Why the study?
Endothelin alters central sympathetic responses, but the resultant effects on arrhythmogenesis are unknown.
Does intracerebroventricular endothelin receptor-A blockade reduce ventricular tachyarrhythmias in rats with acute myocardial infarction?
Does intracerebroventricular endothelin receptor-A blockade reduce ventricular tachyarrhythmias in rats with acute myocardial infarction?
Central endothelin receptor-A blockade significantly reduces the incidence and duration of phase-II ventricular tachyarrhythmias during acute myocardial infarction in a rat model.
Central ET-A blockade effects on post-MI arrhythmias remain preclinical; leaves open human relevance and need for translational studies.
Endothelin alters central sympathetic responses, but the resultant effects on arrhythmogenesis are unknown. We examined ventricular tachyarrhythmias after endothelin receptor-A blockade in the brain of Wistar rats with acute myocardial infarction. For this aim, BQ-123 (n=6) or phosphate-buffered saline (n=6) were injected intracerebroventricularly. After 10 min, the left coronary artery was ligated, followed by implantation of telemetry transmitters. Electrocardiography and voluntary activity (as a surrogate of acute left ventricular failure) were continuously monitored for 24 h. Infarct-size was similar in the two groups. There were fewer episodes of ventricular tachyarrhythmias of shorter average duration in treated rats, leading to markedly shorter total duration (12.3+/-8.9 s), when compared to controls (546.2+/-130.3 s). Voluntary activity increased in treated rats during the last hours of recording, but bradyarrhythmic episodes were comparable between the two groups. Endothelin receptor-A blockade in the brain of rats decreases the incidence of ventricular tachyarrhythmias post-ligation, without affecting bradyarrhythmic episodes. These findings call for further research on the pathophysiologic role of endothelin during acute myocardial infarction.
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Lekkas et al. (2019) studied this question.
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