Thyroid hormone in the pathophysiology of heart failure: clinical evidence

Experimental and clinical findings strongly support the concept that thyroid hormone (TH) has a fundamental role in the cardiovascular homeostasis both in physiological and pathological conditions. THs, in particular the biologically active triiodothyronine (T3), influence cardiac contractility, heart rate, diastolic function and systemic vascular resistance through genomic and non-genomic mediated effects. In heart failure (HF) the main alteration is referred to a "low-T3 syndrorne" characterized by the reduction in serum total T3 (M) and free T3 (FT3) with normal levels of thyroxine (T4) and thyrotropin (TSH). This syndrome, that affects one third of more severe HF patients, is commonly interpreted as an adaptive condition minimizing catabolic phenomena of illness. However, this interpretative hypothesis is actually questioned; new experimental data have shown the potential negative effects of the low-T3 state in the progressive deterioration of cardiac function and myocardial remodeling in HE Also, prognostic studies have shown that low T3 levels represent a powerful predictor of mortality in HF patients, also adding prognostic power to conventional cardiac parameters. All these data, together with the evidence of the benefit of T3 administration in HF patients in pilot studies indicate that placebo controlled large prospective studies are now needed to better define the safety and prognostic effects of the chronic treatment with synthetic thyroid hormones in HE