Patients who had no heart disease had T-wave inversion and prolongation of the QT interval in electrocardiogram after Subarachnoid hemorrhage (SAH), which was reported 70years before. Cardiac complications, including focal myocytolysis, electrocardiographic changes, arrhythmias and left ventricular wall motion abnormalities and pulmonary edema. The autonomic and cardiovascular effects of SAH, 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 SAH, adequate clinical trials are lacking, and the widespread use of these drugs in acute cerebrovascular disease is not supported by evidence. Cardiac injury occurs frequently after SAH, and the most widely investigated form of neurocardiogenic injury.