Author + information
- Jerold S Shinbane, MDA,*,
- Mark A Wood, MD, FACCB,
- D.Nick Jensen, DVMC,
- Kenneth A Ellenbogen, MD, FACCB,
- Adam P Fitzpatrick, MDD and
- Melvin M Scheinman, MD, FACCA
- ↵*Dr. Jerold S. Shinbane, Section of Electrophysiology, University of California San Francisco, 500 Parnassus Avenue, San Francisco, California 94143-1354.
The increasing prevalence of congestive heart failure has focused importance on the search for potentially reversible etiologies of cardiomyopathy. The concept that incessant or chronic tachycardias can lead to ventricular dysfunction that is reversible is supported by both animal models of chronic rapid pacing as well as human studies documenting improvement in ventricular function with tachycardia rate or rhythm control. Sustained rapid pacing in experimental animal models can produce severe biventricular systolic dysfunction. Hemodynamic changes occur as soon as 24 h after rapid pacing, with continued deterioration in ventricular function for up to 3 to 5 weeks, resulting in end-stage heart failure. The recovery from pacing-induced cardiomyopathy demonstrates that the myopathic process associated with rapid heart rates is largely reversible. Within 48 h after termination of pacing, hemodynamic variables approach control levels, and left ventricular ejection fraction shows significant recovery with subsequent normalization after 1 to 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 tachycardias, 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 with cardioversion to sinus rhythm, pharmacologic ventricular rate control and AV junction ablation and permanent ventricular pacing. The investigation 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 affected and optimal therapies.
(J Am Coll Cardiol 1997;29:709–15)
☆ All editorial decisions for this article, including selection of referees, were made by a Guest Editor. This policy applies to all articles with authors from the University of California San Francisco.
- Received November 4, 1996.
- Accepted December 17, 1996.