Antithrombotic Therapy for Cerebrovascular Disorders: Hemorrhagic infarction

Hemorrhagic infarction at autopsy was once believed to be diagnostic of embolic stroke, as distal migration of the embolic fragment caused reperfusion and hemorrhagic transformation of the infarcted area. Clinical studies of hemorrhagic transformation by CT has challenged the specificity, although large areas of hemorrhagic transformation deep within the infarction are more common with cardiogenic brain embolism. Subcortical hemorrhagic infarct has been hypothesized to be particularly indicative of cardiogenic embolism. Overall, about 20% of car-dioembolic strokes will have secondary hemorrhagic transformation if CT is repeated 2-4 days after stroke, larger infarctions having the highest likelihood. Hemorrhagic transformation of infarcts produced by other mechanisms occurs less frequently, is usually less dense, and is confined to the periphery of the infarction.

The presence of a potential cardioembolic source in the absence of cerebrovascular disease in a patient with nonlacunar stroke remains the mainstay of diagnosis. Frequendy, however, some degree of cerebrovascular disease coexists with cardioembolic heart disease, and its role can seldom be completely discounted. Certain cardiac lesions (eg, protruding LV thrombus) are more suggestive than others that have a substantial prevalence in nonstroke patients (eg, mitral valve prolapse, AF). Hemorrhagic infarction occurring deep within the infarction and multiple cortical infarctions in the absence of cerebrovascular atherosclerosis further support a cardioembolic mechanism. The absence of relatively sensitive and specific clinical diagnostic criteria for cardioembolic stroke remains a major problem. More sensitive techniques of cardiac imaging include ultra-fast CT, magnetic resonance imaging, transesophageal echocardiography” and isotope-labeled platelet scintigraphy may aid in the diagnosis in the future. At present, the diagnosis remains “an elusive butterfly” in many patients.