Endocrine Abstracts

The cardiovascular system is one of the major targets of thyroid hormone action, sensitive enough to detect the effects of thyroid hormone excess or deficiency at tissue level. Triiodothyronine (T3) acts on the heart and vascular system by classic genomic as well as non-genomic mechanisms and influences heart rate, systolic and diastolic function and systemic vascular resistance thereby affecting cardiac performance. In human short-term overt hyperthyroidism, the increase in left ventricular performance is predominantly sustained by the increased preload with enhanced left ventricular diastolic function. The combination of reduced systemic vascular resistance, coupled with the increased venous return and preload, increases cardiac output. The cardiovascular risk of subclinical and overt long-term hyperthyroidism is related to short-term effects due to the electrophysiological effects of thyroid hormones, and to the long-term effects resulting from increased left ventricular mass and increased cardiac workload. The frequency of atrial fibrillation is increased to a similar degree in patients with overt and subclinical hyperthyroidism. The significant increase in left ventricular mass represents the most consistent cardiac abnormality reported in patients with long-standing overt and subclinical hyperthyroidism and is responsible for diastolic dysfunction and systolic dysfunction during effort. Long-standing hyperthyroidism exerts many relevant effects on the cardiovascular system and it may induce abnormalities that may lead to more severe cardiovascular disease, thus potentially contributing to the increased risk of cardiovascular morbidity and mortality observed in these patients. The cardiovascular risk in patients with overt and subclinical hypothyroidism results from the changes in cardiovascular function and from accelerated atherosclerosis. The decreased cardiac output in hypothyroid patients at rest depends largely on changes in diastolic relaxation and hemodynamic loading conditions. The reduced cardiac preload, in combination with bradycardia and slightly depressed myocardial contractility, accounts for a subnormal cardiac output in overt hypothyroidism, whereas peripheral vascular resistance are remarkably increased. The most consistent cardiac abnormality recognized in patients with subclinical hypothyroidism is the impairment of left ventricular diastolic function with an impaired left ventricular systolic function on effort. The negative effect induced by subclinical hypothyroidism on the cardiovascular system is reverted, restoring euthyroidism with L-T4 therapy. Several epidemiological studies examined the linkage between SH and atherosclerosis showing conflicting results. Diastolic hypertension, dyslipidemia, endothelial dysfunction, elevated C reactive protein levels and coagulation abnormalities represent the atherosclerotic risk factors associated with subclinical hypothyroidism and may be reversible with euthyroidism after L-T4 therapy.