Advertisement
Research Article Free access | 10.1172/JCI106849
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: JCI | 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: JCI | 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: JCI | 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: JCI | PubMed | Google Scholar
Published March 1, 1972 - More info
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.