Abstract

Background In ST elevation myocardial infarction (STEMI) context, clinical studies have shown the deleterious effect of high aldosterone levels on ventricular arrhythmia (VA) occurrence as well as on cardiac mortality. However, the mechanisms of such harmful effects remain unknown. Methods and results We used an in vitro model of “border zone” using rabbit ventricle and standard microelectrode technique, completed by cellattached experiments of freshly isolated rabbit ventricular cardiomyocytes to assess the acute electrophysiological impact of aldosterone. During simulated ischemia, aldosterone (10 and 100 nmol/L) increased the APD dispersion at 90% between ischemic and normoxic zones (from 95±4 ms to 117±5 ms and 131±6 ms respectively, P Conclusions In this in vitro model of “border zone”, aldosterone had a deleterious impact via a rapid and MR-independent IK1 current activation. These conclusions may help to better understanding recent clinical studies results underlying the involvement of aldosterone in VA occurrence in STEMI context.

Full Text
Published version (Free)

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call