For nearly fifty years, attention has repeatedly been drawn to electrocardiographic changes accompanying acute stroke. The mechanism was unknown. These alterations, which are more frequent after hemisphere than brain stem infarction, are not solely due to concomitant myocardial ischemia. Recently, cardiac chronotropic organization has been shown within the posterior rat insular cortex. Stimulation of that site mimics both the electrocardiographic changes and the cardiac pathology accompanying acute stroke. These effects are attended by increased sympathetic activity. In addition, stimulation of the human right insula increases sympathetic cardiovascular tone, whereas parasympathetic increases are more frequent during left insula stimulation. It is suggested that right middle cerebral artery infarction disinhibits insular function, resulting in increased sympathetic cardiovascular tone and the cardiac consequences of stroke.