Ventricular Resynchronization

Abstract

Cardiac resynchronization therapy (CRT) is a new therapy that improves hemodynamics and symptoms in patients with advanced heart failure (HF).1 In HF, ventricular dyssynchrony results most commonly from left bundle-branch block (LBBB). Resynchronization pacing can influence hemodynamics by improving mechanical synchrony both between and within the right and left ventricles, as well as by optimizing atrioventricular synchrony. Biventricular pacing devices, first implanted in 1994, were approved by the U.S. Food and Drug Administration in 2001. Currently available devices may also have defibrillation capacity. Much of the information regarding the clinical benefits of CRT derives from clinical trials2–4 (Table) that together demonstrate that CRT improves symptoms and exercise tolerance in medically treated patients with persistent, moderate to severe symptoms of HF; poor left ventricular (LV) function; and intraventricular conduction delay. The relatively few scenarios in which this modality has been studied make it possible to argue both for broadening and restricting the use of these devices until further trials are conducted. Here we review the proposed mechanisms of action, potential applicability, and cost impact of CRT of appropriately selected patients. View this table: Published Controlled Studies With Permanent Cardiac Multisite Pacing Both atrioventricular and intraventricular conduction delays further impair LV function in patients with underlying cardiomyopathies. Notably, LBBB (and also possibly right bundle-branch block) changes LV contraction patterns, leading to regions of early and late contraction.5,6 This, in turn, impairs systolic function, reduces cardiac output, and increases end-systolic volume and wall stress.7 In addition to having mechanical consequences, there is preliminary evidence that LBBB, estimated to affect 30% to 50% of patients with advanced HF,7,8 confers an independent risk for mortality.9 Currently, it remains unknown whether ventricular dyssynchrony is fundamental to the pathogenesis of dysfunctional hearts. Early experimental studies demonstrate regional molecular changes in discoordinately contracting myocardium, a …