AUTONOMIC INFLUENCES ON VENTRICULAR ARRHYTHMIAS IN MYOCARDIAL HYPERTROPHY AND HEART-FAILURE

Myocardial hypertrophy and heart failure provoke electrophysiological alterations at the cellular level that might be responsible for any type of arrhythmogenic mechanisms: abnormal automaticity, early and delayed afterdepolarizations, triggered activity, and reentry. With the exception of experimental ischemia, adequate in vivo models of arrhythmias specifically addressing myocardial hypertrophy and dysfunction are not readily available, and the clinical aspects of idiopathic tachyarrhythmias or arrhythmias in cardiomyopathies do not as yet have real equivalents. Whatever the basic electrophysiological mechanism, frequent characteristics are the rate dependence and the autonomic modulation. Autonomic changes are always present in cardiac disease, but their modalities differ in myocardial hypertrophy and heart failure. At variance from the former, the latter includes an elevated plasma level of catecholamines responsible for a downregulation of beta-adrenergic receptors. Accordingly, the heart rate variability diminishes in hypertrophy and even more in heart failure, and it may explain the behavior of arrhythmias. Rate dependence often characterizes the arrhythmia triggers, whereas the adrenergic dependence conditions the substrate responsiveness. These two components have a much greater chance to combine and produce tachyarrhythmias when reduced heart rate variations and a hyperadrenergic state coexist in myocardial dysfunction. The therapeutic implications are important, and beta-blocking therapy has a much greater chance to be effective and much less chance to be deleterious than Na+ channel-blocking antiarrhythmic drugs in this setting.