Left ventricular wall stress distribution in chronic pressure and volume overload: effect of normal and depressed contractility on regional stress-velocity relations

Summary Regional stress-velocity relations were determined in a first group of patients (n=15) with normal (five controls, five patients with aortic stenosis, and five patients with aortic insufficiency) and a second group of patients (n=10) with depressed contractility (five patients with aortic stenosis and five with aortic insufficiency). LV circumferential wall stress was calculated from high-fidelity pressure and frame-by-frame angiocardiographic data using the Wong thick-wall model. Regional wall stress and shortening velocity were calculated from the endo-to the epicardium, and from the equator to the apex at 35 points.Regional LV wall stress was in all patients lower at the epi- than the endocardium, and lower at the apex than the equator. Regional stress-velocity relations were downward shifted from the endo- to the epicardium and from the equator to the apex (family of curves) in both groups. At corresponding LV regions stress-velocity relations showed significantly smaller slopes and intercepts (downward depression) in group 2 than in group 1.Thus, wall stress distribution is inhomogeneous in the normal, as well as in the pressure and volume overloaded left ventricle. Regional differences in stress-velocity relations within groups (family of curves) are probably related to changes in preload rather than to changes in regional contractility. Downward depression of the regional stress-velocity relations in group 2 is caused by depressed myocardial contractility.Supported by the Swiss National Science Foundation