Clinical Research & Data, Hemodynamics, AMI Cardiogenic Shock

Optimal Target MAP in Post-Cardiac Arrest AMI Shock


Do blood pressure targets in the 36 hours after ICU admission affect outcomes in patients with AMI complicated by cardiogenic shock after cardiac arrest? To investigate this question Koen Ameloot, MD and colleagues recently published “Optimum Blood Pressure in Patients With Shock After Acute Myocardial Infarction and Cardiac Arrest” in JACC. Dr. Ameloot is an interventionalist and intensivist in Genk, Belgium.

While current guidelines recommend that clinicians use inotropes and vasopressors in cardiogenic shock to support end-organ perfusion, Dr. Ameloot explains that guidelines do not specify hemodynamic goals that should be targeted. “So, the question we had when we designed this study, was ‘What is the optimal MAP of a cardiogenic shock patient freshly being revascularized in the cath lab?’ So what balances, actually, afterload, myocardial oxygen consumption, and coronary perfusion?”

This post hoc pooled analysis of patients from the Neuroprotect and COMACARE randomized controlled trials investigated whether targeting a lower conventional mean arterial pressure (MAP) goal (65 mmHg) versus a higher MAP target (80/85 to 100 mmHg) would affect myocardial injury and arrhythmogenic risk in this patient population. The primary endpoint was area under the troponin T curve for the first 72 hours.

“And surprisingly, what we found,” Dr. Ameloot reports, “is that targeting a higher mean arterial pressure—so with more inotropes, more vasopressive agents—actually leads to a 37% relative reduction in the area under the troponin curve. So, it’s a reduction in infarct size with targeting higher mean arterial pressures.”

Dr. Ameloot briefly discusses the limitations of troponin to assess infarct size, noting that the gold standard to study infarct size is cardiac MRI at day 5; however, he explains that MRI was not part of the protocol due in part to the challenges associated with undergoing MRI in this unstable shock population. He also describes a future investigation that he and colleagues are designing to test the hypothesis that increasing diastolic blood pressure will increase coronary perfusion and ultimately lead to a reduction in infarct size.

When asked how he would treat a post-cardiac arrest patient with shock after AMI today, as he awaits further data, Dr. Ameloot explains that prior to the outcome of this study he would have gone for the lowest MAP that preserves end-organ perfusion. “But now at least we have some preliminary data to support an 80 or 85 mmHg target,” he states, “and personally I think based on these aspects, I would attempt to go for a higher blood pressure.”



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