Abstract
The myocardial cell hypertrophies as an adaptive response to a mechanical overload. However, cardiac hypertrophy induced by chronic pressure overload results in a variety of structural and functional changes. These include alterations in morphology, metabolism, hemodynamics, contraction, and electrophysiology. Despite these adaptations, or because of these alterations, patients with left ventricular hypertrophy have high risk of cardiovascular morbidity and mortality. Electrophysiological abnormalities may be partly responsible for the increased mortality rate with left ventricular hypertrophy. Several recent clinical studies have demonstrated an increased incidence of ventricular arrhythmias and sudden cardiac death presumably due to ventricular fibrillation or tachycardia in association with left ventricular hypertrophy (1–3). In addition, superimposition of ischemia enhances arrhythmogenesis in hypertrophied hearts. Experimentally, it has been demonstrated that the incidence of ischemia- and reperfusion-induced ventricular fibrillation and sudden death are significantly higher in rats and dogs with left ventricular hypertrophy (4–6). However, the precise mechanisms of electrophysiological abnormalities and enhanced arrhythmogenesis in cardiac hypertrophy remain unsettled.