Should mechanical dyssynchrony be assessed in patients with implantable cardioverter-defibrillators?

Implantable cardioverter-defibrillator (ICD) therapy represents a cornerstone treatment in patients at risk for sudden cardiac death. Indications for ICD therapy have evolved considerably from survivors of sustained ventricular tachycardia or ventricular fibrillation to patients with depressed left ventricular (LV) systolic function (LV ejection fraction (LVEF) \ 30-40%), regardless of prior ventricular tachyarrhythmias. The merits of ICD therapy have been demonstrated in several large randomized trials. The first Multicenter Automatic Defibrillator Implantation Trial (MADIT) was one of the first studies evaluating the effectiveness of defibrillator therapy on the reduction of arrhythmic death in patients with depressed LV systolic function. The prospectively designed study evaluated whether prophylactic ICD implantation showed improved survival when compared to conventional medical therapy alone. Over a 5-year course, 196 patients with a prior myocardial infarction and depressed LV systolic function (LVEF B 35%) were enrolled and randomly assigned to ICD therapy (n = 95) or medical therapy alone (n = 101). During a mean follow-up of 27 months, all-cause mortality was significantly lower in patients with ICD therapy as compared to patients with conventional medication alone (16% vs 39%, P \ .05). The MADIT I trial has shown that the use of prophylactic ICD therapy was associated with a significantly improved survival as compared to patients on medical therapy (HR 0.46, 95% CI 0.26-0.82, P \ .01). Even though the efficacy of ICD therapy have been demonstrated in several landmark trials, the risk of cardiac death remained considerably high in patients who underwent ICD implantation. Several randomized trials have shown that a substantial number of ICD recipients died because of progressive heart failure. The recent randomized clinical Immediate Risk Stratification Improves Survival (IRIS) trial, which was designed to evaluate the efficacy of early ICD therapy (within 40 days of myocardial infarction) in patients with depressed LV systolic function, showed that the number of ICD recipients who died because of nonsudden cardiac death was considerably high; more than 15% of the ICD recipients died over a mean follow-up of 37 months. Additionally, post-hoc analysis of the Sudden Cardiac Death in Heart Failure Trial (SCDHeFT) revealed that progressive heart failure contributed significantly to all-cause mortality in patients with ICD treatment. Progressive heart failure was identified as the mode of death in 40% of the ICD recipients who died over a mean follow-up of 45.5 months. Cardiac resynchronization therapy (CRT) represents an effective treatment option in patients with moderateto-severe drug-refractory heart failure. Resynchronization therapy has been shown to improve the inherent electrical cardiac function by stimulating the ventricles in a synchronized manner. The improvement in cardiac performance, induced by synchronized pacing (which restores the intrinsic electrical conduction), has been consistently demonstrated in patients with moderate-to-severe heart failure (NYHA functional class III or IV) and ventricular conduction delay. The Comparison of Medical Therapy, Pacing and Defibrillation in Heart Failure (COMPANION) trial demonstrated that resynchronization therapy resulted in a 19% risk reduction of the primary endpoint (time to death from or hospitalization for any cause) as compared to optimal medical therapy alone in 1520 patients with NYHA functional class III or IV heart failure (HR 0.81, P = .014). Additionally, a recent post-hoc analysis of the COMPANION trial was published evaluating the effect of CRT on the number of hospitalizations during follow-up. In this study, resynchronization therapy was associated with a 44% reduction of heart failure From the Department of Cardiology, Leiden University Medical Center, Leiden, The Netherlands and The Interuniversity Cardiology Institute of the Netherlands, Utrecht, The Netherlands. Reprint requests: Jeroen J. Bax, MD, PhD, Department of Cardiology, Leiden University Medical Center, Albinusdreef 2, 2333 ZA Leiden, The Netherlands; [email protected]. J Nucl Cardiol 2010;17:354–8. 1071-3581/$34.00 Copyright 2010 The Author(s). This article is published with open access at Springerlink.com doi:10.1007/s12350-010-9222-6