Pacemaker therapy in congestive heart failure

The armamentarium of pharmacologic agents used in the treatment of congestive heart failure (CHF) continues to expand and provide symptomatic improvement to many such patients. It is clear that short-term responses to drug therapy do not always predict long-term effect; hemodynamic improvement does not always translate to symptomatic improvement and an increase in exercise performance does not always predict a better prognosis. Most patients with CHF have severe left ventricular (LV) dysfunction with a decrease in ejection fraction (EF) and dilatation at both end-diastole and end-systole; isolated diastolic dysfunction is uncommon. Further, improvement in symptoms with drug therapy often occurs with no or only modest improvement in EF.im3 The Frank-Starling curve depicting the LV function in patients with CHF is shifted to the right and is often flat. Hence, considerable changes in end-diastolic volume may occur with only modest changes in stroke volume. Thus, the left ventricle appears to have exhausted the preload reserve and is very sensitive to changes in afterload. Decrease of the inappropriately high afterload in CHF has been the mainstay of vasodilator therapy because of the inverse relation between afterload and systolic performance. It is possible that symptomatic improvement with vasodilator therapy in part is also due to a decrease in secondary mitral regurgitation because of decrease in LV size and thus, in the size of the mitral valve annu~us.~,~ The decrease in mitral regurgitation improves the forward cardiac output, although the EF may not change. In studies using rapid atria1 pacing, we and others have observed a decrease in LV size that is explained by the decrease in diastolic filling period.6-8 In normal subjects, the decrease in end-diastolic volume is accompanied by a decrease in stroke volume, but no change in cardiac output because of the proportional increase in heart rate. The decrease in end-diastolic volume is accompanied by a decrease in end-diastolic pressure. In patients with coronary artery disease, pacing-induced ischemia may, however, cause increased LV stiffness and an increase in end-diastolic pressure. In 1986, we hypothesized that pacing may be beneficial in some patients with CHF for 2 reasons.’ In pa