[Pathophysiological and clinical correlations between endocrine and cardiovascular systems. An inter-systemic model of internal medicine].

This review focuses on the mechanisms by which thyroid hormones affect the regulation of the cardiovascular system and the thermogenic and hemodynamic variation induced by thyroid disfunction. It is also stressed the hormonal role of the cardiac myocytes realising natriuretic peptides, involved in plasma volume homeostasis and cardiovascular remodelling; its rapid measurement is a useful clinical tool, in the diagnostic and prognostic of left ventricular dysfunction, correlating with the degree of the clinical symptoms. The endothelial layer is a receptor-effector endocrine organ that produces substances that maintain vasomotor balance and vascular-tissue homeostasis. Cardiovascular risk factors causes oxidative stress that alter endothelial function and leads to endothelial dysfunction. On the basis of the present body of evidence there is no doubt that endothelial dysfunction contributes to the initiation, and progression, of atherosclerotic disease and that it could be considered an independent vascular risk factor for the micro- and macrovascular damages in the diabetes disease. In several extrathyroidal pathological condition, as well as in heart failure, the main alteration of the thyroid function is referred to as "low T3 syndrome". This syndrome is due to an adaptative reaction of the metabolic pathway of thyroxine, producing an increased amount of rT3, metabolically inactive, thus decreasing the detrimental metabolic effects of T3, in conditions of critically impaired hemodynamic and metabolic efficiency. Preliminary clinical trials, in heart failure, suggest the prognostic value of the level of circulating T3, as well as usefulness of T3, or of thyromimetic derivatives (DITPA), in chronic treatment of the heart ventricular dysfunction.