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Blood Pressure Targets in Cardiac Arrest Patients With Shock After AMI
Quick Takes
- In patients with AMI complicated by cardiogenic shock (CS) after cardiac arrest, administration of inotropic and vasopressor medications to maintain mean arterial blood pressure between 80 or 85 and 100 mm Hg is associated with reduction in myocardial injury without raising the risk of arrhythmia or recurrent cardiac arrest in a patient-level pooled post hoc analysis of two clinical trials.
- Future randomized clinical trials are needed to compare the clinical outcomes associated with various blood pressure targets in patients with AMI-CS after cardiac arrest and to correlate these with various measurements of coronary perfusion, myocardial metabolites, and myocardial injury.
Study Questions:
What is the optimal mean arterial pressure (MAP) in patients with acute myocardial infarction (AMI)–cardiogenic shock (CS) after cardiac arrest?
Methods:
This study used a 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) and COMACARE (Carbon Dioxide, Oxygen and Mean Arterial Pressure After Cardiac Arrest and Resuscitation) trials, who were randomized to MAP 65 mm Hg or MAP 80/85-100 mm Hg targets during the first 36 hours after admission. In both trials, adult patients aged ≥18 years resuscitated from out-of-hospital cardiac arrest of a presumed cardiac cause and unconscious at hospital admission after a sustained return of spontaneous circulation (ROSC) were eligible for inclusion. The COMACARE trial only included patients with shockable rhythms and time from collapse to ROSC between 10 and 45 minutes; Neuroprotect also included patients with nonshockable rhythms irrespective of the time to ROSC. Shock was defined as the need for vasopressors to maintain assigned MAP targets at any time point during the 36-hour intervention period. The primary endpoint was the area under the 72-hour high-sensitivity troponin T (hs-cTnT) curve. Secondary endpoints included new-onset atrial fibrillation, re-arrest, all-cause mortality, and cerebral performance category score at 180 days.
Results:
Of the initially randomized cardiac arrest patients, 120 out of 235 had AMI with shock. Patients assigned to the higher MAP target (n = 58) received higher doses of norepinephrine and dobutamine and reached higher MAPs. The area under the 72-hour hs-cTnT curve was lower in patients assigned to the higher MAP target. Additional pharmacologic support did not increase the risk of a new cardiac arrest or atrial fibrillation. Survival with good neurological outcome at 180 days was not significantly different between both groups.
Conclusions:
In post-cardiac arrest patients with shock after AMI, targeting MAP between 80/85 mm Hg and 100 mm Hg with additional use of inotropes and vasopressors during the first 36 hours of intensive care unit (ICU) stay was associated with a significant reduction in myocardial injury, as measured by hs-cTnT.
Perspective:
Current American College of Cardiology/American Heart Association guidelines offer Class IIb recommendations for the use of inotropes and vasopressors to maintain systemic perfusion and preserve end-organ function with patients with AMI presenting with low MAPs and severe systolic dysfunction. The optimal level of pharmacologic support that balances coronary perfusion, afterload, myocardial oxygen consumption, and arrhythmogenic risk remains unknown in this vulnerable, critically ill patient population.
The aim of this post hoc pooled analysis of both the Neuroprotect and COMACARE trials was to investigate whether targeting lower versus higher MAP would affect myocardial injury and arrhythmogenic risk within the subgroup of post-cardiac arrest patients with shock after AMI. The authors found that the use of additional inotropes and vasopressors to target a MAP between 80/85 and 100 mm Hg during the first 36 hours of ICU stay in post-cardiac arrest patients with shock after AMI was associated with a significant reduction of myocardial injury. Notably, this finding was consistent across both trials and primarily driven by results obtained in ST-segment elevation MI patients with an acute occlusion or subocclusion of the left anterior descending or left main coronary artery.
The authors appropriately recognize several limitations, including the fact that the hemodynamic profile, angiographic findings, and prognosis of the pooled post-cardiac arrest cohort may be different from nonresuscitated patients with shock after AMI who do not receive targeted temperature management, thereby limiting the generalizability of their findings. Nonetheless, this study represents important hypothesis-generating work. Future randomized controlled trials are needed to establish the optimal blood pressure target, the optimal vasoactive regimen, and the effects on clinical outcomes including short- and long-term mortality in both resuscitated and nonresuscitated cardiac arrest patients with shock after AMI.
Clinical Topics: Acute Coronary Syndromes, Arrhythmias and Clinical EP, Cardiovascular Care Team, Heart Failure and Cardiomyopathies, Prevention, Implantable Devices, SCD/Ventricular Arrhythmias, Atrial Fibrillation/Supraventricular Arrhythmias, Acute Heart Failure
Keywords: Acute Coronary Syndrome, Arrhythmias, Cardiac, Atrial Fibrillation, Blood Pressure, Coronary Occlusion, Critical Illness, Dobutamine, Heart Arrest, Heart Failure, Myocardial Infarction, Norepinephrine, Out-of-Hospital Cardiac Arrest, Resuscitation, Secondary Prevention, Shock, Shock, Cardiogenic, Troponin T
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