Eight-year mortality in the Emory Angioplasty versus Surgery Trial (EAST). J Am Coll Cardiol. 2000; 35: 1116– 21. CrossrefMedlineGoogle Scholar
Rodriguez A, Boullon F, Perez-Balino N,., ERACI Group. Argentine randomized trial of percutaneous transluminal coronary angioplasty versus coronary artery bypass surgery in multivessel disease (ERACI): in-hospital results and 1-year follow-up. J Am Coll Cardiol. 1993; 22: 1060– 7. CrossrefMedlineGoogle Scholar
Rodriguez A, Mele E, Peyregne E,. Three-year follow-up of the Argentine Randomized Trial of Percutaneous Transluminal Coronary Angioplasty Versus Coronary Artery Bypass Surgery in Multi-vessel Disease (ERACI). J Am Coll Cardiol. 1996; 27: 1178– 84. CrossrefMedlineGoogle Scholar
Wahrborg P. Quality of life after coronary angioplasty or bypass surgery. 1-year follow-up in the Coronary Angioplasty versus Bypass Revascularization investigation (CABRI) trial. Eur Heart J. 1999; 20: 653– 8. CrossrefMedlineGoogle Scholar
- 143. The SoS Investigators. Coronary artery bypass surgery versus percutaneous coronary intervention with stent implantation in patients with multivessel coronary artery disease (the Stent or Surgery trial): a randomised controlled trial. Lancet. 2002; 360: 965– 70. CrossrefMedlineGoogle Scholar
Cisowski M, Drzewiecki J, Drzewiecka-Gerber A,. Primary stenting versus MIDCAB: preliminary report-comparision of two methods of revascularization in single left anterior descending coronary artery stenosis. Ann Thorac Surg. 2002; 74: S1334– 9. CrossrefMedlineGoogle Scholar
Cisowski M, Drzewiecka-Gerber A, Ulczok R,. Primary direct stenting versus endoscopic atraumatic coronary artery bypass surgery in patients with proximal stenosis of the left anterior descending coronary artery—a prospective, randomised study. Kardiol Pol. 2004; 61: 253– 61. MedlineGoogle Scholar
Diegeler A, Thiele H, Falk V,. Comparison of stenting with minimally invasive bypass surgery for stenosis of the left anterior descending coronary artery. N Engl J Med. 2002; 347: 561– 6. CrossrefMedlineGoogle Scholar
Drenth DJ, Veeger NJ, Winter JB,. A prospective randomized trial comparing stenting with off-pump coronary surgery for high-grade stenosis in the proximal left anterior descending coronary artery: three-year follow-up. J Am Coll Cardiol. 2002; 40: 1955– 60. CrossrefMedlineGoogle Scholar
Drenth DJ, Veeger NJ, Middel B,. Comparison of late (four years) functional health status between percutaneous transluminal angioplasty intervention and off-pump left internal mammary artery bypass grafting for isolated high-grade narrowing of the proximal left anterior descending coronary artery. Am J Cardiol. 2004; 94: 1414– 7. MedlineGoogle Scholar
Eefting F, Nathoe H, van Dijk D,. Randomized comparison between stenting and off-pump bypass surgery in patients referred for angioplasty. Circulation. 2003; 108: 2870– 6. LinkGoogle Scholar
Goy JJ, Kaufmann U, Goy-Eggenberger D,. A prospective randomized trial comparing stenting to internal mammary artery grafting for proximal, isolated de novo left anterior coronary artery stenosis: the SIMA trial. Stenting vs Internal Mammary Artery. Mayo Clin Proc. 2000; 75: 1116– 23. CrossrefMedlineGoogle Scholar
Hueb W, Soares PR, Gersh BJ,. The medicine, angioplasty, or surgery study (MASS-II): a randomized, controlled clinical trial of three therapeutic strategies for multivessel coronary artery disease: one-year results. J Am Coll Cardiol. 2004; 43: 1743– 51. CrossrefMedlineGoogle Scholar
Kim JW, Lim DS, Sun K,. Stenting or MIDCAB using ministernotomy for revascularization of proximal left anterior descending artery?Int J Cardiol. 2005; 99: 437– 41. CrossrefMedlineGoogle Scholar
Pohl T, Giehrl W, Reichart B,. Retroinfusion-supported stenting in high-risk patients for percutaneous intervention and bypass surgery: results of the prospective randomized myoprotect I study. Catheter Cardiovasc Interv. 2004; 62: 323– 30. CrossrefMedlineGoogle Scholar
Reeves BC, Angelini GD, Bryan AJ,. A multi-centre randomised controlled trial of minimally invasive direct coronary bypass grafting versus percutaneous transluminal coronary angioplasty with stenting for proximal stenosis of the left anterior descending coronary artery. Health Technol Assess. 2004; 8: 1– 43. CrossrefMedlineGoogle Scholar
Rodriguez A, Bernardi V, Navia J,., ERACI II Investigators. Argentine randomized study: coronary angioplasty with stenting versus coronary bypass surgery in patients with multiple-vessel disease (ERACI II): 30-day and one-year follow-up results. J Am Coll Cardiol. 2001; 37: 51– 8. CrossrefMedlineGoogle Scholar
Rodriguez AE, Baldi J, Fernandez PC,. Five-year follow-up of the Argentine randomized trial of coronary angioplasty with stenting versus coronary bypass surgery in patients with multiple vessel disease (ERACI II). J Am Coll Cardiol. 2005; 46: 582– 8. CrossrefMedlineGoogle Scholar
Serruys PW, Unger F, Sousa JE,. Comparison of coronary-artery bypass surgery and stenting for the treatment of multivessel disease. N Engl J Med. 2001; 344: 1117– 24. CrossrefMedlineGoogle Scholar
Serruys PW, Ong AT, van Herwerdens LA,. Five-year outcomes after coronary stenting versus bypass surgery for the treatment of multivessel disease: the final analysis of the Arterial Revascularization Therapies Study (ARTS) randomized trial. J Am Coll Cardiol. 2005; 46: 575– 81. CrossrefMedlineGoogle Scholar
Stroupe KT, Morrison DA, Hlatky MA,. Cost-effectiveness of coronary artery bypass grafts versus percutaneous coronary intervention for revascularization of high-risk patients. Circulation. 2006; 114: 1251– 7. LinkGoogle Scholar
Thiele H, Oettel S, Jacobs S,. Comparison of bare-metal stenting with minimally invasive bypass surgery for stenosis of the left anterior descending coronary artery: a 5-year follow-up. Circulation. 2005; 112: 3445– 50. LinkGoogle Scholar
Hong SJ, Lim DS, Seo HS,. Percutaneous coronary intervention with drug-eluting stent implantation vs. minimally invasive direct coronary artery bypass (MIDCAB) in patients with left anterior descending coronary artery stenosis. Catheter Cardiovasc Interv. 2005; 64: 75– 81. CrossrefMedlineGoogle Scholar
Thiele H, Neumann-Schniedewind P, Jacobs S,. Randomized comparison of minimally invasive direct coronary artery bypass surgery versus sirolimus-eluting stenting in isolated proximal left anterior descending coronary artery stenosis. J Am Coll Cardiol. 2009; 53: 2324– 31. CrossrefMedlineGoogle Scholar
Bravata DM, Gienger AL, McDonald KM,. Systematic review: the comparative effectiveness of percutaneous coronary interventions and coronary artery bypass graft surgery. Ann Intern Med. 2007; 147: 703– 16. CrossrefMedlineGoogle Scholar
Hlatky MA, Boothroyd DB, Bravata DM,. Coronary artery bypass surgery compared with percutaneous coronary interventions for multivessel disease: a collaborative analysis of individual patient data from ten randomised trials. Lancet. 2009; 373: 1190– 7. CrossrefMedlineGoogle Scholar
Briguori C, Condorelli G, Airoldi F,. Comparison of coronary drug-eluting stents versus coronary artery bypass grafting in patients with diabetes mellitus. Am J Cardiol. 2007; 99: 779– 84. CrossrefMedlineGoogle Scholar
Javaid A, Steinberg DH, Buch AN,. Outcomes of coronary artery bypass grafting versus percutaneous coronary intervention with drug-eluting stents for patients with multivessel coronary artery disease. Circulation. 2007; 116: I200– 6. LinkGoogle Scholar
Lee MS, Jamal F, Kedia G,. Comparison of bypass surgery with drug-eluting stents for diabetic patients with multivessel disease. Int J Cardiol. 2007; 123: 34– 42. CrossrefMedlineGoogle Scholar
Park DW, Yun SC, Lee SW,. Long-term mortality after percutaneous coronary intervention with drug-eluting stent implantation versus coronary artery bypass surgery for the treatment of multivessel coronary artery disease. Circulation. 2008; 117: 2079– 86. LinkGoogle Scholar
Tarantini G, Ramondo A, Napodano M,. PCI versus CABG for multivessel coronary disease in diabetics. Catheter Cardiovasc Interv. 2009; 73: 50– 8. CrossrefMedlineGoogle Scholar
Varani E, Balducelli M, Vecchi G,. Comparison of multiple drug-eluting stent percutaneous coronary intervention and surgical revascularization in patients with multivessel coronary artery disease: one-year clinical results and total treatment costs. J Invasive Cardiol. 2007; 19: 469– 75. MedlineGoogle Scholar
Yang JH, Gwon HC, Cho SJ,. Comparison of coronary artery bypass grafting with drug-eluting stent implantation for the treatment of multivessel coronary artery disease. Ann Thorac Surg. 2008; 85: 65– 70. CrossrefMedlineGoogle Scholar
Yang ZK, Shen WF, Zhang RY,. Coronary artery bypass surgery versus percutaneous coronary intervention with drug-eluting stent implantation in patients with multivessel coronary disease. J Interv Cardiol. 2007; 20: 10– 6. CrossrefMedlineGoogle Scholar
Benedetto U, Melina G, Angeloni E,. Coronary artery bypass grafting versus drug-eluting stents in multivessel coronary disease. A meta-analysis on 24 268 patients. Eur J Cardiothorac Surg. 2009; 36: 611– 5. CrossrefMedlineGoogle Scholar
- 174. Deleted in proof. Google Scholar
Ragosta M, Dee S, Sarembock IJ,. Prevalence of unfavorable angiographic characteristics for percutaneous intervention in patients with unprotected left main coronary artery disease. Catheter Cardiovasc Interv. 2006; 68: 357– 62. CrossrefMedlineGoogle Scholar
Chieffo A, Park SJ, Valgimigli M,. Favorable long-term outcome after drug-eluting stent implantation in nonbifurcation lesions that involve unprotected left main coronary artery: a multi-center registry. Circulation. 2007; 116: 158– 62. LinkGoogle Scholar
Tamburino C, Capranzano P, Capodanno D,. Plaque distribution patterns in distal left main coronary artery to predict outcomes after stent implantation. J Am Coll Cardiol Intv. 2010; 3: 624– 31. CrossrefGoogle Scholar
Ben-Gal Y, Mohr R, Braunstein R,. Revascularization of left anterior descending artery with drug-eluting stents: comparison with minimally invasive direct coronary artery bypass surgery. Ann Thorac Surg. 2006; 82: 2067– 71. CrossrefMedlineGoogle Scholar
Cisowski M, Drzewiecka-Gerber A, Ulczok R,. Primary direct stenting versus endoscopic atraumatic coronary artery bypass surgery in patients with proximal stenosis of the left anterior descending coronary artery—a prospective, randomised study. Kardiol Pol. 2004; 61: 253– 61. MedlineGoogle Scholar
Fraund S, Herrmann G, Witzke A,. Midterm follow-up after minimally invasive direct coronary artery bypass grafting versus percutaneous coronary intervention techniques. Ann Thorac Surg. 2005; 79: 1225– 31. CrossrefMedlineGoogle Scholar
Goy JJ, Kaufmann U, Hurni M,. 10-year follow-up of a prospective randomized trial comparing bare-metal stenting with internal mammary artery grafting for proximal, isolated de novo left anterior coronary artery stenosis the SIMA (Stenting versus Internal Mammary Artery grafting) trial. J Am Coll Cardiol. 2008; 52: 815– 7. CrossrefMedlineGoogle Scholar
Aziz O, Rao C, Panesar SS,. Meta-analysis of minimally invasive internal thoracic artery bypass versus percutaneous revascularisation for isolated lesions of the left anterior descending artery. BMJ. 2007; 334: 617. CrossrefMedlineGoogle Scholar
Jaffery Z, Kowalski M, Weaver WD,. A meta-analysis of randomized control trials comparing minimally invasive direct coronary bypass grafting versus percutaneous coronary intervention for stenosis of the proximal left anterior descending artery. Eur J Cardiothorac Surg. 2007; 31: 691– 7. CrossrefMedlineGoogle Scholar
Kapoor , Gienger AL, Ardehali R,. Isolated disease of the proximal left anterior descending artery comparing the effectiveness of percutaneous coronary interventions and coronary artery bypass surgery. J Am Coll Cardiol Intv. 2008; 1: 483– 91. CrossrefGoogle Scholar
Abizaid A, Costa MA, Centemero M,. Clinical and economic impact of diabetes mellitus on percutaneous and surgical treatment of multivessel coronary disease patients: insights from the Arterial Revascularization Therapy Study (ARTS) trial. Circulation. 2001; 104: 533– 8. CrossrefMedlineGoogle Scholar
Kapur A, Hall RJ, Malik IS,. Randomized comparison of percutaneous coronary intervention with coronary artery bypass grafting in diabetic patients. 1-year results of the CARDia (Coronary Artery Revascularization in Diabetes) trial. J Am Coll Cardiol. 2010; 55: 432– 40. CrossrefMedlineGoogle Scholar
Sarnak MJ, Levey AS, Schoolwerth AC,. Kidney disease as a risk factor for development of cardiovascular disease: a statement from the American Heart Association Councils on Kidney in Cardiovascular Disease, High Blood Pressure Research, Clinical Cardiology, and Epidemiology and Prevention. Circulation. 2003; 108: 2154– 69. LinkGoogle Scholar
Roger VL, Go AS, Lloyd-Jones DM,; on behalf of the American Heart Association Statistics Committee and Stroke Statistics Subcommittee. Heart disease and stroke statistics – 2011 update: a report from the American Heart Association. Circulation. 2011; 123: e18– 209. LinkGoogle Scholar
Sedlis SP, Jurkovitz CT, Hartigan PM,. Optimal medical therapy with or without percutaneous coronary intervention for patients with stable coronary artery disease and chronic kidney disease. Am J Cardiol. 2009; 104: 1647– 53. CrossrefMedlineGoogle Scholar
Hemmelgarn BR, Southern D, Culleton BF,. Survival after coronary revascularization among patients with kidney disease. Circulation. 2004; 110: 1890– 5. LinkGoogle Scholar
Reddan DN, Szczech LA, Tuttle RH,. Chronic kidney disease, mortality, and treatment strategies among patients with clinically significant coronary artery disease. J Am Soc Nephrol. 2003; 14: 2373– 80. CrossrefMedlineGoogle Scholar
Bae KS, Park HC, Kang BS,. Percutaneous coronary intervention versus coronary artery bypass grafting in patients with coronary artery disease and diabetic nephropathy: a single center experience. Korean J Intern Med. 2007; 22: 139– 46. CrossrefMedlineGoogle Scholar
Herzog CA, Ma JZ, Collins AJ. Comparative survival of dialysis patients in the United States after coronary angioplasty, coronary artery stenting, and coronary artery bypass surgery and impact of diabetes. Circulation. 2002; 106: 2207– 11. LinkGoogle Scholar
Ix JH, Mercado N, Shlipak MG,. Association of chronic kidney disease with clinical outcomes after coronary revascularization: the Arterial Revascularization Therapies Study (ARTS). Am Heart J. 2005; 149: 512– 9. CrossrefMedlineGoogle Scholar
Koyanagi T, Nishida H, Kitamura M,. Comparison of clinical outcomes of coronary artery bypass grafting and percutaneous transluminal coronary angioplasty in renal dialysis patients. Ann Thorac Surg. 1996; 61: 1793– 6. CrossrefMedlineGoogle Scholar
Szczech LA, Reddan DN, Owen WF,. Differential survival after coronary revascularization procedures among patients with renal insufficiency. Kidney Int. 2001; 60: 292– 9. CrossrefMedlineGoogle Scholar
Jones EL, Craver JM, Guyton RA,. Importance of complete revascularization in performance of the coronary bypass operation. Am J Cardiol. 1983; 51: 7– 12. CrossrefMedlineGoogle Scholar
Bell MR, Bailey KR, Reeder GS,. Percutaneous transluminal angioplasty in patients with multivessel coronary disease: how important is complete revascularization for cardiac event-free survival?J Am Coll Cardiol. 1990; 16: 553– 62. CrossrefMedlineGoogle Scholar
Bourassa MG, Yeh W, Holubkov R,. Long-term outcome of patients with incomplete vs complete revascularization after multi-vessel PTCA. A report from the NHLBI PTCA Registry. Eur Heart J. 1998; 19: 103– 11. CrossrefMedlineGoogle Scholar
Faxon DP, Ghalilli K, Jacobs AK,. The degree of revascularization and outcome after multivessel coronary angioplasty. Am Heart J. 1992; 123: 854– 9. CrossrefMedlineGoogle Scholar
Berger PB, Velianou JL, Aslanidou VH,. Survival following coronary angioplasty versus coronary artery bypass surgery in anatomic subsets in which coronary artery bypass surgery improves survival compared with medical therapy. Results from the Bypass Angioplasty Revascularization Investigation (BARI). J Am Coll Cardiol. 2001; 38: 1440– 9. MedlineGoogle Scholar
Gioia G, Matthai W, Gillin K,. Revascularization in severe left ventricular dysfunction: outcome comparison of drug-eluting stent implantation versus coronary artery by-pass grafting. Catheter Cardiovasc Interv. 2007; 70: 26– 33. CrossrefMedlineGoogle Scholar
O'Keefe JH, Allan JJ, McCallister BD,. Angioplasty versus bypass surgery for multivessel coronary artery disease with left ventricular ejection fraction < or = 40. Am J Cardiol. 1993; 71: 897– 901. CrossrefMedlineGoogle Scholar
Cole JH, Jones EL, Craver JM,. Outcomes of repeat revascularization in diabetic patients with prior coronary surgery. J Am Coll Cardiol. 2002; 40: 1968– 75. CrossrefMedlineGoogle Scholar
Choudhry NK, Singh JM, Barolet A,. How should patients with unstable angina and non-ST-segment elevation myocardial infarction be managed? A meta-analysis of randomized trials. Am J Med. 2005; 118: 465– 74. CrossrefMedlineGoogle Scholar
Fox KA, Poole-Wilson PA, Henderson RA,. Interventional versus conservative treatment for patients with unstable angina or non-ST-elevation myocardial infarction: the British Heart Foundation RITA 3 randomised trial. Randomized Intervention Trial of unstable Angina. Lancet. 2002; 360: 743– 51. CrossrefMedlineGoogle Scholar
Fox KA, Clayton TC, Damman P,. Long-term outcome of a routine versus selective invasive strategy in patients with non-ST-segment elevation acute coronary syndrome a meta-analysis of individual patient data. J Am Coll Cardiol. 2010; 55: 2435– 45. CrossrefMedlineGoogle Scholar
Grines CL, Bonow RO, Casey DE,. Prevention of premature discontinuation of dual antiplatelet therapy in patients with coronary artery stents: a science advisory from the American Heart Association, American College of Cardiology, Society for Cardiovascular Angiography and Interventions, American College of Surgeons, and American Dental Association, with representation from the American College of Physicians. J Am Coll Cardiol. 2007; 49: 734– 9. MedlineGoogle Scholar
Leon MB, Baim DS, Popma JJ,., Stent Anticoagulation Restenosis Study Investigators. A clinical trial comparing three antithrombotic-drug regimens after coronary-artery stenting. N Engl J Med. 1998; 339: 1665– 71. CrossrefMedlineGoogle Scholar
Mauri L, Hsieh WH, Massaro JM,. Stent thrombosis in randomized clinical trials of drug-eluting stents. N Engl J Med. 2007; 356: 1020– 9. CrossrefMedlineGoogle Scholar
McFadden EP, Stabile E, Regar E,. Late thrombosis in drug-eluting coronary stents after discontinuation of antiplatelet therapy. Lancet. 2004; 364: 1519– 21. CrossrefMedlineGoogle Scholar
Eisenstein EL, Anstrom KJ, Kong DF,. Clopidogrel use and long-term clinical outcomes after drug-eluting stent implantation. JAMA. 2007; 297: 159– 68. CrossrefMedlineGoogle Scholar
Bridges CR, Horvath KA, Nugent WC,. The Society of Thoracic Surgeons practice guideline series: transmyocardial laser revascularization. Ann Thorac Surg. 2004; 77: 1494– 502. CrossrefMedlineGoogle Scholar
Vineberg A. Development of an anastomosis between the coronary vessels and a transplanted internal mammary artery. Can Med Assoc J. 1946; 55: 117– 9. Google Scholar
Aaberge L, Rootwelt K, Blomhoff S,. Continued symptomatic improvement three to five years after transmyocardial revascularization with CO(2) laser: a late clinical follow-up of the Norwegian Randomized trial with transmyocardial revascularization. J Am Coll Cardiol. 2002; 39: 1588– 93. CrossrefMedlineGoogle Scholar
Allen KB, Dowling RD, Fudge TL,. Comparison of transmyocardial revascularization with medical therapy in patients with refractory angina. N Engl J Med. 1999; 341: 1029– 36. CrossrefMedlineGoogle Scholar
Frazier OH, March RJ, Horvath KA. Transmyocardial revascularization with a carbon dioxide laser in patients with end-stage coronary artery disease. N Engl J Med. 1999; 341: 1021– 8. CrossrefMedlineGoogle Scholar
Peterson ED, Kaul P, Kaczmarek RG,. From controlled trials to clinical practice: monitoring transmyocardial revascularization use and outcomes. J Am Coll Cardiol. 2003; 42: 1611– 6. CrossrefMedlineGoogle Scholar
Bonatti J, Schachner T, Bonaros N,. Simultaneous hybrid coronary revascularization using totally endoscopic left internal mam-mary artery bypass grafting and placement of rapamycin eluting stents in the same interventional session. The COMBINATION pilot study. Cardiology. 2008; 110: 92– 5. CrossrefMedlineGoogle Scholar
Gilard M, Bezon E, Cornily JC,. Same-day combined percutaneous coronary intervention and coronary artery surgery. Cardiology. 2007; 108: 363– 7. CrossrefMedlineGoogle Scholar
Holzhey DM, Jacobs S, Mochalski M,. Minimally invasive hybrid coronary artery revascularization. Ann Thorac Surg. 2008; 86: 1856– 60. CrossrefMedlineGoogle Scholar
Kon ZN, Brown EN, Tran R,. Simultaneous hybrid coronary revascularization reduces postoperative morbidity compared with results from conventional off-pump coronary artery bypass. J Thorac Cardiovasc Surg. 2008; 135: 367– 75. CrossrefMedlineGoogle Scholar
Reicher B, Poston RS, Mehra MR,. Simultaneous “hybrid” percutaneous coronary intervention and minimally invasive surgical bypass grafting: feasibility, safety, and clinical outcomes. Am Heart J. 2008; 155: 661– 7. CrossrefMedlineGoogle Scholar
Vassiliades TA, Douglas JS, Morris DC,. Integrated coronary revascularization with drug-eluting stents: immediate and seven-month outcome. J Thorac Cardiovasc Surg. 2006; 131: 956– 62. CrossrefMedlineGoogle Scholar
Zhao DX, Leacche M, Balaguer JM,. Routine intraoperative completion angiography after coronary artery bypass grafting and 1-stop hybrid revascularization results from a fully integrated hybrid catheterization laboratory/operating room. J Am Coll Cardiol. 2009; 53: 232– 41. CrossrefMedlineGoogle Scholar
Angelini GD, Wilde P, Salerno TA,. Integrated left small thoracotomy and angioplasty for multivessel coronary artery revascularisation. Lancet. 1996; 347: 757– 8. CrossrefMedlineGoogle Scholar
Simoons ML. Myocardial revascularization—bypass surgery or angioplasty?N Engl J Med. 1996; 335: 275– 7. CrossrefMedlineGoogle Scholar
Sonoda S, Morino Y, Ako J,. Impact of final stent dimensions on long-term results following sirolimus-eluting stent implantation: serial intravascular ultrasound analysis from the Sirius trial. J Am Coll Cardiol. 2004; 43: 1959– 63. CrossrefMedlineGoogle Scholar
Pijls NH, Klauss V, Siebert U,. Coronary pressure measurement after stenting predicts adverse events at follow-up: a multicenter registry. Circulation. 2002; 105: 2950– 4. LinkGoogle Scholar
Ellis SG, Vandormael MG, Cowley MJ,. Coronary morphologic and clinical determinants of procedural outcome with angioplasty for multivessel coronary disease. Implications for patient selection. Multivessel Angioplasty Prognosis Study Group. Circulation. 1990; 82: 1193– 202. LinkGoogle Scholar
Singh M, Lennon RJ, Holmes DR,. Correlates of procedural complications and a simple integer risk score for percutaneous coronary intervention. J Am Coll Cardiol. 2002; 40: 387– 93. CrossrefMedlineGoogle Scholar
Tan K, Sulke N, Taub N,. Clinical and lesion morphologic determinants of coronary angioplasty success and complications: current experience. J Am Coll Cardiol. 1995; 25: 855– 65. CrossrefMedlineGoogle Scholar
Moscucci M, Kline-Rogers E, Share D,. Simple bedside additive tool for prediction of in-hospital mortality after percutaneous coronary interventions. Circulation. 2001; 104: 263– 8. CrossrefMedlineGoogle Scholar
Resnic FS, Ohno-Machado L, Selwyn A,. Simplified risk score models accurately predict the risk of major in-hospital complications following percutaneous coronary intervention. Am J Cardiol. 2001; 88: 5– 9. CrossrefMedlineGoogle Scholar
Singh M, Rihal CS, Lennon RJ,. Comparison of Mayo Clinic risk score and American College of Cardiology/American Heart Association lesion classification in the prediction of adverse cardiovascular outcome following percutaneous coronary interventions. J Am Coll Cardiol. 2004; 44: 357– 61. CrossrefMedlineGoogle Scholar
Peterson ED, Dai D, DeLong ER,. Contemporary mortality risk prediction for percutaneous coronary intervention: results from 588 398 procedures in the National Cardiovascular Data Registry. J Am Coll Cardiol. 2010; 55: 1923– 32. CrossrefMedlineGoogle Scholar
Kimmel SE, Berlin JA, Strom BL,. Development and validation of simplified predictive index for major complications in contemporary percutaneous transluminal coronary angioplasty practice. The Registry Committee of the Society for Cardiac Angiography and Interventions. J Am Coll Cardiol. 1995; 26: 931– 8. CrossrefMedlineGoogle Scholar
Sianos G, Morel MA, Kappetein AP,. The SYNTAX score: an angiographic tool grading the complexity of coronary artery disease. EuroIntervention. 2005; 1: 219– 27. MedlineGoogle Scholar
Alpert JS, Thygesen K, Antman E,. Myocardial infarction redefined—a consensus document of the Joint European Society of Cardiology/American College of Cardiology Committee for the redefinition of myocardial infarction. J Am Coll Cardiol. 2000; 36: 959– 69. CrossrefMedlineGoogle Scholar
Thygesen K, Alpert JS, White HD. Universal definition of myocar-dial infarction. Eur Heart J. 2007; 28: 2525– 38. CrossrefMedlineGoogle Scholar
Alcock RF, Roy P, Adorini K,. Incidence and determinants of myocardial infarction following percutaneous coronary interventions according to the revised Joint Task Force definition of troponin T elevation. Int J Cardiol. 2010; 140: 66– 72. CrossrefMedlineGoogle Scholar
Testa L, Van Gaal WJ, Biondi Zoccai GG,. Myocardial infarction after percutaneous coronary intervention: a meta-analysis of troponin elevation applying the new universal definition. QJM. 2009; 102: 369– 78. CrossrefMedlineGoogle Scholar
Yang EH, Gumina RJ, Lennon RJ,. Emergency coronary artery bypass surgery for percutaneous coronary interventions: changes in the incidence, clinical characteristics, and indications from 1979 to 2003. J Am Coll Cardiol. 2005; 46: 2004– 9. CrossrefMedlineGoogle Scholar
Kutcher MA, Klein LW, Ou FS,. Percutaneous coronary interventions in facilities without cardiac surgery on site: a report from the National Cardiovascular Data Registry (NCDR). J Am Coll Cardiol. 2009; 54: 16– 24. CrossrefMedlineGoogle Scholar
Roy P, de Labriolle A, Hanna N,. Requirement for emergent coronary artery bypass surgery following percutaneous coronary intervention in the stent era. Am J Cardiol. 2009; 103: 950– 3. CrossrefMedlineGoogle Scholar
Seshadri N, Whitlow PL, Acharya N,. Emergency coronary artery bypass surgery in the contemporary percutaneous coronary intervention era. Circulation. 2002; 106: 2346– 50. LinkGoogle Scholar
Aggarwal A, Dai D, Rumsfeld JS,. Incidence and predictors of stroke associated with percutaneous coronary intervention. Am J Cardiol. 2009; 104: 349– 53. CrossrefMedlineGoogle Scholar
Dukkipati S, O'Neill WW, Harjai KJ,. Characteristics of cerebrovascular accidents after percutaneous coronary interventions. J Am Coll Cardiol. 2004; 43: 1161– 7. CrossrefMedlineGoogle Scholar
Duvernoy CS, Smith DE, Manohar P,. Gender differences in adverse outcomes after contemporary percutaneous coronary intervention: an analysis from the Blue Cross Blue Shield of Michigan Cardiovascular Consortium (BMC2) percutaneous coronary intervention registry. Am Heart J. 2010; 159: 677– 83. CrossrefMedlineGoogle Scholar
Hamon M, Baron JC, Viader F,. Periprocedural stroke and cardiac catheterization. Circulation. 2008; 118: 678– 83. LinkGoogle Scholar
Adams HP, del Zoppo G, Alberts MJ,. Guidelines for the early management of adults with ischemic stroke: a guideline from the American Heart Association/American Stroke Association Stroke Council, Clinical Cardiology Council, Cardiovascular Radiology and Intervention Council, and the Atherosclerotic Peripheral Vascular Disease and Quality of Care Outcomes in Research Interdisciplinary Working Groups. Circulation. 2007; 115: e478– 534. LinkGoogle Scholar
Levine GN, Kern MJ, Berger PB,. Management of patients undergoing percutaneous coronary revascularization. Ann Intern Med. 2003; 139: 123– 36. CrossrefMedlineGoogle Scholar
Ahmed B, Piper WD, Malenka D,. Significantly improved vascular complications among women undergoing percutaneous coronary intervention: a report from the Northern New England Percutaneous Coronary Intervention Registry. Circ Cardiovasc Interv. 2009; 2: 423– 9. LinkGoogle Scholar
Applegate RJ, Sacrinty MT, Kutcher MA,. Trends in vascular complications after diagnostic cardiac catheterization and percutaneous coronary intervention via the femoral artery, 1998 to 2007. J Am Coll Cardiol Intv. 2008; 1: 317– 26. CrossrefGoogle Scholar
Jolly SS, Amlani S, Hamon M,. Radial versus femoral access for coronary angiography or intervention and the impact on major bleeding and ischemic events: a systematic review and meta-analysis of randomized trials. Am Heart J. 2009; 157: 132– 40. CrossrefMedlineGoogle Scholar
Nikolsky E, Mehran R, Halkin A,. Vascular complications associated with arteriotomy closure devices in patients undergoing percutaneous coronary procedures: a meta-analysis. J Am Coll Cardiol. 2004; 44: 1200– 9. MedlineGoogle Scholar
Patel MR, Jneid H, Derdeyn CP,. Arteriotomy closure devices for cardiovascular procedures: a scientific statement from the American Heart Association. Circulation. 2010; 122: 1882– 93. LinkGoogle Scholar
Piper WD, Malenka DJ, Ryan TJ,. Predicting vascular complications in percutaneous coronary interventions. Am Heart J. 2003; 145: 1022– 9. CrossrefMedlineGoogle Scholar
Seto AH, Abu-Fadel MS, Sparling JM,. Real-time ultrasound guidance facilitates femoral arterial access and reduces vascular complications: FAUST (Femoral Arterial Access With Ultrasound Trial). J Am Coll Cardiol Intv. 2010; 3: 751– 8. CrossrefGoogle Scholar
Rao SV, Cohen MG, Kandzari DE,. The transradial approach to percutaneous coronary intervention: historical perspective, current concepts, and future directions. J Am Coll Cardiol. 2010; 55: 2187– 95. CrossrefMedlineGoogle Scholar
Stella PR, Kiemeneij F, Laarman GJ,. Incidence and outcome of radial artery occlusion following transradial artery coronary angioplasty. Cathet Cardiovasc Diagn. 1997; 40: 156– 8. CrossrefMedlineGoogle Scholar
Freestone B, Nolan J. Transradial cardiac procedures: the state of the art. Heart. 2010; 96: 883– 91. CrossrefMedlineGoogle Scholar
Ellis SG, Ajluni S, Arnold AZ,. Increased coronary perforation in the new device era. Incidence, classification, management, and outcome. Circulation. 1994; 90: 2725– 30. LinkGoogle Scholar
Javaid A, Buch AN, Satler LF,. Management and outcomes of coronary artery perforation during percutaneous coronary intervention. Am J Cardiol. 2006; 98: 911– 4. CrossrefMedlineGoogle Scholar
Feit F, Voeltz MD, Attubato MJ,. Predictors and impact of major hemorrhage on mortality following percutaneous coronary intervention from the REPLACE-2 Trial. Am J Cardiol. 2007; 100: 1364– 9. CrossrefMedlineGoogle Scholar
Manoukian SV, Feit F, Mehran R,. Impact of major bleeding on 30-day mortality and clinical outcomes in patients with acute coronary syndromes: an analysis from the ACUITY Trial. J Am Coll Cardiol. 2007; 49: 1362– 8. CrossrefMedlineGoogle Scholar
Mehran R, Pocock SJ, Nikolsky E,. A risk score to predict bleeding in patients with acute coronary syndromes. J Am Coll Cardiol. 2010; 55: 2556– 66. CrossrefMedlineGoogle Scholar
Nikolsky E, Mehran R, Dangas G,. Development and validation of a prognostic risk score for major bleeding in patients undergoing percutaneous coronary intervention via the femoral approach. Eur Heart J. 2007; 28: 1936– 45. CrossrefMedlineGoogle Scholar
Subherwal S, Bach RG, Chen AY,. Baseline risk of major bleeding in non-ST-segment-elevation myocardial infarction: the CRUSADE (Can Rapid risk stratification of Unstable angina patients Suppress ADverse outcomes with Early implementation of the ACC/AHA Guidelines) Bleeding Score. Circulation. 2009; 119: 1873– 82. LinkGoogle Scholar
Mehran R, Aymong ED, Nikolsky E,. A simple risk score for prediction of contrast-induced nephropathy after percutaneous coronary intervention: development and initial validation. J Am Coll Cardiol. 2004; 44: 1393– 9. MedlineGoogle Scholar
Moscucci M, Rogers EK, Montoye C,. Association of a continuous quality improvement initiative with practice and outcome variations of contemporary percutaneous coronary interventions. Circulation. 2006; 113: 814– 22. LinkGoogle Scholar
Bader BD, Berger ED, Heede MB,. What is the best hydration regimen to prevent contrast media-induced nephrotoxicity?Clin Nephrol. 2004; 62: 1– 7. CrossrefMedlineGoogle Scholar
Mueller C, Buerkle G, Buettner HJ,. Prevention of contrast media-associated nephropathy: randomized comparison of 2 hydration regimens in 1620 patients undergoing coronary angioplasty. Arch Intern Med. 2002; 162: 329– 36. CrossrefMedlineGoogle Scholar
Solomon R, Werner C, Mann D,. Effects of saline, mannitol, and furosemide to prevent acute decreases in renal function induced by radiocontrast agents. N Engl J Med. 1994; 331: 1416– 20. CrossrefMedlineGoogle Scholar
Trivedi HS, Moore H, Nasr S,. A randomized prospective trial to assess the role of saline hydration on the development of contrast nephrotoxicity. Nephron Clin Pract. 2003; 93: C29– 34. CrossrefMedlineGoogle Scholar
Marenzi G, Assanelli E, Campodonico J,. Contrast volume during primary percutaneous coronary intervention and subsequent contrast-induced nephropathy and mortality. Ann Intern Med. 2009; 150: 170– 7. CrossrefMedlineGoogle Scholar
McCullough PA, Wolyn R, Rocher LL,. Acute renal failure after coronary intervention: incidence, risk factors, and relationship to mortality. Am J Med. 1997; 103: 368– 75. CrossrefMedlineGoogle Scholar
Russo D, Minutolo R, Cianciaruso B,. Early effects of contrast media on renal hemodynamics and tubular function in chronic renal failure. J Am Soc Nephrol. 1995; 6: 1451– 8. MedlineGoogle Scholar
Gonzales DA, Norsworthy KJ, Kern SJ,. A meta-analysis of N-acetylcysteine in contrast-induced nephrotoxicity: unsupervised clustering to resolve heterogeneity. BMC Med. 2007; 5: 32. Published online November 14. doi:10.1186/1741-7015-5-32. CrossrefMedlineGoogle Scholar
Ozcan EE, Guneri S, Akdeniz B,. Sodium bicarbonate, N-acetylcysteine, and saline for prevention of radiocontrast-induced nephropathy. A comparison of 3 regimens for protecting contrast-induced nephropathy in patients undergoing coronary procedures. A single-center prospective controlled trial. Am Heart J. 2007; 154: 539– 44. MedlineGoogle Scholar
Thiele H, Hildebrand L, Schirdewahn C,. Impact of high-dose N-acetylcysteine versus placebo on contrast-induced nephropathy and myocardial reperfusion injury in unselected patients with ST-segment elevation myocardial infarction undergoing primary percutaneous coronary intervention: the LIPSIA-N-ACC (Prospective, Single-Blind, Placebo-Controlled, Randomized Leipzig Immediate PercutaneouS Coronary Intervention Acute Myocardial Infarction N-ACC) trial. J Am Coll Cardiol. 2010; 55: 2201– 9. MedlineGoogle Scholar
Webb JG, Pate GE, Humphries KH,. A randomized controlled trial of intravenous N-acetylcysteine for the prevention of contrast-induced nephropathy after cardiac catheterization: lack of effect. Am Heart J. 2004; 148: 422– 9. CrossrefMedlineGoogle Scholar
- 283. ACT Investigators. Acetylcysteine for prevention of renal outcomes in patients undergoing coronary and peripheral vascular angiography main results from the randomized Acetylcysteine for Contrast-Induced Nephropathy Trial (ACT). Circulation. 2011; 124: 1250– 9. LinkGoogle Scholar
Klein LW, Sheldon MW, Brinker J,. The use of radiographic contrast media during PCI: a focused review: a position statement of the Society of Cardiovascular Angiography and Interventions. Catheter Cardiovasc Interv. 2009; 74: 728– 46. CrossrefMedlineGoogle Scholar
Tramer MR, von Elm E, Loubeyre P,. Pharmacological prevention of serious anaphylactic reactions due to iodinated contrast media: systematic review. BMJ. 2006; 333: 675. CrossrefMedlineGoogle Scholar
Greenberger PA, Patterson R, Tapio CM. Prophylaxis against repeated radiocontrast media reactions in 857 cases. Adverse experience with cimetidine and safety of beta-adrenergic antagonists. Arch Intern Med. 1985; 145: 2197– 200. CrossrefMedlineGoogle Scholar
Shehadi WH. Adverse reactions to intravascularly administered contrast media. A comprehensive study based on a prospective survey. Am J Roentgenol Radium Ther Nucl Med. 1975; 124: 145– 52. CrossrefMedlineGoogle Scholar
Gill BV, Rice TR, Cartier A,. Identification of crab proteins that elicit IgE reactivity in snow crab-processing workers. J Allergy Clin Immunol. 2009; 124: 1055– 61. CrossrefMedlineGoogle Scholar
Swoboda I, Bugajska-Schretter A, Verdino P,. Recombinant carp parvalbumin, the major cross-reactive fish allergen: a tool for diagnosis and therapy of fish allergy. J Immunol. 2002; 168: 4576– 84. CrossrefMedlineGoogle Scholar
Briguori C, Colombo A, Airoldi F,. Statin administration before percutaneous coronary intervention: impact on periprocedural myocardial infarction. Eur Heart J. 2004; 25: 1822– 8. CrossrefMedlineGoogle Scholar
Briguori C, Visconti G, Focaccio A,. Novel approaches for preventing or limiting events (Naples) II trial: impact of a single high loading dose of atorvastatin on periprocedural myocardial infarction. J Am Coll Cardiol. 2009; 54: 2157– 63. CrossrefMedlineGoogle Scholar
Pasceri V, Patti G, Nusca A,. Randomized trial of atorvastatin for reduction of myocardial damage during coronary intervention: results from the ARMYDA (Atorvastatin for Reduction of MYocar-dial Damage during Angioplasty) study. Circulation. 2004; 110: 674– 8. LinkGoogle Scholar
Patti G, Pasceri V, Colonna G,. Atorvastatin pretreatment improves outcomes in patients with acute coronary syndromes undergoing early percutaneous coronary intervention: results of the ARMYDA-ACS randomized trial. J Am Coll Cardiol. 2007; 49: 1272– 8. CrossrefMedlineGoogle Scholar
Yun KH, Jeong MH, Oh SK,. The beneficial effect of high loading dose of rosuvastatin before percutaneous coronary intervention in patients with acute coronary syndrome. Int J Cardiol. 2009; 137: 246– 51. CrossrefMedlineGoogle Scholar
Zhang F, Dong L, Ge J. Effect of statins pretreatment on periprocedural myocardial infarction in patients undergoing percutaneous coronary intervention: a meta-analysis. Ann Med. 2010; 42: 171– 7. CrossrefMedlineGoogle Scholar
Winchester DE, Wen X, Xie L,. Evidence of pre-procedural statin therapy a meta-analysis of randomized trials. J Am Coll Cardiol. 2010; 56: 1099– 109. CrossrefMedlineGoogle Scholar
Di Sciascio G, Patti G, Pasceri V,. Efficacy of atorvastatin reload in patients on chronic statin therapy undergoing percutaneous coronary intervention: results of the ARMYDA-RECAPTURE (Atorvastatin for Reduction of Myocardial Damage During Angioplasty) randomized trial. J Am Coll Cardiol. 2009; 54: 558– 65. CrossrefMedlineGoogle Scholar
Levey AS, Coresh J, Greene T,. Using standardized serum creatinine values in the modification of diet in renal disease study equation for estimating glomerular filtration rate. Ann Intern Med. 2006; 145: 247– 54. CrossrefMedlineGoogle Scholar
Stevens LA, Nolin TD, Richardson MM,. Comparison of drug dosing recommendations based on measured GFR and kidney function estimating equations. Am J Kidney Dis. 2009; 54: 33– 42. CrossrefMedlineGoogle Scholar
Hassan Y, Al-Ramahi RJ, Aziz NA,. Impact of a renal drug dosing service on dose adjustment in hospitalized patients with chronic kidney disease. Ann Pharmacother. 2009; 43: 1598– 605. CrossrefMedlineGoogle Scholar
Barnathan ES, Schwartz JS, Taylor L,. Aspirin and dipyridamole in the prevention of acute coronary thrombosis complicating coronary angioplasty. Circulation. 1987; 76: 125– 34. LinkGoogle Scholar
Jolly SS, Pogue J, Haladyn K,. Effects of aspirin dose on ischaemic events and bleeding after percutaneous coronary intervention: insights from the PCI-CURE study. Eur Heart J. 2009; 30: 900– 7. CrossrefMedlineGoogle Scholar
Popma JJ, Berger P, Ohman EM,. Antithrombotic therapy during percutaneous coronary intervention: the Seventh ACCP Conference on Antithrombotic and Thrombolytic Therapy. Chest. 2004; 126: 576S– 99S. CrossrefMedlineGoogle Scholar
Schwartz L, Bourassa MG, Lesperance J,. Aspirin and dipyridamole in the prevention of restenosis after percutaneous transluminal coronary angioplasty. N Engl J Med. 1988; 318: 1714– 9. CrossrefMedlineGoogle Scholar
Marshall D, Chambers CE, Heupler F. Performance of adult cardiac catheterization: nonphysicians should not function as independent operators—a position statement. Catheter Cardiovasc Interv. 1999; 48: 167– 9. CrossrefMedlineGoogle Scholar
- 306. Hospital National Patient Safety Goals. UP.01.01.01. Conduct a preprocedure verification process.
Available at: http://www.jointcommission.org/assets/1/6/NPSG_EPs_Scoring_HAP_20110706.pdf. 2011.
Accessed September 9, 2011. Google Scholar
Kwaan MR, Studdert DM, Zinner MJ,. Incidence, patterns, and prevention of wrong-site surgery. Arch Surg. 2006; 141: 353– 7. CrossrefMedlineGoogle Scholar
Nundy S, Mukherjee A, Sexton JB,. Impact of preoperative briefings on operating room delays: a prelimary report. Arch Surg. 2008; 143: 1068– 72. CrossrefMedlineGoogle Scholar
Cameron AA, Laskey WK, Sheldon WC. Ethical issues for invasive cardiologists: Society for cardiovascular angiography and interventions. Catheter Cardiovasc Interv. 2004; 61: 157– 62. CrossrefMedlineGoogle Scholar
Blankenship JC, Mishkel GJ, Chambers CE,. Ad hoc coronary intervention. Catheter Cardiovasc Interv. 2000; 49: 130– 4. CrossrefMedlineGoogle Scholar
Blankenship JC, Klein LW, Laskey WK,. SCAI statement on ad hoc versus the separate performance of diagnostic cardiac catheterization and coronary intervention. Catheter Cardiovasc Interv. 2004; 63: 444– 51. CrossrefMedlineGoogle Scholar
Agard A, Herlitz J, Hermeren G. Obtaining informed consent from patients in the early phase of acute myocardial infarction: physicians' experiences and attitudes. Heart. 2004; 90: 208– 10. CrossrefMedlineGoogle Scholar
Foex BA. Is informed consent possible in acute myocardial infarction?Heart. 2004; 90: 1237– 8. CrossrefMedlineGoogle Scholar
Williams BF, French JK, White HD. Informed consent during the clinical emergency of acute myocardial infarction (HERO-2 consent substudy): a prospective observational study. Lancet. 2003; 361: 918– 22. CrossrefMedlineGoogle Scholar
Ritchie JL, Wolk MJ, Hirshfeld JW,. Task force 4: appropriate clinical care and issues of “self-referral.”J Am Coll Cardiol. 2004; 44: 1740– 6. CrossrefMedlineGoogle Scholar
Hirshfeld JW, Balter S, Brinker JA,. ACCF/AHA/HRS/SCAI clinical competence statement on physician knowledge to optimize patient safety and image quality in fluoroscopically guided invasive cardiovascular procedures. A report of the American College of Cardiology Foundation/American Heart Association/American College of Physicians Task Force on Clinical Competence and Training. Circulation. 2005; 111: 511– 32. LinkGoogle Scholar
Chambers C, Fetterly K, Holzer R,. Radiation safety program for the cardiac catheterization laboratory. Catheter Cardiovasc Interv. 2011; 77: 546– 56. CrossrefMedlineGoogle Scholar
- 318. Deleted in proof. Google Scholar
- 319. Deleted in proof. Google Scholar
Krasuski RA, Beard BM, Geoghagan JD,. Optimal timing of hydration to erase contrast-associated nephropathy: the OTHER CAN study. J Invasive Cardiol. 2003; 15: 699– 702. MedlineGoogle Scholar
Taylor AJ, Hotchkiss D, Morse RW,. PREPARED: Preparation for Angiography in Renal Dysfunction: a randomized trial of inpatient vs outpatient hydration protocols for cardiac catheterization in mild-to-moderate renal dysfunction. Chest. 1998; 114: 1570– 4. CrossrefMedlineGoogle Scholar
Adolph E, Holdt-Lehmann B, Chatterjee T,. Renal Insufficiency Following Radiocontrast Exposure Trial (REINFORCE): a randomized comparison of sodium bicarbonate versus sodium chlo-ride hydration for the prevention of contrast-induced nephropathy. Coron Artery Dis. 2008; 19: 413– 9. MedlineGoogle Scholar
Brar SS, Shen AY, Jorgensen MB,. Sodium bicarbonate vs sodium chloride for the prevention of contrast medium-induced nephropathy in patients undergoing coronary angiography: a randomized trial. JAMA. 2008; 300: 1038– 46. CrossrefMedlineGoogle Scholar
Brar SS, Hiremath S, Dangas G,. Sodium bicarbonate for the prevention of contrast induced-acute kidney injury: a systematic review and meta-analysis. Clin J Am Soc Nephrol. 2009; 4: 1584– 92. CrossrefMedlineGoogle Scholar
Briguori C, Airoldi F, D'Andrea D,. Renal Insufficiency Following Contrast Media Administration Trial (REMEDIAL): a randomized comparison of 3 preventive strategies. Circulation. 2007; 115: 1211– 7. LinkGoogle Scholar
From AM, Bartholmai BJ, Williams AW,. Sodium bicarbonate is associated with an increased incidence of contrast nephropathy: a retrospective cohort study of 7977 patients at Mayo Clinic. Clin J Am Soc Nephrol. 2008; 3: 10– 8. CrossrefMedlineGoogle Scholar
Hoste EA, De Waele JJ, Gevaert SA,. Sodium bicarbonate for prevention of contrast-induced acute kidney injury: a systematic review and meta-analysis. Nephrol Dial Transplant. 2010; 25: 747– 58. CrossrefMedlineGoogle Scholar
Kelly AM, Dwamena B, Cronin P,. Meta-analysis: effectiveness of drugs for preventing contrast-induced nephropathy. Ann Intern Med. 2008; 148: 284– 94. CrossrefMedlineGoogle Scholar
Maioli M, Toso A, Leoncini M,. Sodium bicarbonate versus saline for the prevention of contrast-induced nephropathy in patients with renal dysfunction undergoing coronary angiography or intervention. J Am Coll Cardiol. 2008; 52: 599– 604. CrossrefMedlineGoogle Scholar
Merten GJ, Burgess WP, Gray LV,. Prevention of contrast-induced nephropathy with sodium bicarbonate: a randomized controlled trial. JAMA. 2004; 291: 2328– 34. CrossrefMedlineGoogle Scholar
Pannu N, Manns B, Lee H,. Systematic review of the impact of N-acetylcysteine on contrast nephropathy. Kidney Int. 2004; 65: 1366– 74. CrossrefMedlineGoogle Scholar
Vaitkus PT, Brar C. N-acetylcysteine in the prevention of contrast-induced nephropathy: publication bias perpetuated by meta-analyses. Am Heart J. 2007; 153: 275– 80. CrossrefMedlineGoogle Scholar
- 333. Deleted in proof. Google Scholar
Heinrich MC, Haberle L, Muller V,. Nephrotoxicity of iso-osmolar iodixanol compared with nonionic low-osmolar contrast media: meta-analysis of randomized controlled trials. Radiology. 2009; 250: 68– 86. CrossrefMedlineGoogle Scholar
Kuhn MJ, Chen N, Sahani DV,. The PREDICT study: a randomized double-blind comparison of contrast-induced nephropathy