Ventricular pacing with premature excitation for treatment of hypertensive-cardiac hypertrophy with cavity-obliteration

Hypertensive left ventricular hypertrophy with supranormal systolic ejection and distal cavity obliteration (HHCO) can result in debilitating exertional fatigue and dyspnea. Dual-chamber pacing with ventricular preactivation generates discoordinate contraction, which can limit cavity obliteration an...

Full description

Saved in:
Bibliographic Details
Published in:Circulation (New York, N.Y.) N.Y.), 1999-08, Vol.100 (8), p.807-812
Main Authors: KASS, D. A, CHEN, C.-H, TALBOT, M. W, ROCHITTE, C. E, LIMA, J. A. C, BERGER, R. D, CALKINS, H
Format: Article
Language:English
Subjects:
Arterial hypertension. Arterial hypotension
Biological and medical sciences
Blood and lymphatic vessels
Cardiac Output
Cardiac Pacing, Artificial - methods
Cardiology. Vascular system
Clinical manifestations. Epidemiology. Investigative techniques. Etiology
Cross-Over Studies
Double-Blind Method
Echocardiography, Doppler
Exercise Tolerance
Female
Follow-Up Studies
Humans
Hypertension - complications
Hypertrophy, Left Ventricular - physiopathology
Hypertrophy, Left Ventricular - therapy
Male
Medical sciences
Middle Aged
Quality of Life
Stroke Volume
Ventricular Function, Left
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:Hypertensive left ventricular hypertrophy with supranormal systolic ejection and distal cavity obliteration (HHCO) can result in debilitating exertional fatigue and dyspnea. Dual-chamber pacing with ventricular preactivation generates discoordinate contraction, which can limit cavity obliteration and thereby increase potential ejection reserve. Accordingly, we hypothesized that pacing may improve exercise tolerance long-term in this syndrome. Dual-chamber pacemakers were implanted in 9 patients with exertional dyspnea caused by HHCO. Intrinsic atrial rate was sensed, and ventricular preactivation was achieved by shortening the atrial-ventricular delay. Pacing was on or off for successive 3-month periods (randomized, double-blind, crossover design), followed by 6 additional pacing-on months. Metabolic exercise testing, quality-of-life assessment, and rest and dobutamine-stress echocardiographic/Doppler data were obtained. After 3 months of pacing-on, exercise duration rose from 324+/-133 to 588+/-238 s (mean+/-SD; P=0.001, with 7 of 9 patients improving >/=30%), and maximal oxygen consumption increased from 13.6+/-2.9 to 16.7+/-3.3 mL of O(2). min(-1). kg(-1) (P
ISSN:0009-7322
1524-4539
DOI:10.1161/01.CIR.100.8.807