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(Stroke. 1997;28:1107-1114.)
© 1997 American Heart Association, Inc.
Articles |
From the Maryland Medical Research Institute (M.A.S., T.R.P., M.L.T., S.F., G.L.K.) and the Department of Neurology, University of Maryland School of Medicine (M.A.S., T.R.P.), Baltimore; the Department of Medicine, University of Massachusetts School of Medicine, Worcester (J.M.G.); the Division of Cardiology, St Louis (Mo) University Medical Center (B.R.C.); the Cardiology Division, University of Minnesota, Minneapolis (M.H.); the Division of Cardiology, Albert Einstein College of Medicine, New York, NY (H.M.); the Department of Medicine, University of Alabama Medical Center, Birmingham (W.J.R.); and the Department of Medicine, Brigham and Women's and Beth Israel Hospitals, Harvard Medical School, Boston, Mass (E.B.).
Correspondence to Michael A. Sloan, MD, Maryland Medical Research Institute, 600 Wyndhurst Ave, Baltimore, MD 21210.
Background and Purpose Ischemic cerebral infarction (CI) is a serious complication of acute myocardial infarction (MI). Little information exists on CI after thrombolytic therapy for MI.
Methods Of 3924 MI patients treated with recombinant tissue plasminogen activator (rt-PA) and heparin, 29 (0.7%) developed CI after treatment. All CI patients had detailed neurological evaluations, and 27 (93%) had CT scans centrally reviewed.
Results Age range was 40 to 74 years (mean, 60 years); 25 patients (86%) were men, and 22 (76%) were white. The electrocardiographic location of MI was anterior in 22 (76%) and nonanterior in 7 (24%). Five CIs occurred within 6 hours, 4 between 6 to 24 hours, 8 during the remainder of the first week, 10 during the second week, and 2 others distributed over the 4 weeks after study entry. Six of 29 CIs did not involve the cerebral cortex; 9 patients (31%) had multiple CIs. Of 28 CIs thought to be embolic in origin, 17 showed strong evidence for at least one cardiac abnormality (mural clot, wall-motion abnormality, aneurysm, or atrial fibrillation) known to be associated more specifically with embolism than MI. Eight of 27 CIs (30%) with CT scans had hemorrhagic transformation of varying degrees; 5 were symptomatic.
Conclusions The time of occurrence and sites of CI after rt-PA and heparin therapy for acute MI are similar to those reported during the prethrombolytic era.
Key Words: cerebral infarction heparin myocardial infarction thrombolytic therapy
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