Tachycardia-Induced Cardiomyopathy: A Review of Animal Models and Clinical Studies

Abstract

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.

Diagnostic Approach and Treatment Strategy in Tachycardia‐induced Cardiomyopathy

“…Many rhythms and causes evolve into TIC, which include atrial fibrillation, 13,14 atrial flutter, 15 PSVT, 16 ventricular tachycardia, 17,18 fascicular tachycardia, 7 ventricular ectopy, 19 persistent rapid atrial or ventricular pacing, 20 and even extracardiac causes such as thyrotoxicosis and glucagonoma. 5,21 Heart failure and tachyarrhythmia have a strong association, especially for atrial fibrillation. In general, tachyarrhythmia is a secondary consequence following advanced heart failure.…”

Results of radiofrequency ablation in children with tachycardia-induced cardiomyopathy

“…The mean procedure, fluoroscopy and radiofrequency energy exposure durations were 104±39 minutes (45-195), 24±10 minutes and 191±90 seconds , respectively. Mean follow-up period was 4.8±3.2 years (1)(2)(3)(4)(5)(6)(7)(8)(9)(10). Mean values for pre-RFA left ventricular end-diastolic diameter (LVEDD) and left ventricular ejection fraction (LVEF) were 49.1±9.6 mm and 40.8±13.4% (23-57%), respectively.…”

“…Several experimental models have demonstrated significant reduction in systemic arterial pressure and cardiac output in animals with 24 hours of sustained rapid pacing (3,33). Despite many neurohumoral and cellular activation mechanisms have been postulated, the exact mechanisms that produce these changes are not well understood.…”

“…Tachycardia-induced cardiomyopathy, which results in a clinical feature of heart failure, is characterized by the development of ventricular systolic and/or diastolic dysfunction and ventricular dilatation in the presence of rapid and/or irregular ventricular rhythm, all of which is partially or completely resolve following normalization of heart rate (3)(4)(5). The reversibility of symptoms and cardiac functions in patients with TIC highlights the need for pursuit of an aggressive treatment approach.…”

Pharmacological interventions for clozapine-induced sinus tachycardia

“…Individuals with established psychosis have increased mortality rates compared to the general population due to cardiovascular disease, necessitating that cardiovascular risk factors, such as sinus tachycardia, be minimised in this population. An ongoing resting sinus tachycardia is also recognised as a risk factor for cardiomyopathy (Shinbane 1997), a serious adverse event associated with clozapine treatment. The need to minimise the risk of cardiac adverse events secondary to clozapine use and to reduce the risk of cardiovascular morbidity are pertinent reasons for the symptomatic treatment of sinus tachycardia in clozapinetreated patients.…”