Which Patients with Dilated Cardiomyopathy May Really Benefit from Dual-chamber Pacing?

Abstract

Congestive heart failure is one of the leading causes of morbidity and mortality in our country. In most patients, signs and symptoms of heart failure are the result of an enlarged, poorly contractile left ventricle. Therapy has been directed toward lowering pre-load, reducing after-load, improving contractility and interfering with the detrimental neurohumoral mechanisms activated in heart failure. In 1990, dual-chamber pacing was proposed as a therapeutic alternative for relief of symptoms in patients with dilated cardiomyopathy and severe heart failure who were unresponsive to the optimal medical therapy [1]. Initial reports have demonstrated a subjective abatement in symptoms as well as an objective increase in ejection fraction and cardiac output in patients undergoing dual-chamber pacing with short atrioventricular (AV) intervals [2, 3]. Subsequently these results were partially confirmed [4] or completely contradicted [5, 6], probably because the results were derived from observational studies with small, heterogeneous patient populations. In addition, it is unknown whether all subjects with left ventricular systolic disfunction respond to dual-chamber pacing or whether the beneficial effect is limited to a select subgroup of patients. The hemodynamic mechanisms of this “electrical” therapy may be resumed in three main physiopathologic statements:

• 1) The reduction of mitral regurgitation. Sequential pacing with short AV interval leads to an activated atrium during the expulsive stage of the left ventricle, thus determining the reduction of the ventriculoatrial gradient, the diastolic mitral regurgitation and the early mitral valve closure [1, 7].

• 2) A better utilization of the Frank-Starling mechanism obtained by restoring the atrioventricular synchronization [8].

• 3) A better sequence of the activation-relaxation induced by sequential pacing compared with that realized by the normal conduction pathways [3, 4, 9]. This mechanism may reduce the apical activation delay, that it’s very pronounced in dilated hearts, and, consequently, the wall stress.