Drug-induced cardiomyopathies are becoming widely used as models of heart failure. These models offer the advantage of precise control of the onset time and can often be studied in a longitudinal fashion. Toxin- and tachycardia-induced models, as well as nutritional deficiency models, possess certain clinically relevant features, thereby enhancing their appeal. By studying these types of models, key components of heart disease can be elucidated, and may provide important new insights into the pathophysiology of the clinical and functional end-point: heart failure.