PCI for Acute Myocardial Infarction with Cardiogenic Shock: When Less Is More

Published - Written by Michael Mi, MD

Figure 1. Event Rates of the Primary End Point and Its Components at 30 DaysShown are Kaplan–Meier time-to-event curves for the primary end point of a composite of death from any cause or severe renal failure leading to renal-replacement therapy (Panel A), as well as the individual components of death from any cause (Panel B) and renal-replacement therapy (Panel C), within 30 days after randomization. PCI denotes percutaneous coronary intervention.

When I was a resident in the coronary care unit, we would review on morning rounds the coronary angiograms of new patients who presented with acute myocardial infarction (MI). Many of them had multivessel coronary artery disease (CAD), and the decision to treat all significant stenoses or just the lesion responsible for the MI seemed mystifying. Even the guidelines suggest that this answer may not be so clear. In 2013, the ACC/AHA guideline on the management of ST-elevation MI (STEMI) recommended against percutaneous coronary intervention (PCI) in the noninfarct artery at the time of primary PCI, citing evidence of injury. But in 2015, based on the accumulated evidence of benefit from four randomized clinical trials, the ACC/AHA changed its position to suggest that PCI of a noninfarct artery be considered at the time of primary PCI in selected patients.

One important caveat of the guidelines is that they applied mainly to hemodynamically stable patients because patients with cardiogenic shock were excluded from the clinical trials. Although the U.S. guideline makes no specific recommendation for patients with cardiogenic shock, many cardiologists argue that cardiogenic shock justifies revascularization of noninfarct arteries because better overall myocardial perfusion leads to improved pump function.

To help fill this knowledge gap, investigators of the CULPRIT-SHOCK trial randomized 706 patients (mean age, 70 years) with acute MI, multivessel CAD, and cardiogenic shock to receive either PCI of the culprit lesion only (with the option of staged revascularization of nonculprit lesions based on noninvasive testing or fractional flow reserve) or immediate multivessel PCI of all lesions with >70% stenosis, including chronic total occlusions.  Overall, 62% of patients had STEMI. Median contrast doses were 190 mL and 250 mL, respectively, and median fluoroscopy times were 13 and 19 minutes.

The primary outcome — a composite of death or renal-replacement therapy at 30 days — was significantly lower in the culprit-lesion-only PCI group than in the multivessel PCI group (45.9% vs. 55.4%; relative risk, 0.83; 95% CI, 0.71–0.96). The rate of death at 30 days was also significantly lower (43.3% vs. 51.6%; RR, 0.84; 95% CI 0.72–0.98). Despite a crossover rate of approximately 10% in each group, the primary outcome remained similar in both per-protocol and as-treated populations. Rates of bleeding did not differ significantly between groups.

In an accompanying editorial, Drs. Judith Hochman and Stuart Katz from New York University Langone Health offered some reasons why these results are discordant with those from prior trials. In addition to longer procedure times and greater contrast exposure in the multivessel PCI group, they suggest that the inflammatory and prothrombotic effects of cardiogenic shock increase the risk of ischemia or infarction during PCI of nonculprit lesions and that additional catheter manipulation can lead to more renal and neurologic injury. Ultimately, this study provides compelling evidence that in this population of very critically ill patients, minimizing iatrogenic harm is as important as a timely therapeutic intervention.

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Mike is a 2017-2018 NEJM Editorial Fellow and a hospitalist at Beth Israel Deaconess Medical Center. He graduated from Harvard Medical School and completed his internal medicine training at BIDMC.