Author + information
- Received September 9, 2019
- Revision received June 8, 2020
- Accepted June 12, 2020
- Published online August 10, 2020.
- Koen Ameloot, MDa,b,c,∗∗ (, )@kameloot3,
- Pekka Jakkula, MD, PhDd,∗,
- Johanna Hästbacka, MD, PhDd,
- Matti Reinikainen, MD, PhDe,
- Ville Pettilä, MD, PhDd,
- Pekka Loisa, MD, PhDf,
- Marjaana Tiainen, MD, PhDg,
- Stepani Bendel, MD, PhDh,
- Thomas Birkelund, MDi,
- Ann Belmans, PhDb,
- Pieter-Jan Palmers, MDa,
- Eline Bogaerts, MDb,
- Robin Lemmens, MD, PhDj,k,l,
- Cathy De Deyne, MD, PhDc,m,
- Bert Ferdinande, MDa,
- Matthias Dupont, MDa,
- Stefan Janssens, MD, PhDb,
- Joseph Dens, MD, PhDa,c,† and
- Markus B. Skrifvars, MD, PhDd,n,†
- aDepartment of Cardiology, Ziekenhuis Oost-Limburg, Genk, Belgium
- bDepartment of Cardiology, University Hospitals Leuven, Leuven, Belgium
- cFaculty of Medicine and Life Sciences, University Hasselt, Diepenbeek, Belgium
- dDepartment of Anaesthesiology, Intensive Care and Pain Medicine, University of Helsinki and Helsinki University Hospital, Helsinki, Finland
- eDepartment of Anaesthesiology and Intensive Care, University of Eastern Finland and Kuopio University Hospital, Kuopio, Finland
- fDepartment of Intensive Care, Päijät-Häme Central Hospital, Lahti, Finland
- gDepartment of Neurology, University of Helsinki and Helsinki University Hospital, Helsinki, Finland
- hDepartment of Intensive Care, Kuopio University Hospital, Kuopio, Finland
- iAarhus University Hospital, Aarhus, Denmark
- jDepartment of Neurology, University Hospitals Leuven, Leuven, Belgium
- kVIB, Center for Brain & Disease Research, Laboratory of Neurobiology, Leuven, Belgium
- lKU Leuven-University of Leuven, Department of Neurosciences, Experimental Neurology, and Leuven Brain Institute (LBI), Leuven, Belgium
- mDepartment of Anesthesiology and Critical Care Medicine, Ziekenhuis Oost-Limburg, Genk, Belgium
- nDepartment of Emergency Medicine and Services, University of Helsinki and Helsinki University Hospital, Helsinki, Finland
- ↵∗Address for correspondence:
Dr. Ameloot, Ziekenhuis Oost-Limburg, Schiepse Bos 6, 3600 Genk, Belgium.
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.
↵∗ Drs. Ameloot and Jakkula are joint first authors.
↵† Drs. Dens and Skrifvars are joint senior authors.
The authors have reported that they have no relationships relevant to the contents of this paper to disclose.
The authors attest they are in compliance with human studies committees and animal welfare regulations of the authors’ institutions and Food and Drug Administration guidelines, including patient consent where appropriate. For more information, visit the JACC author instructions page.
- Received September 9, 2019.
- Revision received June 8, 2020.
- Accepted June 12, 2020.
- 2020 American College of Cardiology Foundation
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