Chamber compliance and myocardial stiffness in left ventricular hypertrophy.

Abstract

Left ventricular chamber stiffness is determined by the level of operating pressure and the diastolic pressurevolume relation. This relation is curvilinear and the slope of a tangent to the pressure-volume curve (operative chamber stiffness) increases as the chamber progressively fills. Such preload dependent changes in compliance occur during any acute alteration in ventricular volume. At a given diastolic pressure, operative chamber stiffness is determined by the relative values for ventricular volume and muscle mass and by the stiffness of a unit of myocardium. Thus, there may be a leftward shift of the diastolic pressure-volume curve (increase in the modulus of chamber stiffness) as a consequence of ventricular hypertrophy or an increase in the stiffness of heart muscle itself (increase in the modulus of muscle stiffness). To assess the stiffness of heart muscle, the myocardial stressstrain and stiffness-stress relations must be defined. Although some controversy exists with regard to the stiffness of hypertrophied myocardium, clinical studies suggest that chamber stiffness and myocardial stiffness can be normal or increased in the presence of left ventricular hypertrophy. These studies also suggest that increased myocardial stiffness develops in the presence of increased interstitial fibrosis. Moreover, isolated cardiac muscle experiments indicate that the increase in myocardial stiffness can be prevented when the connective tissue response is prevented. Quantitative measures of left ventricular chamber and myocardial stiffness contribute to the understanding of the pathophysiology of cardiac dyspnea and provide insight into functional and structural defects of hypertrophied myocardium.