Physiologic Dual-Chamber Pacing with Short Atrioventricular Delay in Dilated Cardiomyopathy: Which Hemodynamic Effects and Clinical Results?

Abstract

Congestive heart failure is one of the leading causes of morbidity and mortality in the western world. Therapy has been directed toward lowering preload, reducing afterload, improving contractility, and interfering with the detrimental neurohumoral mechanism activated in heart failure. Despite considerable improvement in the pharmacologic treatment of severe left ventricular dysfunction, the problem of treating drug-resistant, end-stage heart failure remains. In 1990 Hochleitner (1) introduced the use of physiologic dual-chamber (DDD) pacing with a shortened atrioventricular (AV) delay as an alternative, new approach in the treatment of patients with dilated cardiomyopathy and severe heart failure unresponsive to optimal medical therapy. The author demonstrated that left ventricular function and clinical symptoms improved considerably after stimulation. These results have been only partially confirmed (2–4), probably because they were derived from observational studies in a small, nonhomogeneous group of patients. The beneficial effects of this “electrical” therapy were explained by different hemodynamic mechanisms. Some authors considered the reduction of ventriculoatrial regurgitation obtained by shortening of AV delay to be the determining factor; others pointed out the modification of preload or the optimization of mechanical AV synchrony.