Hemorrhagic transformation in cerebral embolism

• Published in: Stroke (1970) Vol. 20; no. 5; pp. 598 - 603
• Main Authors: Okada, Y, Yamaguchi, T, Minematsu, K, Miyashita, T, Sawada, T, Sadoshima, S, Fujishima, M, Omae, T
• Format: Journal Article
• Language: English
• Published: United States 01.05.1989
• Subjects: Adolescent; Adult; Aged; Aged, 80 and over; Cerebral Hemorrhage - diagnostic imaging; Cerebral Hemorrhage - etiology; Cerebral Hemorrhage - physiopathology; Female; Humans; Intracranial Embolism and Thrombosis - complications; Intracranial Embolism and Thrombosis - diagnostic imaging; Intracranial Embolism and Thrombosis - etiology; Intracranial Embolism and Thrombosis - physiopathology; Male; Middle Aged; Myocardial Infarction - complications; Time Factors; Tomography, X-Ray Computed
• ISSN: 0039-2499; 1524-4628
• DOI: 10.1161/01.str.20.5.598

We studied the mechanism of hemorrhagic infarction after acute cerebral embolism in 160 patients by brain computed tomography and angiography. Hemorrhagic infarction during the month after the embolic event was evident in 65 patients (40.6%). Initial angiography a median of 1.5 (range 1-60) days after the event revealed occlusion of the cerebral arteries in 117 of 142 patients (82.4%), and reopening of the vessels was observed in 56 (94.9%) of 59 patients who had follow-up angiography a median of 20 (range 3-47) days after the event. The incidence of hemorrhagic infarction was higher in patients greater than or equal to 70 years old (31 of 61, 50.8%) than in those aged 50-69 years (27 of 72, 37.5%) or less than 50 years (seven of 27, 25.9%) (greater than or equal to 70 vs. less than 50, p less than 0.05). In patients with moderate or large infarcts, hemorrhagic infarction developed in 50.0% or 51.5%, respectively, while in those with small infarcts it developed in only 2.9% (p less than 0.05). No correlation was found between hemorrhagic infarction and history of hypertension or blood pressure during the acute stage of stroke. Thrombolytic and/or anticoagulant therapy did not affect the incidence of hemorrhagic infarction (40.0% with vs. 40.7% without therapy) but tended to cause massive hematoma. Our results indicate that hemorrhagic transformation in cerebral embolism is caused not only by reopening of the occluded vessels but also by other factors such as age and size of the infarct. Hypertension per se seems to be less important for hemorrhagic infarction.