Key result
Patients with compensated nonischemic cardiovascular disease exhibited significantly lower glucose tolerance and reduced insulin response compared to normal subjects.
Why the study?
Does compensated nonischemic cardiovascular disease alter glucose tolerance and insulin response compared to normal subjects?
Observational (n=13)
Does compensated nonischemic cardiovascular disease alter glucose tolerance and insulin response compared to normal subjects?
Glucose intolerance in compensated nonischemic cardiac disease appears to be an acquired metabolic disorder likely driven by enhanced sympathetic stimulation.
May warrant glucose monitoring in compensated nonischemic CVD; leaves open sympathetic causality pending prospective studies.
Intravenous infusion of glucose in patients with compensated nonischemic cardiovascular disease has demonstrated that the glucose disappearance slope, G K , is significantly lower than in normal subjects. Immunoassay of plasma insulin in 13 of these cardiac patients showed a reduced insulin response to hyperglycemia in the majority. All had a delayed decline of plasma insulin values. Plasma free fatty acids (FFA) were significantly elevated in the fasting state but were not significantly correlated with the reduced G K . During the acute hyperglycemia, plasma free fatty acid, potassium, and inorganic phosphate concentrations declined as in the normal subjects. Although cardiac index was reduced in most patients, a linear correlation with G K was not obtained. To examine the possible role of enhanced sympathetic stimulation seen in cardiac patients, norepinephrine was infused into normal subjects during a glucose-tolerance test (GTT). A decline in glucose tolerance and plasma insulin was observed to levels approximating those seen in the cardiac patients, suggesting a neurohumoral mechanism for the glucose intolerance in cardiac patients. It would therefore appear that the glucose intolerance in compensated cardiac subjects with a reduced cardiac output is frequently an acquired rather than a genetically determined metabolic disorder.
No takes yet. Share an insight, caveat, or question.
Ettinger et al. (1968) conducted an observational in Compensated nonischemic cardiovascular disease (n=13). Intravenous infusion of glucose vs. Normal subjects was evaluated on Glucose disappearance slope and plasma insulin response. Patients with compensated nonischemic cardiovascular disease exhibited significantly lower glucose tolerance and reduced insulin response compared to normal subjects.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: