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(Stroke. 1998;29:235-238.)
© 1998 American Heart Association, Inc.

Case Reports

Depressed Platelet Status in an Elderly Patient With Hemorrhagic Stroke After Thrombolysis for Acute Myocardial Infarction

Victor L. Serebruany, MD, PhD; Paul A. Gurbel, MD; Andrew R. Shustov, MD; Margaret R. Dalesandro, PhD; Cindy I. Gumbs, BS; Laura B. Grabletz, BS; Raymond D. Bahr, MD; E. Magnus Ohman, MD; Eric J. Topol, MD; for the GUSTO-III Investigators

From the Union Memorial Hospital, Baltimore, Md (V.L.S., P.A.G., A.R.S.); Centocor, Inc, Malvern, Pa (M.R.D., C.I.G., L.B.G.); St Agnes Hospital, Baltimore, Md (R.D.B.); Duke Clinical Research Institute, Durham, NC (E.M.O.); and Cleveland Clinic, Cleveland, Ohio (E.J.T.).

Correspondence to Dr Victor L. Serebruany, Sinai Center for Thrombosis Research, 2401 W Belvedere Ave, Schapiro Research Building-R202, Baltimore, MD 21215. E-mail Heartdrug{at}aol.com

Abstract

Background—Impaired platelet function has been reported in acute myocardial infarction (AMI) and stroke. However, prospective data on the changes of platelet status in patients before the occurrence of hemorrhagic stroke after thrombolytic therapy are unavailable.

Case Description—An 86-year-old male patient was among the 23 AMI patients enrolled in the platelet study for the GUSTO-III trial. He received 325 mg of aspirin daily for at least 6 years, suffered an AMI, and was successfully reperfused with alteplase, but after 44 hours developed a large hemorrhagic stroke resulting in paraplegia. Platelet aggregation and receptor expression were measured by flow cytometry and ELISA before thrombolysis and at 3, 6, 12, and 24 hours thereafter. The percentage of platelet aggregation was lower in the stroke patient at every time point when induced by 5 µmol/L of ADP, by 10 µmol/L of ADP, and by thrombin than in the rest of the AMI group. Ristocetin and collagen-induced aggregability were within the group range. Decreased platelet glycoprotein Ib, IIb, IIIa, and IIb/IIIa and vitronectin receptor expression were observed in the stroke patient. No other differences in p24 (CD9), very late antigen-2, P-selectin, and platelet/endothelial cell adhesion molecule-1 expression were determined.

Conclusions—Profound depression of platelet status preceded the occurrence of hemorrhagic stroke in an elderly long-term aspirin user treated with thrombolytic therapy. Initial "exhausted" platelets may be responsible for the increased risk for hemorrhagic stroke after coronary thrombolysis.

Key Words: hemorrhagic stroke • myocardial infarction • platelets • thrombolysis

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