Key result
Targeting higher MAP reduces myocardial injury ~27% vs 65 mm Hg in post-arrest AMI shock.
Why the study?
In patients with shock after AMI, the optimal level of pharmacologic support and optimal mean arterial pressure target after cardiac arrest were unknown.
Does targeting a higher mean arterial pressure (80/85 to 100 mm Hg) reduce myocardial injury in post-cardiac arrest patients with shock after acute myocardial infarction?
RCT (n=120)
randomized
Yes
Does targeting a higher mean arterial pressure (80/85 to 100 mm Hg) reduce myocardial injury in post-cardiac arrest patients with shock after acute myocardial infarction?
In post-cardiac arrest patients with shock after AMI, targeting a higher MAP (80/85-100 mm Hg) reduced myocardial injury (measured by hs-TnT) without increasing the risk of new cardiac arrest or atrial fibrillation.
Answers are grounded in this paper and cite their sources.
May warrant higher MAP targets in post-arrest AMI shock; extends pooled RCT evidence but leaves hard outcome benefit open.
BACKGROUND: In patients with shock after acute myocardial infarction (AMI), the optimal level of pharmacologic support is unknown. Whereas higher doses may increase myocardial oxygen consumption and induce arrhythmias, diastolic hypotension may reduce coronary perfusion and increase infarct size. OBJECTIVES: This study aimed to determine the optimal mean arterial pressure (MAP) in patients with AMI and shock after cardiac arrest. METHODS: This study used patient-level pooled analysis of post-cardiac arrest patients with shock after AMI randomized in the Neuroprotect (Neuroprotective Goal Directed Hemodynamic Optimization in Post-cardiac Arrest Patients; NCT02541591) and COMACARE (Carbon Dioxide, Oxygen and Mean Arterial Pressure After Cardiac Arrest and Resuscitation; NCT02698917) trials who were randomized to MAP 65 mm Hg or MAP 80/85 to 100 mm Hg targets during the first 36 h after admission. The primary endpoint was the area under the 72-h high-sensitivity troponin-T curve. RESULTS: Of 235 patients originally randomized, 120 patients had AMI with shock. Patients assigned to the higher MAP target (n = 58) received higher doses of norepinephrine (p = 0.004) and dobutamine (p = 0.01) and reached higher MAPs (86 ± 9 mm Hg vs. 72 ± 10 mm Hg, p < 0.001). Whereas admission hemodynamics and angiographic findings were all well-balanced and revascularization was performed equally effective, the area under the 72-h high-sensitivity troponin-T curve was lower in patients assigned to the higher MAP target (median: 1.14 μg.72 h/l [interquartile range: 0.35 to 2.31 μg.72 h/l] vs. median: 1.56 μg.72 h/l [interquartile range: 0.61 to 4.72 μg. 72 h/l]; p = 0.04). Additional pharmacologic support did not increase the risk of a new cardiac arrest (p = 0.88) or atrial fibrillation (p = 0.94). Survival with good neurologic outcome at 180 days was not different between both groups (64% vs. 53%, odds ratio: 1.55; 95% confidence interval: 0.74 to 3.22). CONCLUSIONS: In post-cardiac arrest patients with shock after AMI, targeting MAP between 80/85 and 100 mm Hg with additional use of inotropes and vasopressors was associated with smaller myocardial injury.
No takes yet. Share an insight, caveat, or question.
Ameloot et al. (2020) conducted an RCT in Shock after acute myocardial infarction and cardiac arrest (n=120). Higher mean arterial pressure (MAP) target vs. MAP 65 mm Hg target was evaluated on Area under the 72-h high-sensitivity troponin-T curve (p=0.04). Targeting a mean arterial pressure of 80/85 to 100 mm Hg in post-cardiac arrest patients with shock after AMI reduced myocardial injury (median troponin-T AUC 1.14 vs 1.56 μg.72 h/l; p=0.04).
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: