LEFT-VENTRICULAR DIASTOLIC FUNCTION IN HYPERTENSION AND ROLE OF PLASMA-GLUCOSE AND INSULIN - COMPARISON WITH DIABETIC HEART

Background Experimental production of glucose intolerance has been ass ociated with increased diastolic stiffness of the left ventricle. acco mpanied hv interstitial fibrosis. Because carbohydrate metabolism is a ltered in hypertension. wt undertook the present study to assess the r elation of diastolic dysfunction in hypertension to plasma glucose and insulin concentrations. The latter are also affected by obesity. To f acilitate this analysis, we studied moderately obese hypertensives. El ucidation of these relations was then sought in diabetic subjects. Met hods and Results Subjects undergoing catheterization for chest pain we re included in the study when significant coronary disease was not pre sent. In groups 1 (lean), 2 (obese), 3 (lean hypertensive), and 4 (obe se hypertensives), intraventricular pressures and volumes were determi ned. Fasting plasma glucose, insulin, hemoglobin(AIC), and glucose tol erance were assessed. Basal ejection fraction and end-systolic wall st ress were normal in the four groups. Chamber stiffness was significant ly elevated in the hypertensives and was higher in group 4 than in gro up 3 (P<.05). Diastolic dysfunction was correlated with fasting blood glucose (r=.69, P<.006) but not with plasma insulin or left ventricula r mass. Chamber stiffness was also increased in diabetics, with a larg er effect in the obese. Conclusions Hypertension is associated with in creased diastolic stiffness of the left ventricle, which is enhanced b y moderate obesity, and abnormal carbohydrate metabolism. Experimental ly and in humans, hypertension is associated with interstitial fibrosi s of mycardium, the presumed basis for the diastolic dysfunction. Cham ber stiffness in group 4 hypertensives was similar to that in the lean diabetics but less than that in the obese diabetics. Although the lat ter exhibited a correlation with plasma hemoglobin(AIC), the large ris e in stiffness suggests a potential role for growth factors in further alteration of myocardial composition.