Abstract

In the experimental animal, acute ischemia by interruption of coronary blood supply is accompanied by a steepening of the slope of the left ventricular pressure-volume and pressure-segment length relations. This increase in chamber stiffness is associated with an increase in myocardial stiffness assessed from the slope of the diastolic stress-strain relation. Supply-type ischemia in humans brought about by balloon inflation during coronary angioplasty leads to an upward shift of the pressure-length relation of the ischemic and the adjacent segment combined with a steepening of the slope. In demand ischemia produced by rapid pacing in patients with coronary artery disease, an increased radial stiffness modulus at any level of radial stress was present when compared with that during the resting state. These alterations of the stress-strain relation suggest that the physical properties of the myocardium change during both supply and demand ischemia. The increased diastolic myocardial stiffness appears to result, at least in part, from increased residual interaction between actin and myosin filaments.

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