This review discusses the clinically relevant effects of thyroid hormone excess on the heart. Tachycardia and atrial fibrillation are usually reversible after euthyroidism is restored. Atrial fibrillation may, however, take several months to return to sinus rhythm. The increase in contractility leads to an increase of cardiac output. The development of a relative myocardial hypertrophy following long-term high-dose therapy with thyroid hormones is controversial. Cardiac failure at stress in spite of an increased cardiac output at rest is a phenomenon typical for thyrotoxicosis. Reports of dilated cardiomyopathy associated with Graves' disease and evidence for TSH-receptors in the human myocardium suggest a relationship between these two diseases. Endomyocardial biopsy studies have, however, failed to prove this hypothesis. Mitral valve prolapse is more frequent in hyperthyroid patients than in normals. Thyroid hormone excess as well as the autoimmune origin of the disease are suggested as etiology for this phenomenon. The frequently observed angina pectoris seems to be a consequence of the increase in consumption of oxygen in the presence of an unchanged oxygen supply rather than of obstruction of coronary circulation. Well documented cases of myocardial infarction patients with thyroid hormone excess and normal coronary arteries in angiography substantiate this theory. Finally diagnostic and therapeutic options of the two forms of thyrotoxicosis induced by the antiarrhythmic drug amiodarone are presented.