In MI with cardiogenic shock, PCI of only culprit lesions is safer

In patients with acute myocardial infarction and multivessel coronary artery disease with cardiogenic shock, 30-day rates of death and renal-replacement therapy were lower when patients underwent percutaneous coronary intervention (PCI) of the culprit lesion as opposed to multivessel PCI.

The difference appeared to be driven by mortality, as the renal endpoint alone was not significant.

As many as 80% of patients with cardiogenic shock also present with multivessel coronary artery disease, and this is associated with worse mortality. It is unclear whether immediate PCI of clinically important stenoses of major nonculprit coronary arteries is of benefit, and previous randomized trials comparing the procedures did not look at patients with cardiogenic shock, Holger Thiele, MD, reported at the Transcatheter Cardiovascular Therapeutics annual educational meeting.

^{Bruce Jancin/Frontline Medical News}

Dr. Holger Thiele

European guidelines suggest that PCI of nonculprit lesions should be considered in patients with cardiogenic shock, while U.S. guidelines offer no opinion, but recent appropriate use criteria recommend revascularization of a nonculprit artery if cardiogenic shock continues after the culprit artery has been repaired. It is thought that immediate revascularization of all coronary arteries with clinically important stenoses might improve overall myocardial perfusion and function in patients with cardiogenic shock, but the procedure could also have drawbacks, including additional ischemia, volume overload, and renal impairment from higher doses of contrast material.

To better understand outcomes in these patients, the Culprit Lesion Only PCI versus Multivessel PCI in Cardiogenic Shock (CULPRIT-SHOCK) trial randomized 706 patients to culprit-only PCI or multivessel PCI, in which PCI was performed on all major coronary arteries with more than 70% stenosis. Patients receiving culprit-only PCI could also undergo optional staged revascularization due to residual ischemic lesions, symptoms, or clinical or neurologic status.

At 30 days, death and/or renal-replacement therapy occurred in 45.9% of the culprit-only group, compared to 55.4% in the multivessel group (relative risk, 0.83; 95% confidence interval, 0.71-0.96; P = .01). A per-protocol analysis showed similar results (RR, 0.81; 95% CI, 0.69-0.96; P =.01), as did an analysis of the as-treated population (RR, 0.83; 95% CI, 0.72-0.97; P = .02).

All-cause mortality was lower in the culprit-only group (43.3% versus 51.6%; RR, 0.84; 95% CI, 0.72-0.98; P=.03). The rate of renal-replacement therapy was higher in the multivessel group (16.4% versus 11.6%), but this did not reach statistical significance (P = .07).

There were no statistically significant differences between the two groups with respect to recurrent myocardial infarction, rehospitalization for heart failure, bleeding, or stroke, Dr. Thiele reported at the meeting, which was sponsored by the Cardiovascular Research Foundation.

Some limitations of the study included its unblinded nature, and the fact that 75 patients originally assigned to one treatment category crossed over to the other, including 14 in the culprit-lesion only category who underwent immediate multivessel PCI. This suggests that treatment strategy may need to be adopted to a patient’s clinical circumstances.

The CULPRIT-SHOCK results were published online at the time of Dr. Thiele’s presentation (N Engl J Med. 2017 Oct 30. doi:10/056/NEJMoa1710261).

Several of the study’s authors reported financial ties to the pharmaceutical industry.