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Mitral valve prolapse and embolic stroke.

formed routinely in every patient between the 7th and 14th day after admission. In the event of neurologic worsening, the patient was immediately reevaluated and a new CT done. The second CT scan showed intracranial hemorrhage in five of twenty-four patients (20.8%) with large infarction 1,3,8, 13, and 20 days after admission respectively. Of these, three patients had been on IV-heparin and the other two on SCheparin. Anticoagulation was withdrawn in all five patients and in another patient due to hematuria. Three patients died and another had new embolic stroke. There were recurrent embolic strokes in the other patients. We agree with Shields et al that early anticoagulation therapy following embolic brain infarction in non-hypertensive patients appears to reduce the risk of early embolic recurrence. Three of their five patients were hypertensive. Treatment may lead to intracranial hemorrhage in patients with large clinical or CT infarcts and in these patients it would be wise to avoid inmediate anticoagulation therapy. Taking into account that hemorrhage was detected by initial CT scan in 2-5% of embolic infarcts, Furlan considered that it may be safest to delay the initial CT for 24 to 48 hours after onset, because this delay should increase detection of hemorrhagic stroke with initially microscopic hemorrhagic infarction. However, two out of five of Shield's patients and three out of five patients suffered clinical hemorrhagic transformation seven days after anticoagulation was begun. We think this delay would not be useful, and hemorrhagic complication can occur while receiving heparin therapy. Further studies are needed on the subgroup of patients with large infarcts, who may be a risk for hemorrhagic transformation. J. Matias-Guiu, M.D. J. Alvarez, M.D. C. Cervera, M.D. A. Codina, M.D. Service of Neurology Universilad Anlonoma Hospital del Valle de Hebron Barcelona, Spain