Mechanism of acute mechanical benefit from VDD pacing in hypertrophied heart: similarity of responses in hypertrophic cardiomyopathy and hypertensive heart disease.
BACKGROUND
Dual-chamber pacing can improve symptoms in hypertrophic cardiomyopathy (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 benefits from this mechanism do not depend on the presence of resting outflow pressure gradients or obstruction.


RESULTS
Eleven patients with NYHA class III symptoms, 5 with HCM, and 6 with hypertensive hypertrophy 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 preexcitation. Left ventricular cavity pressure was simultaneously recorded at basal and apical sites, with pressure at the basal site used to generate 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% (range, -65% to -12%), respectively (P<0.05). Preload declined by 3% to 10% because of the short PR interval. Preload-corrected contractility indexes and myocardial workload declined by approximately 10% (P<0.001). Diastolic compliance and relaxation time were unchanged. Pacing made apical pressure-volume loops discoordinate, limiting cavity obliteration and reducing distal systolic pressures. Results in both patient groups 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 compression and cardiac work. These effects likely contribute to reduced metabolic demand and improved symptoms.
Pak
P H
PH
Department of Medicine, Johns Hopkins Medical Institutions, Baltimore, MD, USA. peterpak@welchlink.welch.jhu.edu
Maughan
W L
WL
Baughman
K L
KL
Kieval
R S
RS
Kass
D A
DA
D000328:Adult; D001794:Blood Pressure / Q000502:physiology; D002304:Cardiac Pacing, Artificial / Q000379:methods*; D006332:Cardiomegaly / Q000503:physiopathology* / Q000628:therapy*; D002312:Cardiomyopathy, Hypertrophic / Q000503:physiopathology / Q000628:therapy; D003971:Diastole; D005260:Female; D006321:Heart / Q000503:physiopathology; D006801:Humans; D006973:Hypertension / Q000503:physiopathology / Q000628:therapy; D008297:Male; D008875:Middle Aged; D009200:Myocardial Contraction / Q000502:physiology; D013318:Stroke Volume / Q000502:physiology; D013599:Systole