ABSTRACT

Heart failure combines multiple abnormalities, including molecular and structural cardiac remodeling, neurohormonal stimulation, excessive loading, and vascular insufficiency – all conspiring to limit cardiac pump performance. Typically, heart failure therapy has relied on moderating fluid balance, and blocking both the rennin-angiotensin-aldosterone and b-adrenergic systems (see recent reviews1,2). However, mechanical factors also play a role in the pathophysiology of heart failure, particularly those affecting the intrachamber synchrony of contraction and atrial and ventricular timing intervals. Atrial activation that occurs too close or well prior to ventricular activation results in suboptimal cardiac filling and a net fall in ejection.3-5

Initial clinical trials with pacing therapy in heart failure focused on this effect, and tried to optimize atrioventricular (AV) delay time using right ventricular (RV) single-site pacing.6