The relationship between thyroid disease states and cardiovascular hemodynamics is well recognized. Although the long-term effects of thyroid hormone are thought to result from changes in myocardial gene expression, attention has recently focused on acute, non-nuclear-mediated actions of L-triidothyronine (T3), the biologically active form of the hormone. Various lines of evidence have documented that T3 can act as a vasodilator and inotrope. With this recognition have come novel treatment strategies targeted at specific clinical conditions including heart failure and cardiac surgery that are associated with impaired cardiovascular performance and low serum T3 levels. An understanding of the mechanisms of action of thyroid hormone on the heart and peripheral vasculature is essential for the rational implementation of thyroid hormone as a therapeutic agent. As outlined in this review, initial clinical experience suggests that the ability of thyroid hormone to increase cardiac output and to lower systemic vascular resistance may provide a novel treatment option for physicians caring for patients with cardiovascular illness.