Editorials
Still a Long Way to Go in Treating Cardiogenic Shock in Acute Myocardial Infarction
2020 Volume 84 Issue 9 Pages 1461-1463
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2020 Volume 84 Issue 9 Pages 1461-1463
Acute myocardial infarction (AMI) is the single most common cause of cardiogenic shock (CS),1 which is due to severe impairment of myocardial performance that results in diminished cardiac output, end-organ hypoperfusion, and hypoxia. The primary insult is an imbalance between myocardial oxygen supply and/or demand that results in reduction in myocardial contractility, reduction in cardiac output, and hypotension. A compensatory peripheral vasoconstriction initially improves coronary and peripheral perfusion; however, eventually it contributes to an increase in the cardiac afterload and leads to a further reduction in myocardial function. A vicious cycle between myocardial dysfunction and organ hypoperfusion deteriorates the patient and can lead to death. To be specific, the mortality rate of AMI complicated with CS has been reported to be as high as 50%,2 which is in sharp contrast with that in patients with noncardiogenic shock AMI who have a mortality rate of <5%.3 The etiologies resulting in CS are described in the Table.
| AMI without mechanical complications |
| 1. Severe left heart dysfunction (systolic dysfunction and diastolic dysfunction) |
| 2. Severe right heart dysfunction (systolic dysfunction and diastolic dysfunction) |
| 3. Fatal arrhythmia (associated to reperfusion, associated with heart dysfunction) |
| AMI with mechanical complications |
| 1. Ventricle wall rupture (ventricular septal defect, free wall rupture) |
| 2. Mitral regurgitation with or without ischemic papillary muscle rupture |
| 3. Iatrogenic complications (coronary perforation, cardiac tamponade, etc.) |
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Among various treatment options for AMI complicated with CS, a vast amount of evidence endorses early revascularization by percutaneous coronary intervention (PCI).4,5 Early revascularization is essential to restore myocardial blood supply, and current guidelines recommend primary PCI in patients presenting with ST-segment elevation MI complicated by CS.6 Moreover, the extent of revascularization is currently in the limelight, with a randomized trial reporting that death did not differ significantly between culprit only vs. multivessel revascularization groups at 1-year follow-up.7 Despite the tremendous effort to achieve urgent revascularization together with aggressive medical therapy, mortality in patients presenting with AMI complicated by CS remains very high and management remains challenging despite advances in therapeutic options. To overcome the especially high early mortality rate in these patients, various types of mechanical circulatory support (MCS) devices have been used to provide mechanical hemodynamic support, independent of myocardial contractility (i.e., devices such as intra-aortic balloon pump [IABP], Impella, TandemHeart and extracorporeal membrane oxygenation [ECMO]), which are still under investigation (Figure).8 An ideal MCS device provides effective hemodynamic support, is easy to operate and maintain, and is associated with a minimal complications.
Schematic of current commercially available percutaneous mechanical support devices for cardiogenic shock. (A) Intra-aortic balloon pump (IABP); (B) Impella; (C) TandemHeartT; (D) extracorporeal membrane oxygenation (ECMO). Adapted with permission from Thiele H, et al.8
Until the previous decade, IABP was the mainstay MCS for AMI patients with CS. However, after the IABP SHOCK-II study, which reported that IABP could not demonstrate any benefit as a routinely used device, utilization has markedly decreased. The Impella (Abiomed Inc.) and TandemHeart (CardiacAssist Inc.) are promising new devices that can provide hemodynamic performance superior to IABP, but still need more evidence to be recognized as a standard device for AMI patients with CS. This leaves ECMO as the “currently most commonly used” MCS device.
ECMO is unique in giving both cardiac and pulmonary support. By draining the venous blood, passing it through an oxygenator, and returning the oxygenated blood to the systemic circulation using a centrifugal pump, ECMO can provide fully oxygenated blood at a sufficient flow rate up to 4–5 L/min. Since its first application in the 1970 s by Hill et al as a successful support for severe respiratory failure, it has evolved greatly,9 especially the development of a miniaturized system, more durable membrane oxygenator and biocompatible circuits, which have widened the indication of ECMO. In particular, veno-arterial ECMO (VA-ECMO) is nowadays widely used as circulatory support for CS and has played a pivotal role in refractory cardiac arrest.
In this issue of the Journal, Choi et al10 demonstrate that early initiation of VA-ECMO before revascularization therapy was associated with a significantly lower risk of composite in-hospital mortality, left ventricular assistance device implantation, and heart transplantation, compared with VA-ECMO insertion after revascularization in patients with AMI complicated by refractory CS. Similar results have been reported,11 but interestingly in the current study the patients who received VA-ECMO after revascularization had a similar event rate as the reference cohort (cardiac arrest with E-CPR before revascularization). Noticing that the reference cohort was the population with the worst clinical outcomes, the authors stress the importance of early initiation of VA-ECMO. Although this was a single-center retrospective study with a relatively small number of patients, the study results should be emphasized, because of the valuable insights on the benefits of early initiation of VA-ECMO in AMI patients complicated by refractory CS, as such research cannot be performed in a randomized study.
As can be seen from the results of this study, the optimal timing of ECMO support initiation remains unclear, which is also a difficult issue for other MCS devices. The authors explain that a more stable insertion procedure, and minimizing complications during revascularization by full VA-ECMO support were potential explanations of the favorable outcomes in the ‘ECMO before revascularization’ arm. In particular, the most vulnerable timepoints of fatal arrythmias are the point of reperfusion, when there is a surge of cellular calcium release, and the immediate post-PCI recovery period. Obviously, full support during this period can reduce fatal clinical events. Additionally, it is well known that once the features of end-organ damage have developed, mortality remains very high, despite vigorous treatment. As described earlier, there are plausible explanations for the benefit of earlier ECMO application.
On the other hand, various aspects should be considered when applying VA-ECMO in AMI patients with CS. First, despite the full circulatory support provided by VA-ECMO, it can be associated with significant complications, such as pump thrombosis, bleeding, ischemic limb events, and the Harlequin syndrome. An antegrade sheath placed in the superficial femoral artery to improve distal limb perfusion, adequate anticoagulation and balance between thrombosis and bleeding events, and meticulous monitoring and medical treatment are needed to minimize the risk of these complications. Second, especially in patients with peripheral VA-ECMO, the retrograde flow from femoral artery cannulation can increase the systemic afterload and increase the left ventricular end-diastolic pressure. This retrograde pressure on the left ventricle will further depress native cardiac output, induce congestion in the lungs and heart, and have a negative effect on long-term prognosis unless the left ventricle is decompressed.12 Various methods are used to ‘unload’ the left ventricle, such as a concomitant use of Impella or IABP with ECMO, percutaneous trans-septal venting and direct surgical venting. Although many methods are used to solve the hemodynamic alteration during VA-ECMO, it remains a clinical challenge to foresee which patients will benefit from adjunct interventions.
VA-ECMO is often used as the MCS device for AMI patients complicated by refractory CS. The strongest benefit is that it provides rapid and adequate cardiopulmonary support. Yet with regard to the specific protocol that may benefit the patient, there is much that needs to be elucidated. Also, intrinsic complications induced by ECMO application also need to be reduced. Ongoing prospective registry-based studies, such as the National Cardiogenic Shock Initiative (ClinicalTrial.gov Identifier: NCT03677180), RESCUE II (ClinicalTrials.gov Identifier: NCT04143893), and ECLS-SHOCK (ClinicalTrials.gov Identifier: NCT03637205) will give us invaluable insights of the usage of ECMO in CS.
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