Mechanical Complications of Acute Myocardial Infarction: A Scientific Statement From the American Heart Association

Over the past 30 years, improvements in timely reperfusion within regionalized systems of care together with advancement in optimal medical therapies have contributed to reduced mortality rates of AMI.^3,7 However, these improvements are challenged by the aging of the US population and the higher burden of comorbidities that have been identified as risk factors for post-AMI mechanical complications.^4,8 Although there has been a temporal decline in the proportion of patients presenting with STEMI, contemporary patients with mechanical complications tend to be older, female, have a history of heart failure, chronic kidney disease, and are often presenting with their first AMI.^7,9,10 Furthermore, differences in the socioeconomic factors can play a significant role in influencing health outcomes after AMI.¹¹ For example, prior research has reported that Medicare beneficiaries with the highest income category presented to the hospital earlier, were more likely to be treated by a specialized staff in the cardiac catheterization facilities, and received higher rates of guideline-directed medical therapy, in comparison with beneficiaries with lower socioeconomic class.¹¹ Despite improvements in revascularization strategies and processes of care for STEMI, the incidence of mechanical complications has remained relatively unchanged over time. This can be explained, in part, by the growing prevalence of recognized cardiovascular risk factors and the aging of the US population.^10,12,13

The introduction of fibrinolytic therapy marked the beginning of an era of reperfusion therapies for treating STEMI, resulting in a 40% reduction in overall mortality rate.¹⁴ Beginning in the early 1990s, and continuing over the next decade, numerous studies supported a strategy of primary PCI, which was shown to be a safer and a more effective therapy to restore myocardial blood flow, resulting in a further reduction in short- and long-term mortality.^15,16 With the adoption of primary PCI as the preferred reperfusion strategy, the focus was now placed on improving systems of care to maximize the proportion of patients receiving PCI and emphasize timely percutaneous revascularization.¹⁷ Studies have demonstrated that, when emergency medical services and hospital systems work together using coordinated protocols of care, mortality is further reduced for STEMI and cardiogenic shock.^18,19

Over the past 2 decades, the systematic adoption of early percutaneous revascularization for patients with AMI has had a favorable impact on the global incidence of mechanical complications of AMI. The most notable minor reduction was observed during the era of primary PCI when the focus was placed on systems of care for STEMI (Figure 1).^8,13,20,21 Despite these improvements, studies reporting on outcomes among those with mechanical complications have shown conflicting results.^{8,10,12,20,21} Some studies have shown improved outcomes, but most reported that the case fatality rates for mechanical complications have remained flat despite an increase in the use of mechanical circulatory support devices, the use of percutaneous therapies for managing some complications of shock, and improvements in surgical techniques and outcomes over time.^8,10,13 In contemporary studies, close to three-fourths of these patients presented with cardiogenic shock and most required vasopressors, a balloon pump, or a percutaneous left ventricular support device.²² Diminished cardiac output secondary to cardiogenic shock leads to systemic hypoperfusion and maladaptive cycles of ischemia, inflammation, vasoconstriction, and volume overload culminating in multisystem failure and death.²³ Recent evidence from clinical trials has suggested that there is no mortality difference between primary PCI and fibrinolysis combined with adjunctive medical therapy.²⁴ Although it is difficult to ascertain 1 causal mechanism to explain the stable incidence rate over time despite the improvement in the management of AMI, possible explanations include (1) the rapid aging of the US population, which increases the cohort at risk for mechanical complications; (2) improvements in cardiac imaging and the diagnostic ability to detect mechanical complications; and (3) the growth of specialized cardiac centers with multidisciplinary care and advanced hemodynamic support systems to accept and triage these patients.

The incidence of acute severe mitral regurgitation (MR) from papillary muscle rupture (PMR), like other mechanical complications of AMI, has declined in the reperfusion era (range, 0.05%–0.26%),^9,25 but the reported hospital mortality rate remains high between 10% and 40%.^9,25,26 The mitral valve is supported by 2 papillary muscles, the anterolateral branch that has a dual arterial blood supply from the left anterior descending artery (LAD) and the diagonal or marginal branch of the circumflex coronary artery and the posteromedial papillary muscle that has a single blood supply from the circumflex coronary artery or the right coronary artery, depending on dominance. Thus, anterolateral PMR is extremely uncommon and posteromedial PMR typically occurs in association with inferior or lateral STEMIs. PMR may be complete or partial, which may influence the severity of the clinical symptoms.

Risk factors for PMR include older age, female sex, a history of heart failure, chronic kidney disease, and a delayed presentation with a first AMI.^7,9,10,27 PMR commonly occurs within days of AMI, and roughly half of patients present with pulmonary edema that may quickly progress to cardiogenic shock (Table 1).¹² A murmur may be absent because of the rapid equalization of left atrial and left ventricular pressures. The modern cardiac intensive care unit (CICU) has adopted the use of bedside echocardiography or point-of-care ultrasound for the management of acute cardiovascular illness, which can be helpful in establishing the diagnosis of acute MR secondary to PMR, although it should be recognized that a transthoracic echocardiography study can be nondiagnostic in cases of partial PMR, and transesophageal echocardiography has a high diagnostic sensitivity. Left ventricular ejection fraction is often normal or low-normal, and coronary angiography will most often demonstrate single- or 2-vessel coronary artery disease, with total occlusion of the infarct-related artery.⁸

Initial medical care and resuscitation efforts in the CICU may include the need for vasoactive drugs and respiratory support with invasive mechanical ventilation.²⁸ The use of positive-pressure ventilation can improve gas exchange and cardiovascular hemodynamics by reducing left ventricular (LV) preload and afterload and MR and augmenting cardiac output.²⁹ In hemodynamically stable patients, intravenous nitroglycerin or nitroprusside can be administered in the critical care environment to reduce LV afterload. According to an AHA scientific statement on contemporary management of cardiogenic shock secondary to severe MR,²⁸ norepinephrine or dopamine is a good initial vasoactive agent that can be used for hemodynamic support, but after the hemodynamic stabilization is achieved, the addition of an inotropic agent is suggested for patients with pump failure.²⁸ However, it should be noted that the use of vasopressors and inotropic support for mechanical complications of AMI has not been tested in clinical trials. In cases with advanced forms of cardiogenic shock, multiple organ failure, or other contraindications to surgery, a Heart Team discussion may lead to medical optimization in CICU and temporary mechanical support. Large v waves from placement of the pulmonary catheter in a wedge position should be delineated from the pulmonary arterial waveform. Although it is a rare complication of Swan-Ganz catheter, unrecognized prolonged balloon inflation in the wedge position can lead to catheter-associated pulmonary infarct. Patients who do not initially present with cardiogenic shock commonly experience rapid hemodynamic deterioration. The proportion of patients who experienced acute MR attributable to PMR and required mechanical circulatory support before mitral valve surgery was in excess of 70%.²⁵ In the APEX-AMI trial (Assessment of Pexelizumab in Acute Myocardial Infarction), patients who underwent surgical repair had a markedly improved survival rate at 90 days, in comparison with those who were treated medically (surgical treatment, 69% versus medical treatment, 33%). Although the IABP-Shock II trial (Intraaortic Balloon Pump in Cardiogenic Shock II) did not show a mortality benefit from the use of an intra-aortic balloon pump (IABP) in patients with AMI complicated by cardiogenic shock,³⁰ the study excluded patients with mechanical complications, and IABP placement is still recommended by guidelines as a bridge to therapy because of its presumed ability to reduce afterload in patients with severe MR attributable to PMR. The use of IABP provides ≈0.5 L/min of cardiac output for mechanical circulatory support by using balloon counterpulsation.²³ This mechanism increases the aortic pressure during diastole while decreasing the mean arterial pressure during ejection, which in turn reduces the impedance (ie, afterload) for the ejected blood from the LV during systole and at the same time increases coronary blood flow during diastole.²³ The reduction in the afterload during severe MR attributable to PMR decreases the regurgitant volume and regurgitant fraction, which may ultimately increase the cardiac index.²⁸ The experience with mechanical circulatory support, including percutaneous ventricular assist devices and venoarterial extracorporeal membrane oxygenation (ECMO) for stabilization in PMR, is limited to small case series, but can be considered as a bridge to decision or definitive surgical or percutaneous therapies.³¹

In contemporary cardiovascular practice, the incidence of ventricular septal defect (VSD) after AMI is ≈0.3%.^40,41 Risk factors include older age, female sex, and delayed reperfusion.^7,9,10,27 Typically occurring 3 to 5 days after infarction, presentations range from an incidental murmur to circulatory collapse (Figure 2). Symptoms may include dyspnea and orthopnea, and clinical examination often reveals hypotension, cool peripheries, and oliguria attributable to low cardiac output, and a new pansystolic murmur, commonly at the lower left sternal edge, with signs of pulmonary venous congestion. A 12-lead ECG may identify ongoing ischemia, evolving myocardial infarction, Q wave in the affected territory (anterior or inferior), and associated ventricular arrythmias.

Echocardiography is diagnostic for evaluating the size and location of a left-to-right shunt, biventricular function, and MR. Right heart catheterization shows a diagnostic step-up in oxygenation between the right atrium and pulmonary artery and elevated pulmonary-to-systemic flow ratio (up to 8:1 depending on the defect size). Left heart catheterization often performed during the initial ischemic presentation guides concomitant revascularization and commonly shows a complete coronary obstruction without collateral circulation. Anterior and apical ischemic VSDs are caused by infarcts in the LAD territory, but posterior VSDs are caused by inferior infarcts. Right ventricular infarction or ischemia with severe dysfunction is an important feature of VSDs caused by acute proximal right coronary occlusion. Posterior VSDs are often accompanied by MR commonly secondary to ischemic tethering (Figure 2). The locations of VSD have been reported in 1 study and tend to occur more frequently in the anterior than inferior/lateral wall infarction (70% versus 29%), but inferior infarcts are associated with “complex VSDs, those with multiple, irregular, and/or variable interventricular connections.”⁴¹

Given the high mortality rate associated with uncorrected defects approaching 80% at 30 days, conservative medical therapy alone is limited to patients with hemodynamically insignificant defects, or those with prohibitive surgical risk.^40,42–44 Effective afterload reduction to decrease the left-to-right shunt is essential: IABPs with pharmacotherapy are used in >80% of emergency and 65% of urgent repairs.^5,45 In the SHOCK Trial Registry, IABPs were used in up to 75% of postinfarct VSDs. Within 30 minutes of the initiation of IABP, the median systolic blood pressure was increased from 81 mm Hg to 102 mm Hg.⁴⁶ When a patient presents with multiorgan failure, potential support with ECMO may be considered to allow for improvements in end-organ failure as a bridge to surgical candidacy. In patients without clinical symptoms of end-organ failure, a delayed treatment may allow for connective tissue or scar formation around the defect, resulting in a better anchor for suture material and a lower potential for patch dehiscence. Therefore, the patient with early shock and no evidence of multiorgan failure is potentially the best candidate for emergency surgery.^47–49 Similar hemodynamic stability as a bridge to definitive therapy has been reported using ECMO,⁵⁰ Impella, and TandemHeart.^51,52 Patients severely compromised by multiorgan failure may benefit from biventricular mechanical support or ECMO with percutaneous or surgical LV vents, allowing end-organ recovery before definitive surgery. The purpose of LV venting is to reduce LV afterload/preload, reduce the pulmonary shunt fraction, and thereby reduce pulmonary edema and improve gas exchange. The venting may be necessary to reduce acute lung injury and harlequin (North/South) syndrome. In addition, the LV vent may improve LV flow, and the therapy minimizes the risk of LV or aortic thrombosis. However, venting strategies may also have potential drawbacks in patients with VSD, including the aspiration of deoxygenated blood from the right side to the left and embolization of necrotic LV debris with the use of Impella. In VSDs, the right ventricular flow may minimize the risk of LV thrombosis and increase the risk of aortic thrombosis. Careful considerations of LV venting in patients with ECMO and in patients with postinfarct VSD should be exercised. We suggest that a multidisciplinary team carefully weigh the risk and benefits of LV venting in patients supported with ECMO.^53,54 Emergency surgery is indicated for patients with cardiogenic shock and pulmonary edema refractory to mechanical circulatory support. Lower mortality is reported when surgery is delayed for a week after diagnosis, although selection and survival bias may explain these reported outcomes.⁵¹ The rationale for delaying surgery in hemodynamically stable patients is to avoid bleeding from antiplatelet medication and allow improved patient selection for optimal outcomes.

Although free wall rupture is the most commonly reported mechanical complication of AMI, its true incidence is unknown because it usually presents as out-of-hospital sudden cardiac death and there is a lack of routine autopsy. Although the overall incidence of rupture has decreased with prompt acute reperfusion therapy for STEMI, the initial trials of fibrinolysis versus placebo showed an early increased risk of free wall rupture after 24 hours with fibrinolytic therapy that supports a higher risk of rupture with delayed reperfusion therapy.⁵ This is attributed to intramyocardial hemorrhage, myocardial dissection, and subsequent rupture.²⁰

Free wall rupture should be suspected in any patient with hemodynamic instability or collapse after AMI, especially in the setting of delayed or ineffective reperfusion therapy. The clinical examination classically shows jugular venous distension, a pulsus-paradoxus or frank electromechanical disassociation, and muffled heart sounds in the setting of cardiovascular collapse. It is sometimes preceded by chest pain and nausea, and ECG may show new ST-segment elevation because contact with blood irritates the pericardium. Free wall rupture is rapidly fatal, but occasionally a prompt bedside echocardiogram confirms the diagnosis and warrants emergency surgical correction. Although surgery can be lifesaving, the hospital mortality for patients who have undergone surgical repair is >35%.^61,62 A variant of frank rupture characterized by a friable infarct zone with an oozing bloody pericardial effusion should be recognized. In cases of circulatory collapse, immediate placement on ECMO support may provide an opportunity to stabilize the circulation and perform definitive repair with acceptable results, but poor venous return in cases with tamponade may limit ECMO blood flow.⁶²

Pseudoaneurysms of the LV develop when cardiac rupture is contained by pericardial adhesions.^65–68 Although they may occur after cardiovascular surgery, after blunt or penetrating chest trauma, or as a result of infective endocarditis, pseudoaneurysms are most commonly associated with prior AMI.^65–67 Compared with true aneurysms, pseudoaneurysms more often involve the inferior or lateral wall, perhaps the result of dependent pericardial adhesions developing in the recumbent, convalescing patient after infarction.⁶⁷ Although acute anterior wall rupture is thought to result in massive hemopericardium, catastrophic tamponade, and immediate death, other pseudoaneurysms can remain undiagnosed for several months or longer.^65–68

Patients with pseudoaneurysm may present with a myriad of signs or symptoms, none of which can be considered pathognomonic for the condition (Table 1). Although previous case series have argued that nearly half of afflicted individuals will be asymptomatic at the time of diagnosis,⁶⁶ more contemporary studies and systematic reviews instead note that the majority will be expected to present with congestive heart failure, chest pain, or shortness of breath.^67,68 Others may develop symptomatic arrhythmias, signs of systemic embolization, and even sudden cardiac death. Most patients are male, and will have both electrocardiographic (eg, ST-segment changes) and radiographic (eg, mass-like protuberance on plain film or cardiomegaly) abnormalities at presentation.⁶⁷ Diagnosis requires a high index of suspicion, and often necessitates the use of multiple complimentary imaging tools; among these are coronary angiography and ventriculography, 2-dimensional transthoracic echocardiography, transesophageal echocardiography, cardiac computed tomography, and magnetic resonance imaging.^65–68 Pseudoaneurysms usually have a narrow neck and lack the normal structural elements found in an intact cardiac wall (Figure 2).^65–68

Although commonly a delayed complication of AMI, LV aneurysm is associated with an increased risk of angina pectoris, in part, secondary to an increased LV end-diastolic pressure, thrombus formation, worsening heart failure, and hemodynamically significant ventricular tachyarrhythmia.⁶⁹ The aneurysm is made of a thin, scarred, or fibrotic myocardial wall and it most commonly involves the anterior or apical walls of the LV. The most common pathogenesis is a total thrombotic occlusion of the LAD, but involvement to the inferior or basal walls secondary to the occlusion of the right coronary artery can also be observed.⁶⁹ For most cases, the management is conservative.⁶⁹

In patients who are not suitable candidates for surgical and transcatheter therapies, including those with significant biventricular failure and with associated end-organ impairment, evaluation for orthotopic heart transplantation or mechanical circulatory support may be considered. The new United Network for Organ Sharing transplant allocation system gives preference to patients on full circulatory support with venoarterial ECMO. Increasing numbers of patients are undergoing orthotopic heart transplantation while on full circulatory support (INTERMACS 1 [Interagency Registry for Mechanically Assisted Circulatory Support] or SCAI E [Society for Cardiovascular Angiography and Interventions Clinical Expert Consensus Statement on the Classification of Cardiogenic Shock]).⁷⁷ Although concerns linger regarding perioperative mortality in these patients, this therapeutic option may be a successful bridge or destination therapy for select patients with mechanical complications of AMI if surgery or catheter-based therapies are not feasible.⁷⁸

Mechanical complications usually present with hemodynamic instability initially or after admission for AMI. Early diagnosis is critical, and a high degree of clinical suspicion is warranted.

Table 2 highlights other clinical conditions that may be considered in the clinical differential.

Heightened recognition of the complexities associated with contemporary cardiovascular care has led to a reappraisal of management practices and staffing requirements within the modern CICU.⁷⁹ Multiorgan system injury is now commonplace^79,80 and often requires multidisciplinary input for optimal management. Shared decision-making, orchestrated by a critical care–trained physician, has been shown to enhance collaboration and communication,⁸¹ streamline transitions of care, and even improve patient survival.⁸² Patient-centered, team-based care can also optimize adherence to best practice guidelines, decrease adverse events,⁸³ reduce costs of care, and result in patient and family satisfaction.⁸¹

Patients with mechanical complications of AMI are at high risk for multisystem sequelae, will frequently require critical care support for end-organ dysfunction, and are likely to benefit from a team-based approach for decision-making in the CICU. Mechanical complications have a spectrum of presentations for clinical acuity ranging from minimally symptomatic to cardiogenic shock; in patients with Society for Cardiovascular Angiography and Interventions stage B through E shock, we suggest that multidisciplinary shock team assessment and management has the potential to improve clinical outcomes.^84,85 In addition to the aforementioned cardiac intensivist, these collaborative care teams will include nurses, respiratory therapists, pharmacists, interventional cardiologists, cardiovascular surgeons, social workers, dieticians, and others (Figure 5). In most cases, the mechanical complications of AMI are surgical emergencies and need an emergency surgical consultation to avoid undue delays for medical optimization. The multidisciplinary Heart Team discussion is critically important in nonstraightforward cases. Palliative care experts and geriatricians will be frequently called on to help determine patient-centered goals of care and to assist in end-of-life discussions.⁸⁶ Patients and family members are pivotal partners in treatment decision-making.^87,88 In response, critical care societies have emphasized the importance of including well-delineated patient and family engagement pathways as part of routine intensive care delivery; this may include such practices as the engagement of patients and families during team rounds and the presence of family members during cardiopulmonary resuscitative efforts.⁸⁹ Figure 5 summarizes and illustrates the key perspectives necessary for optimal treatment decision-making and team-based care for critically ill patients with mechanical complications of AMI. It should be noted that these principles should not only include patients with mechanical complications in the CICU only, but they also include these patients if they were cared for in the emergency department, medical intensive care unit, and surgical intensive care unit. Figure 6 highlights a treatment pathway for the management of stable and unstable mechanical complications of AMI.

Palliative care is a medical specialty that emphasizes interprofessional team, patient- and family-centered care with the goal of optimizing quality of life by anticipating, preventing, and treating symptoms.⁹⁰ In critically ill cardiac patients, such as those experiencing mechanical complications of AMI, palliative care specialists can play a vital role in identifying the patient’s and family’s values and care preferences, which can then be matched with appropriate cardiac, life-sustaining, and comfort care treatment options. Values-based decision-making and goals of care are tantamount to patient- and family-centered care, regardless of evidence of a therapy’s effectiveness in a given population.⁹¹ Palliative care consultation can provide value-added service to the multidisciplinary team by helping to balance potentially evidence-based treatment choices with individual patient and family cultural, spiritual, and quality-of-life contexts.⁹¹

Although numerous guidelines and reviews have recommended integration of palliative care for all patients with advanced stage cardiac conditions, regular use has been low.^5,28,91 In a nationwide sample of almost a million patients with AMI from 2002 to 2016, palliative care consultation increased over time but still averaged only 1.3%. Even for high-risk patients, like those with cardiogenic shock who experience an estimated 30% to 40% in-hospital mortality, the consultation rate was only 6.5%.⁹² Another large, contemporary study found that only 2.5% of all patients with AMI and 24% of patients with AMI who died had palliative care specialist consultations.⁹³

Barriers to palliative care use include patients’ uncertain prognosis, lack of understanding of risks and benefits of therapy, and conflation of palliative care with hospice and death.^28,92,94 These biases likely explain the common use of palliative care only when death seems certain.⁹² Professional societies have begun to identify appropriate triggers for palliative care referral, including the presence of advanced heart failure and objective, subjective, and patient-centric markers of critical cardiac illness.^28,94 Based on indicators and potential benefits of decision support, values-based care, symptom control, quality of life, and resource use, extrapolated from many critical cardiac conditions, regular referral to palliative care for patients with mechanical complications of AMI is currently routine practice in many centers.^28,91–94

Mechanical complications are rare and occur in <1% of patients with AMI. Their presentation is acute and requires a high intensity of care and clinical expertise, available only in select tertiary or quaternary care centers. Therefore, systematic enrollment of these patients in pragmatic clinical trials to develop pathways of care is extremely challenging. The variability in care of patients with mechanical complications is influenced by factors, such as difficulties in early diagnosis, limited availability of LV assist devices, experienced multidisciplinary teams, risk-averse medical behaviors, and lack of equipoise among physicians caring for these patients. In this setting, randomized controlled trials become exceptionally difficult to perform, likely with unrepresentative patient samples. However, reliance on observational data is not satisfactory. Mechanical complications could be studied in a fashion similar to rare diseases, with study designs that require only a fraction of the number of subjects necessary for an adequately powered randomized controlled trial.⁹⁵ Because of similarities in the presentation and early mortality rate between mechanical complications and aortic dissection, a registry similar to the International Registry of Acute Aortic Dissection in selected referral centers could shed light on and help develop pathways of care for the diagnosis and management of mechanical complications.⁹⁶

Multiple gaps remain in the care of mechanical complications of AMI (Table 3); these include the role of point-of-care echocardiography in the initial assessment of complicated infarcts, the use of other imaging modalities such as computed tomography and magnetic resonance imaging, the role and timing of new temporary LV support devices or ECMO, and the timing of corrective intervention, either percutaneous or surgical. Of note, the surge of new procedures for structural heart disease could be extended to the management of mechanical complications, including customized solutions using 3-dimensional printing technology.⁹⁷

Mechanical complications of AMI are high-acuity and time-sensitive conditions associated with high morbidity and mortality rates. We propose that early recognition, diagnosis, and multidisciplinary stakeholder involvement in medical resuscitation and stabilization together with patient-centered planning and timing of appropriate surgical intervention, percutaneous technologies, mechanical circulatory support, and palliative specialist support has the potential to improve disease- and patient-centered outcomes. We acknowledge the paucity of controlled studies in these infrequent conditions, and we advocate for more collaborative international efforts to develop registries and conduct pragmatic trials to address the identified knowledge gaps and guide the optimal treatment strategies and pathways.

The authors would like to acknowledge (1) Dr Alan W. Heldman for providing the case study for percutaneous repair of left ventricular pseudoaneurysm; (2) Ms Devon Stuart and Mr Patrick Lane for their assistance with medical illustration; and (3) Dr Paul St. Laurent, Senior Science and Medicine Advisor (Lead), for his assistance and administrative role with this AHA scientific statement.