Cardiac complications, including focal myocytolysis, electrocardiographic changes, arrhythmias and left ventricular wall motion abnormalities, frequently occur following stroke and contribute to worsen the prognosis. Their clinical spectrum seems to be related to the type of cerebrovascular disease and its localization. Thus, the incidence of arrhythmias and pulmonary edema is significantly higher in subarachnoid hemorrhage than in ischemic stroke, and the lesions in the right insular cortex are a major risk for complex arrhythmias and sudden death. Elevated plasma norepinephrine levels are frequently associated with these events and strongly suggest an underlying sympathetically mediated mechanism. The autonomic and cardiovascular effects of stroke, however, are modulated by concomitant factors such as pre-existent cardiac diseases, electrolyte disorders and, probably, by genetic alterations in the ionic control of myocyte repolarization. Although beta-blockers have been reported to prevent myocardial damage following stroke, adequate clinical trials are lacking, and the widespread use of these drugs in acute cerebrovascular disease is not supported by evidence.