MECHANISM OF ACUTE MECHANICAL BENEFIT FROM VDD PACING IN HYPERTROPHIED HEART - SIMILARITY OF RESPONSES IN HYPERTROPHIC CARDIOMYOPATHY AND HYPERTENSIVE HEART-DISEASE

Background-Dual-chamber Facing can improve symptoms in hypertrophic ca rdiomyopathy (HCM), but the mechanism remains unclear. We hypothesized that pacing generates discoordinate contraction and a rightward shift of the end-systolic pressure-volume relation (ESPVR) and that benefit s from this mechanism do not depend on the presence of resting outflow pressure gradients or obstruction. Methods and Results-Eleven patient s with NYHA class lm symptoms, 5 with HCM, and 6 with hypertensive hyp ertrophy and cavity obliteration, were studied by invasive conductance catheter methods, No patient had coronary artery or primary valvular disease. Pressure-volume relations were recorded before and during VDD pacing by use of a short (75-millisecond) PR interval to achieve pree xcitation. Left ventricular cavity pressure was simultaneously recorde d at basal and apical sites, with pressure at the basal site used to g enerate the ESPVRs. VDD pacing shifted the ESPVR rightward, increasing end-systolic volume by 45% (range, 17% to 151%; P=0.002), Resting and provokable gradients declined by 20% (range, -56% to +3%) and 30% (ra nge, -65% to -12%), respectively (P<0.05). Preload declined by 3% to 1 0% because of the short PR interval. Preload-corrected contractility i ndexes and myocardial workload declined by approximate to 10% (P<0.001 ). Diastolic compliance and relaxation time were unchanged. Pacing mad e apical pressure-volume loops discoordinate, limiting cavity oblitera tion and reducing distal systolic pressures. Results in both patient g roups were similar. Conclusions-VDD pacing shifts the ESPVR rightward in HCM patients with cavity obliteration with or without. obstruction, increasing end-systolic volumes and reducing apical cavity compressio n and cardiac work, These effects likely contribute to reduced metabol ic demand and improved symptoms.