[Arrhythmia-induced dilated cardiomyopathies]

Abstract

Arrhythmic cardiomyopathies are due to ventricular dysfunction following prolonged or chronic tachycardia; the clinical pictures one of congestive heart failure, which is totally reversible after the treatment of tachycardia and the restoration of sinus rhythm. Since Whipple's first description of this model of heart failure, several teams have shown that ventricular or atrial pacing at rates exceeding 220 beats per minute produces a profound and largely reversible depression of ventricular function, and a constellation of neuroendocrine abnormalities and metabolic, electrophysiological and anatomic alterations of the myocardium. The associated heart failure generally starts to improve within days of achieving ventricular rhythm control, but clinical recovery may take several weeks or months. All forms of chronic tachycardia may induce heart failure, but the onset of cardiomyopathy depends more on the heart rate and the duration of the arrhythmia than on its type. The pathophysiological mechanisms are multiple and complex, and include abnormalities in the structure and function of cardiomyocytes and disturbances in excitation-contraction coupling. Treatment consists of restoring and maintaining sinus rhythm, or at least of controlling the ventricular rate. Because of its curative effect, selective radiofrequency ablation is the treatment of choice when the arrhythmogenic substrate is localized. Control of the ventricular rate by radiofrequency modification of atrioventricular conduction is the treatment of choice for chronic atrial fibrillation.