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Cardiac Arrest in Pigs With 48 hours of Post‐Resuscitation Care Induced by 2 Methods of Myocardial Infarction: A Methodological Description

BACKGROUND: Systematic reviews have disclosed a lack of clinically relevant cardiac arrest animal models. The aim of this study was to develop a cardiac arrest model in pigs encompassing relevant cardiac arrest characteristics and clinically relevant post‐resuscitation care. METHODS AND RESULTS: We...

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Detalles Bibliográficos
Autores principales: Vammen, Lauge, Munch Johannsen, Cecilie, Magnussen, Andreas, Povlsen, Amalie, Riis Petersen, Søren, Azizi, Arezo, Løfgren, Bo, Andersen, Lars W., Granfeldt, Asger
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley and Sons Inc. 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9075364/
https://www.ncbi.nlm.nih.gov/pubmed/34854307
http://dx.doi.org/10.1161/JAHA.121.022679
Descripción
Sumario:BACKGROUND: Systematic reviews have disclosed a lack of clinically relevant cardiac arrest animal models. The aim of this study was to develop a cardiac arrest model in pigs encompassing relevant cardiac arrest characteristics and clinically relevant post‐resuscitation care. METHODS AND RESULTS: We used 2 methods of myocardial infarction in conjunction with cardiac arrest. One group (n=7) had a continuous coronary occlusion, while another group (n=11) underwent balloon‐deflation during arrest and resuscitation with re‐inflation after return of spontaneous circulation. A sham group was included (n=6). All groups underwent 48 hours of intensive care including 24 hours of targeted temperature management. Pigs underwent invasive hemodynamic monitoring. Left ventricular function was assessed by pressure‐volume measurements. The proportion of pigs with return of spontaneous circulation was 43% in the continuous infarction group and 64% in the deflation‐reinflation group. In the continuous infarction group 29% survived the entire protocol while 55% survived in the deflation‐reinflation group. Both cardiac arrest groups needed vasopressor and inotropic support and pressure‐volume measurements showed cardiac dysfunction. During rewarming, systemic vascular resistance decreased in both cardiac arrest groups. Median [25%;75%] troponin‐I 48 hours after return of spontaneous circulation, was 88 973 ng/L [53 124;99 740] in the continuous infarction group, 19 661 ng/L [10 871;23 209] in the deflation‐reinflation group, and 1973 ng/L [1117;1995] in the sham group. CONCLUSIONS: This article describes a cardiac arrest pig model with myocardial infarction, targeted temperature management, and clinically relevant post‐cardiac arrest care. We demonstrate 2 methods of inducing myocardial ischemia with cardiac arrest resulting in post‐cardiac arrest organ injury including cardiac dysfunction and cerebral injury.