Koen Ameloot1, Pekka Jakkula2, Johanna Hästbacka2, Matti Reinikainen3, Ville Pettilä2, Pekka Loisa4, Marjaana Tiainen5, Stepani Bendel6, Thomas Birkelund7, Ann Belmans8, Pieter-Jan Palmers9, Eline Bogaerts8, Robin Lemmens10, Cathy De Deyne11, Bert Ferdinande9, Matthias Dupont9, Stefan Janssens8, Joseph Dens12, Markus B Skrifvars13. 1. Department of Cardiology, Ziekenhuis Oost-Limburg, Genk, Belgium; Department of Cardiology, University Hospitals Leuven, Leuven, Belgium; Faculty of Medicine and Life Sciences, University Hasselt, Diepenbeek, Belgium. Electronic address: Koen.ameloot@zol.be. 2. Department of Anaesthesiology, Intensive Care and Pain Medicine, University of Helsinki and Helsinki University Hospital, Helsinki, Finland. 3. Department of Anaesthesiology and Intensive Care, University of Eastern Finland and Kuopio University Hospital, Kuopio, Finland. 4. Department of Intensive Care, Päijät-Häme Central Hospital, Lahti, Finland. 5. Department of Neurology, University of Helsinki and Helsinki University Hospital, Helsinki, Finland. 6. Department of Intensive Care, Kuopio University Hospital, Kuopio, Finland. 7. Aarhus University Hospital, Aarhus, Denmark. 8. Department of Cardiology, University Hospitals Leuven, Leuven, Belgium. 9. Department of Cardiology, Ziekenhuis Oost-Limburg, Genk, Belgium. 10. Department of Neurology, University Hospitals Leuven, Leuven, Belgium; VIB, Center for Brain & Disease Research, Laboratory of Neurobiology, Leuven, Belgium; KU Leuven-University of Leuven, Department of Neurosciences, Experimental Neurology, and Leuven Brain Institute (LBI), Leuven, Belgium. 11. Faculty of Medicine and Life Sciences, University Hasselt, Diepenbeek, Belgium; Department of Anesthesiology and Critical Care Medicine, Ziekenhuis Oost-Limburg, Genk, Belgium. 12. Department of Cardiology, Ziekenhuis Oost-Limburg, Genk, Belgium; Faculty of Medicine and Life Sciences, University Hasselt, Diepenbeek, Belgium. 13. Department of Anaesthesiology, Intensive Care and Pain Medicine, University of Helsinki and Helsinki University Hospital, Helsinki, Finland; Department of Emergency Medicine and Services, University of Helsinki and Helsinki University Hospital, Helsinki, Finland.
Abstract
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.
RCT Entities:
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 arrestpatients with shock after AMI randomized in the Neuroprotect (Neuroprotective Goal Directed Hemodynamic Optimization in Post-cardiac ArrestPatients; 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 arrestpatients 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.
Authors: Travis W Murphy; Scott A Cohen; Charles W Hwang; K Leslie Avery; Meenakshi P Balakrishnan; Ramani Balu; Muhammad Abdul Baker Chowdhury; David B Crabb; Yasmeen Elmelige; Carolina B Maciel; Sarah S Gul; Francis Han; Torben K Becker Journal: J Am Coll Emerg Physicians Open Date: 2022-07-14
Authors: Ole Broch; Lars Hummitzsch; Jochen Renner; Patrick Meybohm; Martin Albrecht; Peter Rosenthal; Ann-Christine Rosenthal; Markus Steinfath; Berthold Bein; Matthias Gruenewald Journal: Sci Rep Date: 2021-03-05 Impact factor: 4.379
Authors: Johannes Grand; Christian Hassager; Henrik Schmidt; Jacob E Møller; Simon Mølstrøm; Benjamin Nyholm; Jesper Kjaergaard Journal: Resusc Plus Date: 2021-12-10