Optimum Blood Pressure in Patients With Shock After Acute Myocardial Infarction and Cardiac Arrest.
Arterial Pressure
/ drug effects
Atrial Fibrillation
/ etiology
Blood Pressure Determination
/ methods
Cardiotonic Agents
/ administration & dosage
Coronary Angiography
/ methods
Female
Heart Arrest
/ complications
Hemodynamics
/ drug effects
Humans
Male
Middle Aged
Myocardial Infarction
/ blood
Outcome Assessment, Health Care
Shock
/ complications
Survivors
Troponin T
/ analysis
Vasoconstrictor Agents
/ administration & dosage
acute myocardial infarction
cardiac arrest
cardiogenic shock
Journal
Journal of the American College of Cardiology
ISSN: 1558-3597
Titre abrégé: J Am Coll Cardiol
Pays: United States
ID NLM: 8301365
Informations de publication
Date de publication:
18 08 2020
18 08 2020
Historique:
received:
09
09
2019
revised:
08
06
2020
accepted:
12
06
2020
entrez:
15
8
2020
pubmed:
15
8
2020
medline:
23
1
2021
Statut:
ppublish
Résumé
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. This study aimed to determine the optimal mean arterial pressure (MAP) in patients with AMI and shock after cardiac arrest. 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. 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). 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.
Sections du résumé
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.
Identifiants
pubmed: 32792079
pii: S0735-1097(20)35740-5
doi: 10.1016/j.jacc.2020.06.043
pii:
doi:
Substances chimiques
Cardiotonic Agents
0
Troponin T
0
Vasoconstrictor Agents
0
Banques de données
ClinicalTrials.gov
['NCT02541591', 'NCT02698917']
Types de publication
Journal Article
Randomized Controlled Trial
Langues
eng
Sous-ensembles de citation
IM
Pagination
812-824Commentaires et corrections
Type : CommentIn
Informations de copyright
Copyright © 2020 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.