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Brief sympathetic activation precedes the development of ventricular tachycardia and ventricular fibrillation in hibernating myocardium

2006; Elsevier BV; Volume: 39; Issue: 4 Linguagem: Inglês

10.1016/j.jelectrocard.2006.05.026

1532-8430

Matthew Pizzuto, Arturo Valverde, Brendan M. Heavey, Michael D. Banas, Nickolaos Michelakis, Gen Suzuki, James A. Fallavollita, John M. Canty,

Cardiovascular Effects of Exercise

Hibernating myocardium develops inhomogeneity in myocardial sympathetic innervation with spontaneous sudden cardiac death (SCD) because of ventricular fibrillation (VF). The triggers and prodromal arrhythmias initiating SCD in this substrate are unknown. Swine chronically instrumented with a proximal left anterior descending coronary artery stenosis underwent placement of an implantable telemetry unit capable of continuously recording digitized electrocardiogram and left ventricular pressure signals at 1 kHz in conscious unrestrained animals for periods of up to 5 months. Spontaneous SCD (n = 10) was initiated by a close-coupled premature ventricular contraction followed by ventricular tachycardia (VT) that degenerated into VF during brief sympathetic activation. Peak heart rates were similar in animals that developed SCD vs survivors (250 ± 12 vs 261 ± 6 bpm). Electrocardiogram evidence of ischemia preceding VT/VF occurred in only 1 animal, and there was no significant infarction. Spontaneous VT/VF in hibernating myocardium develops during brief sympathetic activation with only rare evidence of acute ischemia. This supports the notion that the regional remodeling accompanying hibernating myocardium may be a novel substrate for the development of SCD in chronic ischemic heart disease.