Optimum Blood Pressure in Patients With Shock After Acute Myocardial Infarction and Cardiac Arrest

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  • Koen Ameloot, East Limburg Hospital, KU Leuven, Hasselt University
  • ,
  • Pekka Jakkula, University of Helsinki
  • ,
  • Johanna Hästbacka, University of Helsinki
  • ,
  • Matti Reinikainen, University of Eastern Finland
  • ,
  • Ville Pettilä, University of Helsinki
  • ,
  • Pekka Loisa, Päijät-Häme Central Hospital
  • ,
  • Marjaana Tiainen, University of Helsinki
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  • Stepani Bendel, University of Eastern Finland
  • ,
  • Thomas Birkelund
  • ,
  • Ann Belmans, KU Leuven
  • ,
  • Pieter Jan Palmers, East Limburg Hospital
  • ,
  • Eline Bogaerts, KU Leuven
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  • Robin Lemmens, KU Leuven, Flanders Institute for Biotechnology, KU Leuven-University of Leuven
  • ,
  • Cathy De Deyne, Hasselt University, East Limburg Hospital
  • ,
  • Bert Ferdinande, East Limburg Hospital
  • ,
  • Matthias Dupont, East Limburg Hospital
  • ,
  • Stefan Janssens, KU Leuven
  • ,
  • Joseph Dens, East Limburg Hospital, Hasselt University
  • ,
  • Markus B. Skrifvars, University of Helsinki

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.

OriginalsprogEngelsk
TidsskriftJournal of the American College of Cardiology
Vol/bind76
Nummer7
Sider (fra-til)812-824
Antal sider13
ISSN0735-1097
DOI
StatusUdgivet - 18 aug. 2020

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