Need for Critical Reappraisal of Intra-aortic Balloon Counterpulsation

Abstract

DESPITE CONSIDERABLE ORGANIZATIONAL, TECHNOlogical, and pharmacological advancements in the treatment of patients with acute ST-segment elevation myocardial infarction (STEMI) and even with percutaneous coronary intervention (PCI), the efficacy of reperfusion is still suboptimal, mortality remains high, and novel therapeutic interventions are needed. Intraaortic balloon counterpulsation (IABC) was first used to treat cardiogenic shock in 1968; since then, it has been used in various clinical conditions to provide mechanical cardiac assistance. Use of IABC is associated with immediate hemodynamic effects leading to increased diastolic pressure, increased coronary perfusion pressure, and reduced left ventricular afterload. In the setting of STEMI, left ventricular unloading by IABC may prevent early infarct extension and ventricular remodeling. Experimental studies have shown that IABC reduces infarct size. Currently, IABC is widely used in patients with STEMI complicated by cardiogenic shock. In addition, IABC has been used as a circulatory support in PCI procedures for patients at high risk for hemodynamic instability such as those with complex coronary lesions, post-MI refractory angina, and severely compromised left ventricular function as well as an intervention in the last remaining vessel and in unprotected left main coronary artery disease. Nevertheless, the issue of IABC use during high-risk PCI procedures or in STEMI remains controversial. The report of the Counterpulsation to Reduce Infarct Size Pre-PCI Acute Myocardial Infarction (CRISP AMI) trial by Patel and colleagues in this issue of JAMA helps to clarify this controversy. CRISP AMI was an open-label, multicenter randomized controlled trial that included 337 patients with STEMI involving the anterior wall who presented within 6 hours of chest pain onset and without cardiogenic shock. Patients were randomly assigned to receive IABC, which was placed prior to PCI and was continued for at least 12 hours, or primary PCI alone. The primary outcome of the trial was infarct size measured by cardiac magnetic resonance imaging. The mean infarct size (estimated a median of 4 days after the onset of symptoms) was 42.1% of the left ventricle in patients assigned to IABC plus PCI and 37.5% of the left ventricle in the patients assigned to PCI alone (P=.06), showing no benefit with IABC. No significant differences between the IABC plus PCI group and the PCI alone group were observed regarding clinical end points. The authors concluded that the routine use of IABC in patients with anterior wall STEMI without cardiogenic shock does not lead to a reduction in infarct size or to an improvement in clinical outcomes at 6 months. Autopsy studies have shown that cardiogenic shock is generally associated with loss of 40% or more of the left ventricular mass, and the association between necrosis of 40% or more and the development of cardiogenic shock has been accepted in the field of cardiology during the last 40 years. Therefore, the finding in the CRISP AMI trial that the mean infarct size estimated by cardiac magnetic resonance imaging was 40% and patients were hemodynamically stable at presentation seems surprising. Moreover, infarct size was recorded after primary PCI, a reperfusion strategy that leads to an average salvage index (proportion of area at risk salvaged by reperfusion) of about 50% according to studies with serial measurements of both the initial area at risk and the final infarct size after reperfusion. Based on the T2weighted imaging obtained from the single magnetic resonance imaging study performed after reperfusion, the authors computed a mean salvage index of 35%. Although the reasons underlying these findings remain largely unclear, possible explanations include an overestimation of infarct size by cardiac magnetic resonance imaging, premature timing of imaging at a point when the recovery of myocardial perfusion is not complete, or dissociation of the link between myocardial necrosis and the development of cardiogenic shock in the contemporary era of STEMI care. Five previous randomized trials have assessed the role of IABC in patients with AMI without cardiogenic shock. However, neither these trials nor the CRISP AMI trial were sufficiently powered for the evaluation of clinical outcomes with IABC, with only 21 deaths among 518 patients in the IABC groups and 21 deaths among 536 patients in the control groups across the studies.