Thyroid hormone action has profound consequences for the heart, ranging from 
atrial fibrillation to hemodynamic collapse. It has long been known that the 
cardiovascular signs and symptoms seen in thyrotoxicosis resemble those seen in 
states of catecholamine excess. However, measured concentrations of serum 
catecholamines in patients with thyrotoxicosis are typically normal or even low, 
suggesting an increase in the adrenergic responsiveness of the thyrotoxic heart. 
In spite of several decades of work, the question of whether thyroid hormone 
increases cardiac adrenergic responsiveness is still controversial. In this 
brief review, we consider the reasons underlying this controversy, focusing on 
the complexity of the adrenergic signaling cascade.