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15 September 1993 | Volume 119 Issue 6 | Pages 466-473
Objective: To test, by studying the acute effects of drugs that influence active processes, the hypothesis that in humans with marked ventricular hypertrophy, reduced chamber compliance is primarily caused by passive structural changes.
Design: An uncontrolled (before-after) study.
Setting: University Medical Center.
Patients: Fourteen patients with ventricular hypertrophy (19 ± 4.5-mm diastolic-wall thickness) and normal resting systolic function were studied while they had invasive cardiac catheterization.
Intervention: Intravenous ß-blocker (esmolol) or calcium channel blocker (verapamil) or both.
Measurements: Left ventricular function was determined by pressure-volume relations. Volume was measured using conductance catheter, providing a continuous voltage signal proportional to chamber volume. Pressure was measured by micromanometer. Cardiac-specific assessment of change in chamber contractility and diastolic compliance due to each drug was determined.
Results: Both drugs lowered contractility by approximately 30% (P < 0.01). Esmolol slowed relaxation and reduced early peak filling rate, whereas verapamil delayed the time to peak filling (all P < 0.05). In contrast to the effects of both drugs on active contraction and early diastole, late-diastolic compliance was unaltered, and end-diastolic pressure-volume relations were almost identical.
Conclusion: Neither ß-receptor nor calcium channel blockade acutely alters left ventricular compliance despite substantial active effects manifest in systole and early diastole. This supports the notion that chamber compliance is principally determined by passive structural elements in the heart rather than by active processes.
Author and Article Information
From The Johns Hopkins Medical Institutions, Baltimore, Maryland, and Veterans General Hospital, Taipei, Taiwan, R.O.C.
ARTICLE
Diastolic Compliance of Hypertrophied Ventricle Is Not Acutely Altered by Pharmacologic Agents Influencing Active Processes
Requests for Reprints: David A. Kass, MD, Carnegie 538, Division of Cardiology, The Johns Hopkins Hospital, 600 North Wolfe Street, Baltimore, MD 21205.
Acknowledgments: The authors thank Drs. Gary Gerstenblith, Kenneth L. Baughman, and Thomas A. Traill for review of the manuscript and Karen Augustine for preparation of the manuscript.
Grant Support: National Institutes of Health grants HL-01820, HL-33243, and HL-01610, a grant from Academica Sinica, VGH, Taipei, Taiwan, and a Visiting Fellowship of the Internal Medicine Department, National Defense Medical Center, Taiwan, Republic of China, to Dr. Liu. Dr. Kass is an Established Investigator of the American Heart Association.
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