atrial-natriuretic-factor and Euthyroid-Sick-Syndromes

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.

Topics: Atrial Natriuretic Factor; Cardiovascular System; Diabetes Mellitus; Endocrine System; Endothelium, Vascular; Euthyroid Sick Syndromes; Heart Failure; History, 19th Century; History, 20th Century; Humans; Internal Medicine; Oxidative Stress; Prognosis; Risk Factors; Triiodothyronine

The relationship between the pituitary-thyroid axis and the cardiovascular system in patients with congestive heart failure (CHF) remains unknown. Therefore, we attempted to determine serum levels of thyroid hormones in relation to plasma atrial natriuretic peptide (ANP) levels and left ventricular (LV) function in patients with CHF. The echocardiographic ejection fraction significantly correlated with the thyroid stimulating hormone (TSH) (p < 0.005) and free triiodothyronine (FT3)/free thyroxine (FT4) ratio (p < 0.005), respectively, in patients with CHF but not in control subjects. TSH was positively correlated with the FT3/FT4 ratio (p < 0.01) in CHF. In patients with CHF, TSH and thyroid hormones may participate in regulatory mechanisms of the cardiovascular system and altered thyroid hormone metabolism, which was characterized by a euthyroid sick syndrome.

Topics: Aged; Atrial Natriuretic Factor; Cardiovascular System; Euthyroid Sick Syndromes; Female; Heart Failure; Humans; Male; Pituitary Gland; Thyroid Gland; Thyrotropin; Thyroxine; Triiodothyronine; Ventricular Function, Left

Topics: Aldosterone; Angiotensin II; Arginine Vasopressin; Atrial Natriuretic Factor; Brain Death; Euthyroid Sick Syndromes; Humans; Renin; Tissue Donors

The present prospective study was conducted in order to investigate the effect of an acute decrease in serum T3 levels on ANP, aldosterone, angiotensin II, renin and ADH. All patients showed a pathologic TRH stimulation test prior to organ harvesting. Our patients developed secondary T3 hypothyroidism of different severity dependent on intensive care unit (ICU) stay. T3 values in group 1 (ICU stay > or = 77 h) were smaller than 70 ng/dl, those of group 2 (ICU stay < or = 53 h) were greater than 70 ng/dl. In both groups a severe elevation of plasma renin activity was measured, with almost high-normal values for ANP in group 1 and slightly elevated values in group 2 [not significant (n.s.)]. Results demonstrate that, contrary to patients who are not critically ill, brain-dead patients develop a dissociation of the renin-angiotensin-aldosterone mechanism. No statistical significant difference was found between the groups in serum levels of ADH and aldosterone. This endocrine dissociation, however, seems to have no clinical significance with regard to organ function after transplantation in kidney recipients.

Topics: Aldosterone; Angiotensin II; Atrial Natriuretic Factor; Euthyroid Sick Syndromes; Hemodynamics; Humans; Kidney Transplantation; Renin; Thyrotropin; Thyrotropin-Releasing Hormone; Thyroxine; Tissue Donors; Triiodothyronine; Triiodothyronine, Reverse