Physiology of cardiac resynchronization

Abstract

Dyssynchronous ventricular contraction, often associated with delayed electrical activation, contributes to worsened clinical status in patients with chronic dilated heart failure. There are three levels of impaired electromechanical synchrony that can be recognized and potentially improved with pacing methods. Prolonged atrioventricular (AV) delay can promote presystolic mitral regurgitation and impaired left ventricular (LV) filling. Interventricular conduction delay with right ventricular (RV) activation preceding LV activation often occurs in the setting of left bundle branch block or RV apical pacing, and can result in impeded LV filling and ejection. Activation delays within the LV itself (intraventricular dyssynchrony) can cause decreased efficiency of contraction, increased mitral regurgitation, and abnormal ventricular remodeling. Cardiac resynchronization therapy (CRT) can improve ventricular performance in two thirds of patients selected based on QRS duration alone. Improved understanding of the pathophysiology of cardiac dyssynchrony will aid in patient selection and in assessment and optimization of response to CRT.