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Research Article Free access | 10.1172/JCI106849

Early Increase in Left Ventricular Compliance after Myocardial Infarction

James S. Forrester, George Diamond, William W. Parmley, and H. J. C. Swan

Department of Cardiology, Cedars-Sinai Medical Center, Los Angeles, California 90029

Department of Medicine, University of California, Los Angeles, California 90024

Find articles by Forrester, J. in: PubMed | Google Scholar

Department of Cardiology, Cedars-Sinai Medical Center, Los Angeles, California 90029

Department of Medicine, University of California, Los Angeles, California 90024

Find articles by Diamond, G. in: PubMed | Google Scholar

Department of Cardiology, Cedars-Sinai Medical Center, Los Angeles, California 90029

Department of Medicine, University of California, Los Angeles, California 90024

Find articles by Parmley, W. in: PubMed | Google Scholar

Department of Cardiology, Cedars-Sinai Medical Center, Los Angeles, California 90029

Department of Medicine, University of California, Los Angeles, California 90024

Find articles by Swan, H. in: PubMed | Google Scholar

Published March 1, 1972 - More info

Published in Volume 51, Issue 3 on March 1, 1972
J Clin Invest. 1972;51(3):598–603. https://doi.org/10.1172/JCI106849.
© 1972 The American Society for Clinical Investigation
Published March 1, 1972 - Version history
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Abstract

The left ventricular (LV) pressure-volume (P-V) relationship is a resultant of several determinants, including initial ventricular volume, geometry, and wall stiffness. A quantitative index of one of these determinants, LV wall stiffness, was developed from a mathematical analysis of the isolated P-V relationship. Since this relationship was exponential, stiffness (dP/dV) could be expressed by the equation dP/dV = aP + b, where a and b are constants. The a constant, termed the passive elastic modulus, was independent of both pressure and volume, was modified only slightly by changes in geometry, and thus was primarily affected by changes in wall stiffness. LV wall stiffness was assessed by determination of the passive elastic modulus in eight normal canine hearts and in five hearts 1 hr after acute myocardial infarction. The value of the passive elastic modulus for the normal canine LV was found to be 0.099±0.006 cc-1. In the five infarcted hearts there was a modest, but statistically insignificant, shift of the P-V curves from control, such that for the same pressure the infarcted hearts contained greater volume. However, the passive elastic modulus decreased 41% to 0.057±0.006 cc-1 (P < 0.001). Thus, although LV wall stiffness may increase later in the course of myocardial infarction, it is concluded that it was significantly decreased 1 hr after infarction. Calculation of the passive elastic modulus provided a sensitive means of detecting such changes, whereas P-V curves alone were generally insensitive.

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