Diabetes and thyroid-hormone-induced changes in cardiac function and their molecular basis.

Abstract

The heart is a major target organ for insulin and thyroid hormone action, and marked changes in cardiac function occur in patients with hyper- or hypothyroidism and diabetes mellitus. Cardiac contractility is increased in the hyperthyroid state and decreased in hypothyroidism, and changes in specific proteins mediating cardiac contraction accompany these alterations. Changes in thyroid status mediate their influence on cardiac function by a combination of direct thyroid hormone effects on the heart, alterations in the responsiveness of the cardiac sympathoadrenal system, and hemodynamic effects generated in the periphery. Cardiovascular complications of diabetes mellitus are a major contributor to mortality and morbidity in the diabetic population. In addition to cardiac small and large vessel disease, an autonomic neuropathy and a cardiomyopathy occur in diabetic patients. The cardiomyopathy results in congestive failure and is independent of large vessel disease. Studies in diabetic animal models point to a metabolic basis for the cardiomyopathy, which is accompanied by changes in specific contractile proteins.