Triiodothyronine (T3) and cardiovascular therapeutics: a review.

Hypothyroidism is associated with an abnormal hemodynamic state characterized by decreased heart rate, stroke volume, output, and contractility, and increased systemic vascular resistance. Since cardiopulmonary bypass (CPB) and surgical stress can induce profound decreases in triiodothyronine (T3) levels, the hemodynamic consequences of "stress-induced" hypothyroidism and T3 repletion are of increasing clinical interest. Available data generally support the likelihood of a beneficial effect associated with T3 replacement in brain-dead organ donors and in cases of low cardiac output following CPB. Although hypotheses have been advanced to account for these salutary effects, the mechanism by which T3 may augment hemodynamic performance has not been precisely defined, particularly in the acute setting. Although additional research is needed to clarify these and other issues, preliminary findings with T3 replacement indicate that such investigation is warranted.