TACHYCARDIA-INDUCED CARDIOMYOPATHY - A REVIEW OF ANIMAL-MODELS AND CLINICAL-STUDIES

The increasing prevalence of congestive heart failure has focused impo rtance on the search for potentially reversible etiologies of cardiomy opathy, The concept that incessant or chronic tachycardias can lead to ventricular dysfunction that is reversible is supported by both anima l models of chronic rapid pacing as well as human studies documenting improvement in ventricular function with tachycardia rate or rhythm co ntrol, Sustained rapid pacing in experimental animal models can produc e severe biventricular systolic dysfunction, Hemodynamic changes occur as soon as 24 h after rapid pacing, with continued deterioration in v entricular function for up to 3 to 5 weeks, resulting in end-stage hea rt failure, The recovery from pacing-induced cardiomyopathy demonstrat es that the myopathic process associated with rapid heart rates is lar gely reversible, Within 48 h after termination of pacing, hemodynamic variables approach control levels, and left ventricular ejection fract ion shows significant recovery with subsequent normalization after 1 t o 2 weeks, In humans, descriptions of reversal of cardiomyopathy with rate or rhythm control of incessant or chronic tachycardias have been reported with atrial tachycardias, accessory pathway reciprocating tac hycardias, atrioventricular (AV) node reentry and atrial fibrillation (AF) with rapid ventricular responses, Control of AF rapid ventricular responses has been demonstrated to improve ventricular dysfunction wi th cardioversion to sinus rhythm, pharmacologic ventricular rate contr ol and AV junction ablation and permanent ventricular pacing, The inve stigation of potential tachycardia-induced cardiomyopathy in patients with heart failure requires further prospective confirmation in larger numbers of patients, with study of mechanisms, patient groups affecte d and optimal therapies. (C) 1997 by the American College of Cardiolog y.