Glucose intolerance in nonischemic cardiac disease. Role of cardiac output and adrenergic function.

Abstract

To investigate hemodynamic and neurohumoral factors as a basis for glucose intolerance in cardiac patients without ischemic heart disease, intravenous glucose tolerance tests were performed on 70 patients aged 14 to 69 years. The mean glucose fractional disappearance rate (G k ) for 41 patients less than age 50 was 1.19 ± 0.07% fall in glucose/min, while in 19 normal subjects, it was 1.60 ± 0.14, P <0.01. The decreased G k was independent of age and lipid levels, and was directly related to a reduced plasma concentration of immunoreactive insulin. The glucose response to tolbutamide of 40 patients was similarly reduced and correlated with G k . Since enhanced adrenergic stimulation may be present in cardiac patients with resultant reduction of insulin secretion, the effects of alpha-and beta-adrenergic blockade were examined in two groups of cardiac patients. G k was unchanged after administration of phenoxybenzamine and propranolol. Since a reduced cardiac output correlated with diminished G k , the influence of sustained improvement after corrective cardiac surgery was evaluated in 13 patients. Postsurgical increments of resting cardiac output were usually associated with lower fasting insulin levels, enhanced clearance of administered glucose, and a more rapid rise of plasma insulin to higher peak levels, followed by a relatively rapid decline. Enhanced insulin response to tolbutamide after surgery in seven of these patients was also demonstrated. It is suggested that chronically reduced levels of cardiac output can result in reduced insulin secretion and in glucose intolerance and that these may be reversed with improved cardiac function.