Left Ventricular Diastolic Function in Hypertension and Role of Plasma Glucose and Insulin

BACKGROUND: Experimental production of glucose intolerance has been associated with increased diastolic stiffness of the left ventricle, accompanied by interstitial fibrosis. Because carbohydrate metabolism is altered in hypertension, we undertook the present study to assess the relation of diastolic dysfunction in hypertension to plasma glucose and insulin concentrations. The latter are also affected by obesity. To facilitate this analysis, we studied moderately obese hypertensives. Elucidation of these relations was then sought in diabetic subjects. METHODS AND RESULTS: Subjects undergoing catheterization for chest pain were included in the study when significant coronary disease was not present. In groups 1 (lean), 2 (obese), 3 (lean hypertensive), and 4 (obese hypertensives), intraventricular pressures and volumes were determined. Fasting plasma glucose, insulin, hemoglobinAIC, and glucose tolerance were assessed. Basal ejection fraction and end-systolic wall stress were normal in the four groups. Chamber stiffness was significantly elevated in the hypertensives and was higher in group 4 than in group 3 (P < .05). Diastolic dysfunction was correlated with fasting blood glucose (r = .69, P < .006) but not with plasma insulin or left ventricular mass. Chamber stiffness was also increased in diabetics, with a larger effect in the obese. CONCLUSIONS: Hypertension is associated with increased diastolic stiffness of the left ventricle, which is enhanced by moderate obesity, and abnormal carbohydrate metabolism. Experimentally and in humans, hypertension is associated with interstitial fibrosis of mycardium, the presumed basis for the diastolic dysfunction. Chamber stiffness in group 4 hypertensives was similar to that in the lean diabetics but less than that in the obese diabetics. Although the latter exhibited a correlation with plasma hemoglobinAIC, the large rise in stiffness suggests a potential role for growth factors in further alteration of myocardial composition.