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Diastolic Compliance of Hypertrophied Ventricle Is Not Acutely Altered by Pharmacologic Agents Influencing Active Processes

David A. Kass, MD; Matthew R. Wolff, MD; Chih-Tai Ting, MD; Chun-Pen Liu, MD; Mau-Song Chang, MD; Willie Lawrence, MD; and W. Lowell Maughan, MD
[+] Article and Author Information

From The Johns Hopkins Medical Institutions, Baltimore, Maryland, and Veterans General Hospital, Taipei, Taiwan, R.O.C. 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.


Copyright 2004 by the American College of Physicians


Ann Intern Med. 1993;119(6):466-473. doi:10.7326/0003-4819-119-6-199309150-00004
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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 -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 -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.

Figures

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Figure 1.
Measurement of systolic and diastolic chamber properties from pressure-volume relations loops and relations in humans.

Left ventricular pressure-volume data are recorded continuously by conductance catheter during gradual mechanical reduction of inferior vena cava inflow. Several cycles are combined to generate systolic (upper left-hand corners) and diastolic (lower right-hand corners) pressure-volume boundaries. The systolic boundary is fit by linear regression and its slope (end-systolic elastance) provides a relatively load-insensitive measure of chamber contractility. This slope has units of millimeters of mercury per milliliter and was 3.02 mm Hg/mL in this patient. The lower boundary, defined by points taken from late diastole, is also fit by linear regression. The slope of the diastolic boundary is also elastance; however, more commonly the inverse slope (compliance) is reported (Delta V/Delta P). This slope was 2.29 mL/mm Hg for this patient.

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Figure 2.
Pressure-volume systolic and diastolic relations before and after administration of esmolol and of verapamil.Figure 1dashed line

Data are from one patient and were generated in a similar fashion to those shown in . Baseline systolic and diastolic pressure-volume relations are reproduced in each corresponding lower panel (solid lines). The left-hand panels show baseline and esmolol data, and the right-hand panels show second baseline and verapamil data. Both drugs lowered contractility, as shown by the reduced slope of the end-systolic pressure-volume relation ( ). In contrast, they had minimal effect on diastolic compliance, indicated by the similar slope of the diastolic pressure-volume relation.

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Figure 3.
Minimal influence of esmolol or verapamil on end-diastolic pressure-volume relation.12Table 3

End-diastolic pressure-volume data before and after esmolol (upper panels, left, middle, and right) and verapamil (lower panels, left, middle, and right) are shown for three typical patients. The individual points were derived from the latter 30% of chamber filling, using the multiple pressure-volume loops measured during transient preload reduction (as shown in Figures and ). These diastolic data reflect passive chamber properties and were not altered by either drug. Group compliance data are provided in . solid diamonds = baseline 1; open diamonds = esmolol; solid triangles = baseline 2; open triangles = verapamil.

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