| Summary: | Alessandro Pingitore, Giorgio IervasiInstitute of Clinical Physiology, CNR, Pisa, ItalyIntroductionCurrently, there is little doubt that activation of the neuroendocrine (NE) system is predominately responsible for the progressive decline of heart function in heart failure (HF). This is due to the complex action of neurotransmitters, hormonal factors, and/or immunological pathways. Evidence that supports this point of view is the clear prognostic benefit and the reduction of HF progression by using NE-guided therapeutic approaches (SOLVD investigators 1992; Eichhorn and Bristow 1996; Packer et al 1996; Opie 2004; Solomon et al 2004). However, the fact that HF represents one of the major causes of morbidity and mortality in Western countries also suggests that the current portfolio of NE antagonists fails to completely explain and possibly counteract disease progression (Guyatt and Deveraux 2004). In this context, interest in the relationship between thyroid hormones (THs) and HF is increasingly gaining prominence. The chief reason for the latter is the emerging novel actions of THs on the cardiovascular system and, more specifically, the role of TH as a prognostic biomarker of cardiac disease as well as the potential benefit of TH administration in patients with HF.
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