Cardioembolic stroke: topography and pathogenesis.

The preventive and acute treatment of cardioembolic stroke is based upon its pathogenesis and location. Typically, cardioembolic cerebral infarction is multiple, bilateral, and often large and wedge shaped. Less frequently, smaller infarcts are produced, but the incidence of lacunar infarction or small cortico-medullary junction infarction due to cardioembolism is uncertain. Microembolism has been detected by Doppler sonography and may be constant, but the factors leading to symptomatic embolism are poorly understood. The natural lytic properties of endothelium play a role in thrombus formation in the heart and embolus lysis intracranially. In addition, site-specific tissue factors may be important in the production of complications occurring in the wake of embolic infarction: hemorrhagic transformation and edema. The treatment of cardioembolic stroke may involve prevention of both red (fibrin-based) and white (platelet-predominant) clot formation as well as a combination of clot lysis and the use of agents to prevent damage due to the final ischemic cascade after embolism has occurred. This review attempts to clarify the arterial topography, mechanism, and presentation of cardioembolic stroke.