Harmful effects of long-term right ventricular pacing.

摘要

Much evidence has emerged recently about the harmful effects of chronic right ventricular (RV) pacing (mostly apical) on left ventricular (LV) function1"13. The left ventricle (LV) normally contracts rapidly and synchronously with little variation in the onset of electrical and mechanical activation throughout the wall. The pathophysiologic consequences of RV pacing are similar to those of left bundle branch block (LBBB): asynchronous (and delayed) electrical and mechanical LV activation. Endocardial catheter mapping studies have unequivocally demonstrated that RV pacing mimics the endocardial activation patterns of LBBB. It is therefore not surprising that chronic RV pacing imposes basically the same chronic adverse effects as chronic LBBB on LV hemodynamics and function. Long-term RV pacing like chronic LBBB produces structural changes resulting in chronic systolic and diastolic LV dysfunction that contribute to reduced LV pumping function on a long-term basis. The changes include paradoxical septal wall motion, delayed LV lateral wall contraction, reduced LV pressure, mitral regurgitation, increased left atrial diameters, reduced diastolic filling times, and distorted LV geometry. These abnormalities correlate with those documented in experimental animals subjected to long-term RV pacing such as adverse cellular changes with myofibrillar disarray, asymmetric myocardial hypertrophy and LV dilatation as well as biochemical abnormalities.