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Cancellation of the Cardiac Catheterization Lab After Activation for ST-Segment–Elevation Myocardial Infarction

Frequency, Etiology, and Clinical Outcomes
Originally published Cardiovascular Quality and Outcomes. 2018;11:e004464



    Prehospital ECG-based cardiac catheterization laboratory (CCL) activation for ST-segment–elevation myocardial infarction reduces door-to-balloon times, but CCL cancellations (CCLX) remain a challenging problem. We examined the reasons for CCLX, clinical characteristics, and outcomes of patients presenting as ST-segment–elevation myocardial infarction activations who receive emergent coronary angiography (EA) compared with CCLX.

    Methods and Results:

    We reviewed all consecutive CCL activations between January 1, 2012, and December 31, 2014 (n=1332). Data were analyzed comparing 2 groups stratified as EA (n=466) versus CCLX (n=866; 65%). Reasons for CCLX included bundle branch block (21%), poor-quality prehospital ECG (18%), non–ST-segment–elevation myocardial infarction ST changes (18%), repolarization abnormality (13%), and arrhythmia (8%). A multivariate logistic regression model using age, peak troponin, and initial ECG findings had a high discriminatory value for determining EA versus CCLX (C statistic, 0.985). CCLX subjects were older and more likely to be women, have prior coronary artery bypass grafting, or a paced rhythm (P<0.0001 for all). All-cause mortality did not differ between groups at 1 year or during the study period (mean follow-up, 2.186±1.167 years; 15.8% EA versus 16.2% CCLX; P=0.9377). Cardiac death was higher in the EA group (11.8% versus 3.0%; P<0.0001). After adjusting for clinical variables associated with survival, CCLX was associated with an increased risk for all-cause mortality during the study period (hazard ratio, 1.82; 95% CI, 1.28–2.59; P=0.0009).


    In this study, prehospital ECG without overreading or transmission lead to frequent CCLX. CCLX subjects differ with regard to age, sex, risk factors, and comorbidities. However, CCLX patients represent a high-risk population, with frequently positive cardiac enzymes and similar short- and long-term mortality compared with EA. Further studies are needed to determine how quality improvement initiatives can lower the rates of CCLX and influence clinical outcomes.



    • Although first-medical-contact-to-device times and clinical outcomes for ST-segment–elevation myocardial infarction have markedly improved, cancellation of the cardiac catheterization laboratory (CCL) has become an increasing problem.

    • CCL cancellation rates vary widely across ST-segment–elevation myocardial infarction systems because of differences in definition, emergency medical service training, and CCL activation workflow.

    • CCL cancellations are costly to the medical system for a variety of reasons: patient satisfaction and trust, CCL morale and economics, and healthcare resource utilization.


    • To our knowledge, this study is the first to examine the reasons for CCL cancellation and to examine clinical outcomes in this important patient population.

    Approximately 500 000 patients experience acute ST-segment–elevation myocardial infarction (STEMI) each year in the United States.1 Ten years ago, ≤30% of patients with STEMI were not receiving any form of reperfusion therapy (primary percutaneous coronary intervention [PCI] or fibrinolysis). Furthermore, only 40% of those who received PCI were treated within the recommended time frame (first-medical-contact-to-device time, ≤90 minutes).1,2 These shortcomings in reperfusion rates and time-to-treatment stimulated the development of the American College of Cardiology Door-to-Balloon Alliance and the American Heart Association Mission: Lifeline Program. Along with regional STEMI systems of care, these programs have dramatically changed healthcare delivery for patients with STEMI, providing timely access to PCI for an increasing proportion of the population, while decreasing the eligible but untreated population. As a result, time-to-treatment and cardiovascular outcomes have markedly improved during the past decade.27 However, cancellation of the cardiac catheterization laboratory (CCL) has become a challenging problem.817

    CCL cancellations (CCLX) are defined as any CCL-staff activation for possible patients with STEMI who ultimately do not require emergent coronary angiography (EA). CCLX can cause patient confusion, frustration, and perhaps even distrust in the medical providers. In addition, CCLX can cause CCL staff fatigue, burn out, and loss of productivity. Finally, false CCLX are costly to the medical system because staff are often paid overtime wages to take calls and respond to CCL activations, regardless of whether or not the patient receives EA.17,18

    CCLX rates vary according to definition but range in frequency from ≈5% to 60%.816 The reasons for CCLX, as well as clinical characteristics and outcome data, are lacking for this important patient population. The purpose of this study was to characterize the frequency, etiology, and clinical outcomes for CCLX from a consecutive series of patients presenting with possible STEMI.


    The data, analytic methods, and study materials will be made available to other researchers for purposes of reproducing the results or replicating the procedure. Please contact the corresponding author for materials pertaining to this study. Cedars-Sinai Medical Center (CSMC) is a tertiary care cardiovascular center and is among the highest volume STEMI-receiving centers (SRC) in Los Angeles County (LAC). The LAC SRC network has been described previously and relies on prehospital ECG (PH-ECG) activation of the CCL.1921 At the time of this study, the construct of the LAC SRC network mandated that any PH-ECG computer read of ***ACUTE MYOCARDIAL INFARCTION*** be triaged to the closest LAC SRC. LAC SRC protocols for emergency response PH-ECG acquisition and treatment can be found online.22 At CSMC, triage to the SRC based on the PH-ECG computer interpretation triggers CCL staff activation with a single page to the entire STEMI team. The CCL can also be activated by CSMC Emergency Physicians or other staff for patients who self-present to the emergency department or for inpatients who experience a STEMI. Patients presenting as CCL activations receive an expedited evaluation by the on-call interventional cardiologist who decides whether to proceed with EA or whether to cancel the CCL activation. For CCLX, the treating emergency physician subsequently resumes care. The algorithm for determining EA versus CCLX at CSMC is demonstrated in Figure 1.

    Figure 1.

    Figure 1. Study diagram within the construct of the cardiac catheterization laboratory (CCL)-activation algorithm at Cedars-Sinai Medical Center. ED indicates emergency department; MI, myocardial infarction; MD, medical doctor; OSH, outside hospital; PH-ECG, prehospital ECG; RN, registered nurse; RCIS, registered cardiovascular invasive specialist; and STEMI, ST-segment–elevation myocardial infarction.

    Effective January 1, 2012, all consecutive CCL activations were prospectively enrolled in a registry that includes clinical, laboratory, ECG, angiographic, medical decision-making, and follow-up data. Time-to-treatment (first-medical-contact-to-device time and door-to-balloon) is tracked for all CCL activations who receive EA, whereas time-to-cancellation and reason(s) for cancellation is tracked for all patients who do not (CCLX). No patients are excluded from the registry, including patients who die before receiving EA, elderly patients, cardiogenic shock, cardiac arrest, nondiagnostic initial ECG, and atypical presentations.

    Angiographic data are obtained from the cardiac catheterization report and include the culprit artery, number of vessels with obstructive coronary artery disease, type of intervention, and flow according to the TIMI study (Thrombosis in Myocardial Infarction) guidelines before and after PCI, using American College of Cardiology definitions. In cases with >1 potential culprit lesion, the culprit vessel is coded as multiple culprit, and cases without a specific culprit artery are coded as no culprit. All index ECGs were reviewed retrospectively to determine whether criteria for STEMI were met by a cardiologist blinded to the clinical characteristics of the patients (D.C.L.).


    Review of the literature reveals a high degree of variability in the definition and terminology for CCLX.816 Many of these definitions rely on some combination of ECG findings, decision to offer EA, angiographic identification of a culprit vessel, and cardiac biomarker levels. For this study, all patients presenting with ischemic symptoms and ECG findings consistent with STEMI without contraindications to cardiac catheterization were included in the EA group, whereas patients not undergoing emergent cardiac catheterization for STEMI were examined in the CCLX group. ECG findings consistent with STEMI included 2 contiguous leads with ST-segment elevation of ≥0.2 mV in leads V1, V2, or V3 or ≥0.1 mV in other leads and new or presumably new left bundle branch block. Elevated cardiac biomarkers were defined as serum troponin T ≥0.1 ng/dL. Inappropriate cancellations were defined as patients who1 met these ECG criteria for STEMI2; had typical chest pain symptoms for ≤12 hours in duration3; had a rise and fall in cardiac biomarkers4; and had no contraindications to cardiac catheterization who were not taken for EA. A culprit coronary artery was identified by the interventional cardiologist in the cardiac catheterization report and defined as an acute total or subtotal occlusion of a coronary artery or bypass graft or a coronary lesion with visible thrombus responsible for the STEMI. Regular working hours were defined as Monday to Friday 7:00 am to 7:00 pm, whereas nights, weekends, and holidays were considered after working hours. The study was approved by the CSMC Institutional Review Board. The informed consent requirement for human subjects was waived as data collection is for the purposes of quality improvement and reporting.

    Statistical Methods

    Data were organized according to EA and CCLX. Of note, any patient who presented as a STEMI activation but died before receiving EA (n=28) was included in the EA group. Comparisons between the groups were performed using a Student t test for continuous variables with Gaussian distribution (reported as mean±SD) and Wilcoxon rank-sum test for continuous variables with markedly non-normal distribution (reported as median and interquartile rage). Categorical variables were compared using a χ2 test, and mortality data were examined using Kaplan-Meier survival curves. Follow-up time was censored at December 31, 2015, for those patients who did not have mortality reported. All subgroup analyses were planned a priori and multivariate logistic regression models were used to determine associations. Cox proportional hazards modeling was used to determine the associations with survival at 1 year and during the study period. All tests were performed using a 2-sided α level of 0.05, and analyses were performed with SAS, version 9.4 (SAS Institute, Inc, Cary, NC).


    Between January 1, 2012, and December 31, 2014, there were 1332 CCL activations for STEMI. Four hundred sixty-six of the 1332 (34.9%) were included in the EA group, including 28 patients who expired before receiving cardiac catheterization (6% of EA). The remaining 866 subjects were included in the CCLX group (65.1%). Reasons for cancellation are shown in Figure 2 and included bundle branch block (21%, of which 54% were right bundle branch block without STEMI and 46% were prior left bundle branch block), poor-quality PH-ECG (18%), non-STEMI ST changes (18%), repolarization abnormality (13%), and arrhythmia (8%), among others. One hundred fifty-four of the 866 false activations (17.8%) received coronary angiography during the hospitalization.

    Figure 2.

    Figure 2. Reasons for false activation. Cath indicates catheterization; CI, contraindication; Dx, diagnosed; MI, myocardial infarction; and STEMI, ST-segment–elevation myocardial infarction.

    Table 1 shows the baseline demographic information for EA and CCLX. CCLX patients were older, were more commonly women, had a lower mean body mass index, were less likely to have a family history of coronary artery disease, a personal history of dyslipidemia or tobacco abuse, prior history of coronary artery bypass grafting (CABG), and prior history of pacemaker or implantable cardioverter defibrillator (Table 1). Additionally, these same characteristics are presented for between EA and CCLX that received coronary angiography during the same hospitalization. This subgroup of CCLX patients who received elective coronary angiography were also older and more likely to be women when compared with EA (P<0.0001 and P=0.0091, respectively). Additionally, these patients were more likely to have a prior history of hypertension, coronary artery disease, diabetes mellitus, prior CABG, and a history of pacemaker or implantable cardioverter defibrillator implantation (Table 1).

    Table 1. Baseline Clinical Characteristics of CCL-Activation Patients According to EA vs CCLX

    Patient CharacteristicsEA
    CCLX Received Cath
    P Value
    (EA vs CCLX)
    P Value
    (EA vs CCLX Received Cath)
    Age, y (mean±SD)64.48±14.1267.83±17.270.27±12.64<0.0001<0.0001
    Sex, n (% men)331 (71.03%)496 (57.27%)92 (59.74%)<0.00010.0091
    BMI, kg/m2 (mean±SD)27.11±5.1726.58±7.4826.47±5.800.00090.0817
    Family Hx CAD, n (%)98 (21.12%)76 (8.78%)28 (18.18%)<0.00010.4328
    HTN, n (%)275 (59.14%)546 (63.12%)115 (74.68%)0.15430.0005
    Dyslipidemia, n (%)196 (42.24%)278 (32.18%)69 (44.81%)0.00030.5775
    DM, n (%)117 (25.16%)256 (29.6%)54 (35.06%)0.08610.0172
    Smoking Hx, n (%)182 (39.06%)205 (23.67%)49 (31.82%)<0.00010.1073
    Hx CAD, n (%)128 (27.59%)262 (30.29%)70 (45.45%)0.3023<0.0001
    Previous MI, n (%)79 (17.03%)145 (16.74%)35 (22.73%)0.89570.1140
    Previous PCI, n (%)84 (18.1%)124 (14.34%)36 (23.38%)0.07150.1517
    Previous CABG, n (%)22 (4.74%)72 (8.31%)27 (17.53%)0.0154<0.0001
    Previous PM or ICD, n (%)7 (1.51%)92 (10.62%)11 (7.14%)<0.00010.0003

    BMI indicates body mass index; CABG, coronary artery bypass grafting; CAD, coronary artery disease; Cath, catheterization; CCLX, cardiac catheterization laboratory cancellation; DM, diabetes mellitus; EA, emergent angiography; HTN, hypertension; Hx, history; ICD, implantable cardioverter defibrillator; MI, myocardial infarction; PCI, percutaneous coronary intervention; and PM, pacemaker.

    Table 2 demonstrates several of the key clinical characteristics on presentation and throughout the hospital course. There was no difference between the groups in terms of after-working-hour presentations (34.65% for EA versus 33.26% for CCLX; P=0.6108); however, EA patients were more likely to present in cardiogenic shock and were more likely to sustain a cardiac arrest in any phase of care (prehospital, in hospital before cardiac catheterization, or in hospital after cardiac catheterization). As expected, initial and peak troponin levels were significantly higher in the EA group. Finally, a higher proportion of EA patients had positive cardiac biomarkers (88% versus 23%; P<0.0001).

    Table 2. Presentation Characteristics of CCL-Activation Patients According to EA vs CCLX

    CCLX Received Cath
    P Value
    (EA vs CCLX)
    P Value
    (EA vs CCLX Received Cath)
    After working hours presentation, n (%)158 (34.65%)287 (33.26%)59 (38.31%)0.61080.4117
    Cardiogenic shock, n (%)67 (14.38%)49 (5.66%)9 (5.84%)<0.00010.0051
    Cardiac arrest pre-hospital, n (%)61 (13.09%)49 (5.66%)12 (7.79%)<0.00010.0842
    Cardiac arrest in hospital before coronary angiography, n (%)24 (5.15%)15 (1.73%)2 (1.3%)0.00090.0375
    Cardiac arrest in hospital after coronary angiography, n (%)9 (1.93%)4 (0.46%)2 (1.3%)0.01581.0
    Expired before emergent coronary angiography28 (6.0%)NANANANA
    Troponin on presentation, ng/mL; median (IQR)0.11
    Troponin peak, ng/mL; median (IQR)43.75
    0.05 (
    Peak cardiac enzymes >0.78 ng/mL, n (%)410 (87.98%)198 (22.86%)127 (83.01%)<0.00010.0034
    Door-to-balloon time, min; median (IQR)61 (50–73)NANANANA

    Cath indicates catheterization; CCLX, cardiac catheterization laboratory cancellation; EA, emergent angiography; IQR, interquartile range; and NA, not available.

    These key clinical characteristics for CCLX patients who received elective coronary angiography during the same hospitalization are also shown in Table 2. Compared with EA subjects, these patients were also less likely to present in cardiogenic shock, and although the prevalence of cardiac arrest in any phase of care remained higher in the EA group, this only reached statistical significance in the group that sustained a cardiac arrest in hospital before cardiac catheterization. There was no difference in initial troponin between the groups, although peak troponin remained markedly higher in the EA group, as did the proportion of patients with positive cardiac enzymes (Table 2).

    The clinical outcomes for the groups are displayed in Table 3. CCLX patients were far less likely to receive PCI, although there were no differences in the rates of CABG between the 2 groups. Hospital length of stay was longer in the EA group, and mortality in hospital and at 30 days was slightly higher. However, there was no difference in all-cause mortality at 1 year or during the course of the entire study period (mean follow-up, 2.186±1.167 years; Figure 3). Of note, cardiovascular mortality was significantly higher in the EA group during the study period (11.8% versus 3.0%; P<0.0001). When comparing EA with CCLX subjects who received coronary angiography, the increased prevalence of PCI for EA remained; however, CCLX patients who received coronary angiography were more likely to undergo CABG (P<0.01 for all). CCLX subjects who later received elective coronary angiography had a longer length of hospital stay and lower rates of in-hospital, 30-day, and 1-year all-cause and cardiovascular mortality (P<0.05 for all). Findings on coronary angiography, including culprit vessels, are demonstrated in Figure 3. CCLX patients who received elective coronary angiography were more likely to have no culprit lesion or multiple culprit vessels, whereas EA patients were more likely to have a culprit in the right coronary artery (P<0.05 for all).

    Table 3. Clinical Outcomes for CCL Activations Stratified by EA vs CCLX

    CCLX, Received Cath (n=154)P Value
    (EA vs CCLX)
    P Value
    (EA vs CCLX Received Cath)
    PCI, n (%)350 (79.01%)88 (24.31%)85 (57.05%)<0.0001<0.0001
    CABG, n (%)7 (1.51%)9 (1.04%)9 (5.84%)0.45570.0033
    Length of hospital stay, d; median (IQR)3 (2,5)2 (1,6)4 (2,8)<0.00010.0003
    In-hospital death, n (%)61 (13.09%)84 (9.7%)4 (2.6%)0.0061<0.0001
    30-d death, n (%)62 (13.3%)89 (10.28%)4 (2.6%)0.0120<0.0001
    1-y death, n (%)67 (14.38%)122 (14.09%)12 (7.79%)0.93440.0362
    Death, n (%)74 (15.88%)140 (16.17%)17 (11.04%)0.93770.1507
    Cardiac death, n (%)55 (11.8%)26 (3.0%)3 (1.9%)<0.0001<0.0001

    CABG indicates coronary artery bypass grafting; Cath, catheterization; CCLX, cardiac catheterization laboratory cancellation; EA, emergent angiography; IQR, interquartile range; and PCI, percutaneous coronary intervention.

    Figure 3.

    Figure 3. Findings on coronary angiography stratified by emergent angiography (EA) vs cardiac catheterization laboratory (CCL) cancellations who received coronary angiography. LAD indicates left anterior descending artery; LCx, left circumflex artery; RCA, right coronary artery; LM, left main artery. * indicates comparative values where the P was <0.05.

    Figure 4A through 4C demonstrates the Kaplan-Meier survival curves for EA versus CCLX (panel A), EA versus CCLX patients who receive coronary angiography (panel B), and all 3 groups (panel C). Multivariate logistic regression analysis to discriminate EA from CCLX revealed that age, initial ECG findings, and peak troponin were the most important variables in determining EA from CCLX (C statistic, 0.985). After adjusting for variables that were associated with survival, including age, diabetes mellitus (DM), smoking history, cardiogenic shock, cardiac arrest, clinical signs of congestive heart failure, and activation status (EA versus CCLX), Cox proportional hazards modeling revealed that CCLX subjects had a higher risk of death during the course of the study when compared with EA subjects (hazard ratio, 1.82; 95% CI, 1.28–2.58; P=0.0009).

    Figure 4.

    Figure 4. Kaplan-Meier survival curves for emergent angiography (EA) vs cardiac catheterization laboratory cancellations (CCL-X;A), EA vs CCL-X that receive coronary angiography (B), and all 3 groups (C).

    Blinded review of the presenting ECG revealed that 56 patients in the CCLX group had ECGs that met diagnostic criteria for STEMI. Nine of these patients were found to be inappropriate CCLX (0.7%), whereas 18 had contraindications to EA (1.4%), and 29 declined consent because of advanced directives and comfort-focused goals of care (2.2%). All of the 9 inappropriate cancellation patients received coronary angiography during the hospitalization, and 8 of the 9 patients received PCI (89%). The culprit vessel identified was the left anterior descending in 4 subjects (44%) and the right coronary artery in the remaining 5 subjects (56%). Reasons for cancellation included physician decision (n=5; 56%), ST changes that were not felt to meet STEMI criteria (n=3; 33%) and repolarization abnormality (n=1; 11%). There were no deaths in this subgroup during the study period.


    Both the American College of Cardiology/American Heart Association and European Society of Cardiology guidelines recommend primary PCI as the preferred therapy for STEMI, provided it can be performed in a timely manner by an experienced operator, with a goal first-medical-contact-to-device time of ≤90 minutes.23,24 The ECG is an imperfect tool for diagnosing STEMI.25,26 For these reasons, primary PCI for STEMI remains one of the most complex, multidisciplinary, and time-sensitive therapeutic interventions in medicine today: the process is measured in minutes, whereas the outcomes are measured in terms of significant morbidity and mortality. Teamwork, coordination of care, and smooth transitions along every step of the process are critically important.19,27

    Multiple studies have demonstrated decreased time-to-revascularization on implementation of the PH-ECG, with or without transmission or overreading.19,20,2534 However, EA±primary PCI is a precious resource, particularly after working hours and on weekends when CCL staff are not on site. As such, it is desirable to maximize the rate of appropriate CCL activation after PH-ECG—an important quality measure that should be tracked and reported.20,35

    CCLX occur in almost every STEMI system; however, the frequency, reasons, and definitions of CCLX vary considerably.817 Larson et al were the first to report on the subject in 2007. Their study, which included 1345 patients from a regional STEMI network, reported a CCLX rate of only 0.8% (10 of the 1345 subjects).8 In 2010, Kontos et al reported on 249 consecutive emergency physician-initiated CCL activations and noted 5.2% (13 of 249) were unnecessary CCL activations, whereas an additional 4.4% (11 subjects) were not STEMI, and 14.9% (37 subjects) had negative cardiac biomarkers and no culprit on coronary angiography. Clinical outcomes were not reported in this study.11 In 2012, Garvey et al reported on 3973 consecutive CCL activations in North Carolina and found that 15% (596 of 3973 CCL activations) were cancelled because of ECG reinterpretation or contraindications to EA. Of note, an additional 145 (4.3%) appropriate CCL activations did not receive EA because of a change in clinical status. If this patient group was to be reclassified as CCLX, the rate would rise to 18.7% (741 of 3973 CCL activations).12 Cardiac biomarkers and clinical outcome data were not included.

    Mixon et al performed a retrospective analysis of 345 consecutive CCL activations from a STEMI system in Central Texas. They reported 12.8% (44 of the 345 CCL activations) were inappropriate by ECG criteria, whereas an additional 15.6% of all CCL activations did not have a confirmed diagnosis of STEMI. Therefore, ≈28% of all CCL activations failed to have a confirmed diagnosis of STEMI.13 Similar to many previous studies, no clinical outcomes were reported.

    More recently, Bosson et al compared PH-ECG computer read versus PH-ECG transmission in LAC by determining the rates of false-positive CCL activations (defined in this study as CCL activation that did not result in primary PCI or CABG). The overall rate of false-positive activations in this series was 57% in this database of 7768 patients with STEMI on PH-ECG. Successful transmission of the PH-ECG slightly reduced the false activation rate from 61% to 55%, but this difference did not reach statistical significance.35 Importantly, the PH-ECG was transmitted and received by the SRC in only 28% of patients.

    Several important insights can be made based on the available literature. First, CCLX rates vary widely, from as low as ≈5% to as high as ≈60%. Second, this wide range in CCLX prevalence is due, in part, to the variability in definitions for what constitutes an appropriate CCL activation. Common themes used for deciding which CCL activations are true/appropriate include ECG criteria, cardiac biomarkers, and findings on EA. Individual patient goals of care, medical comorbidities, and contraindications to cardiac catheterization further complicate the matter of defining appropriate versus inappropriate CCL activations. These issues highlight the need for universal definitions and terminology.

    A third lesson is that the reasons for CCLX are incompletely reported. Many studies cite incorrect ECG interpretation as the reason for CCLX; however, the specific reasons (ie, bundle branch block, early repolarization, pericarditis, and other STEMI mimics) are not reported. In a recent single-center study based on 231 PH-ECG activations during 3 years, bundle branch block, left ventricular hypertrophy, and nonwhite race were the 3 strongest predictors of CCLX.16 The final observation is that clinical outcomes for CCLX patients have rarely been reported.

    This study builds on the previous reports and provides several novel contributions to our understanding of CCLX patients. Our group recently proposed a universal definition for inappropriate activation of the CCL, defined as any CCL activation that for reasons related to ECG findings, clinical scenarios, goals of care, or medical comorbidities, does not warrant EA.17

    Our finding of 65.1% inappropriate activation of the CCL using this definition is consistent with prior reports from the LAC SRC network.35 Reasons for CCLX included bundle branch block (21%), poor-quality PH-ECG (18%), non-STEMI ST changes (18%), repolarization abnormality (13%), and arrhythmia (8%), among others (Figure 2). This highlights specific shortcomings to the computer algorithm for interpreting PH-ECGs, for example, right bundle branch block without STEMI and poor-quality ECGs frequently triggered CCL activation.

    Our study is the first to define and report the frequency of inappropriate CCLX (ie, patients who presented with ECG findings consistent with STEMI, chest pain for ≤12 hours, and no contraindications to cardiac catheterization and yet did not receive EA). Although a total of 56 patients who presented with STEMI did not receive EA (4.2%), only 9 patients were truly inappropriate CCLX (0.7%). Of the remaining 47 patients, 18 had contraindications to EA (1.4%), and 29 declined consent because of advanced directives and comfort-focused goals of care (2.2%).

    To our knowledge, this study is the first to report on the clinical characteristics of the CCLX patient population. We found that CCLX subjects were older, were more likely to be women, and had unique medical comorbidities when compared with true activations. These medical comorbidities included lower mean body mass index, less family history of coronary artery disease, and lower rates of dyslipidemia and tobacco abuse. In addition, CCLX patients were more likely to have a history of CABG, pacemaker implantation, or implantable cardioverter defibrillator.

    As mentioned previously, clinical outcome data for CCLX patients are severely lacking. Our study demonstrates that a large proportion of CCLX patients had elevated cardiac biomarkers (22.9%) and received elective cardiac catheterization during their index hospitalization (17.8%). However, initial and peak troponin levels of CCLX patients, including those who went on to receive cardiac catheterization, were significantly lower than their EA counterparts. Additionally, CCLX subjects were much more likely to have no culprit (37% versus 15%; P<0.0001) or multiple culprit arteries (14% versus 6%; P=0.0051) on coronary angiography when compared with EA. Along these lines, CCLX patients who later underwent elective angiograms were less likely to receive revascularization via PCI (57.1% versus 79.0%; P<0.0001) but were more likely to undergo CABG for revascularization (5.8% versus 1.5%; P=0.0033). These results, when taken in the context of the low inappropriate CCLX rate and low cardiovascular mortality in the CCLX group, seem to indicate that the CCL team was activated for reasons other than ECG findings of STEMI, such as positive cardiac biomarkers, or sick patients triggering CCL activation.

    Second, our study demonstrates that CCLX, in spite of the relatively high frequency of elevated biomarkers and cardiac catheterization, had a lower incidence of cardiac mortality during the course of the study (3.0% versus 11.8%; P<0.0001). This study included all consecutive patients, including patients who presented in cardiogenic shock and those who experienced out-of-hospital cardiac arrest. These patients are widely excluded from public reporting and other clinical outcome literature.36 Furthermore, the EA cohort in this study included 28 patients (6%) who presented as a CCL activation but experienced a cardiac arrest before coronary angiography and were not successfully resuscitated. These were counted in the EA group because they represent real-life patient experience with CCL activations who would have been offered EA had resuscitation efforts been successful. Excluding these patients would decrease the EA in-hospital mortality and cardiovascular mortality to 7.1% and 5.8%, respectively, consistent with contemporary clinical outcomes for STEMI3,5,7,36 (Figure 4C).

    Finally, in spite of the low cardiovascular mortality for CCLX patients during the study period, this patient population remains a high-risk group. Our study showed no difference in all-cause mortality at 1 year or during the study period (mean follow-up, 988±348 days). Furthermore, after adjusting for other factors that were associated with survival, including age, DM, smoking history, cardiogenic shock, cardiac arrest, clinical signs of congestive heart failure, and cancellation status, we found that having a CCLX was associated with a higher hazard than EA patients for overall survival during the study period (hazard ratio, 1.82; 95% CI, 1.28–2.58; P=0.0009). This illustrates the vulnerable nature of the population.

    In the context of this study, CCLX seems to serve as a marker for sick patients who are not necessarily having a STEMI. Many patients who present with sepsis, advanced malignancy, pulmonary emboli, etc, may have positive cardiac biomarkers or type II non-STEMI but do not warrant EA.37,38 Similar pathophysiology may explain the low-level elevation of cardiac enzymes seen in the CCLX subjects. We think these patients still benefit from triage to an SRC, which are typically tertiary care facilities, but do not necessarily require CCL activation.


    There are several limitations to this study. First, this is a single-center study, which raises the question of generalizability to other STEMI systems. However, the in-depth examination of the reasons for CCLX and clinical outcomes of these patients offer guidance and grounds for hypothesis testing for other STEMI systems with high CCLX rates.18 Second, the study is a retrospective analysis of all consecutive CCL activations. As such, causality cannot be inferred, and the findings should be considered as hypothesis generating, especially the association of CCLX with increased long-term mortality. Further studies will be necessary to determine how changes in CCL activation process affect CCLX rates and clinical outcomes. Finally, although we report on the incidence of CCLX and inappropriate cancellations, we do not currently have a mechanism for identifying missed STEMIs that did not result in a CCL activation.


    This study represents a comprehensive examination of the reasons for CCL cancellation, as well as the clinical characteristics and outcomes of this interesting patient population. The findings build on the current CCLX literature while offering several novel insights. CCLX patients represent a unique population when compared with EA patients, with novel medical comorbidities. CCLX subjects often do have positive cardiac biomarkers and occasionally receive elective cardiac catheterization. Finally, although cardiovascular mortality remains relatively low, CCLX represent a high-risk patient population that may benefit from triage to tertiary care centers. Ongoing, prospective data will be necessary to determine how changes to the CCL activation process affect the rates of CCLX and clinical outcomes of this patient population.


    Correspondence to David C. Lange, MD, The Permanente Medical Group, Kaiser Permanente Santa Clara Medical Center, 700 Lawrence Expressway, Santa Clara, CA 95051. E-mail


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