Evaluation of chamber and myocardial compliance in pressure overload hypertrophy.
The effect of pressure overload hypertrophy on isolated myocardial muscle preparations remains controversial. Moreover, the ultimate effect on the diastolic function of the left ventricle in the pressure overload states of man and the relative changes in chamber and myocardial stiffness remain incompletely studied. We review here the methods as well as results of dynamic diastolic stiffness analysis in 18 patients with valvular aortic stenosis and 5 normal subjects based upon the pressure-volume and circumferential stress-strain relations obtained by simultaneous left ventricular micromanometry and high-speed cineangiography. In addition, complementary analysis of dynamic diastolic stiffness findings in chronically instrumented animals, before and after the induction of hypertrophy, are reviewed. Increased diastolic intracavitary pressures during concentric hypertrophy were found to be attributable to both increased muscle mass as well as enhanced myocardial stiffness. However, both chamber and myocardial stiffness changes during hypertrophy were quite variable with some patients (and 2 of 6 dogs) showing no enhancement of stiffness parameters. In the chronically instrumented animals where dynamic, instantaneous stiffness changes and strain rates are more readily studied than in man, viscous (velocity dependent) effects were noted to be enhanced during hypertrophy. It is postulated that variable increases in diastolic stiffness during concentric hypertrophy in the intact heart results from varying degrees of myofiber architectural distortion and/or inconstant collagen content, and further correlative studies of morphology and mechanical function are needed.
D000818:Animals; D001024:Aortic Valve Stenosis / Q000503:physiopathology* / Q000601:surgery; D001794:Blood Pressure; D006328:Cardiac Catheterization; D002306:Cardiac Volume; D006332:Cardiomegaly / Q000503:physiopathology*; D003187:Compliance; D004285:Dogs; D006350:Heart Valve Prosthesis; D006439:Hemodynamics; D006801:Humans; D009200:Myocardial Contraction