Tachycardia-mediated cardiomyopathy is a cause of ventricular dysfunction due to, at least partially, persistent tachycardia leading to cellular and extracellular perturbations. Cardiomyopathy may take years to develop, but pharmacologic management to achieve rate control and reverse remodeling, as well as cardioversion or ablative strategies to stop the tachycardia, can result in rapid recovery from symptoms and gradual improvement in left ventricular ejection fraction. However, ultrastructural changes can remain and may lead to a rapid decline in ventricular function if tachycardia recurs. Ultrastructural changes may also explain a propensity toward sudden death even if the ejection fraction normalizes. Although the etiology, pathophysiology, and late clinical manifestations of tachycardia-mediated cardiomyopathy are beginning to be understood, investigation continues, focusing on prevention, early recognition, and acute and long-term management in an attempt to lessen heart failure and prevent risk of sudden death.