The recognition of cardiac complications after stroke is of essence for the clinician, as the anticipation of such can guide clinical management and significantly alter patient outcomes after stroke. This chapter focuses mainly on the effects of the brain on the heart, discussing the neuroanatomical and pathophysiological correlates of these conditions, and their clinical and management implications. Pathophysiologically, the major underlying mechanism for myocardial damage in contraction band necrosis is felt to be sudden entry of calcium into the myocytes. Calcium deficiency with loss of intracellular calcium, anoxia followed by reoxygenation of the electron transport system, ischemia followed by reperfusion, or opening of the receptor-operated calcium channels by excessive amounts of locally released norepinephrine can lead to the final common pathway to cell death. Hypertension has been consistently shown in the acute phase of cerebrovascular diseases, even in patients who do not have a prior history of hypertension.