Veno-arterial extracorporeal membrane oxygenation reduces myocardial and mitochondrial damage in acute myocardial infarction.

Abstract

Myocardial infarction (MI) is a common cardiovascular disease with a high fatality rate once accompanied by cardiogenic shock. The efficacy of extracorporeal membrane oxygenation (ECMO) in treating myocardial infarction is controversial. MI was induced by ligating the left anterior descending artery in adult male rats. Groups were defined as follows: MI group, reperfusion for 90 min after 30 min of left anterior descending artery (LAD) occlusion; MI + ECMO group, reperfusion and ECMO were performed for 90 min immediately after 30 min of LAD occlusion; prolonged MI + ECMO group, ECMO was used immediately after 30 minutes of occlusion with persistent occlusion of the LAD for an additional 30 minutes, followed by 90 minutes of reperfusion. The myocardial infarct size and mitochondrial morphology and function data were collected and compared of each group. The ECMO groups had a smaller myocardial infarct size and larger percentage ejection fraction. Compared with the prolonged MI + ECMO group, the immediate reperfusion group had a lower percentage of infarct size (63.28% versus 17.97% versus 31.22%, MI versus MI + ECMO versus prolonged MI + ECMO). Mitochondria isolated from the ischemic zone showed an intact mitochondrial structure, including fewer voids and broken crists, and preserved activity of mitochondrial complex II and complex IV in ECMO groups. ECMO support in myocardial infarction can reduce myocardial injury despite delayed coronary reperfusion.