Rapid decline of cerebral microemboli of arterial origin after intravenous acetylsalicylic acid

• Published in: Stroke (1970) 1999, Vol.30 (1), p.66-69
• Main Authors: GOERTLER, M, BAEUMER, M, KROSS, R, BLASER, T, LUTZE, G, JOST, S, WALLESCH, C.-W
• Format: Article
• Language: English
• Subjects: Adult; Aged; Aspirin - administration & dosage; Biological and medical sciences; Blood. Blood coagulation. Reticuloendothelial system; Carotid Stenosis - diagnostic imaging; Carotid Stenosis - physiopathology; Cerebral Arteries - physiopathology; Cerebrovascular Disorders - diagnostic imaging; Cerebrovascular Disorders - drug therapy; Female; Fibrinolytic Agents - administration & dosage; Humans; Injections, Intravenous; Intracranial Embolism and Thrombosis - diagnostic imaging; Intracranial Embolism and Thrombosis - drug therapy; Ischemic Attack, Transient - diagnostic imaging; Ischemic Attack, Transient - drug therapy; Male; Medical sciences; Microcirculation; Middle Aged; Pharmacology. Drug treatments; Platelet Aggregation Inhibitors - administration & dosage; Ultrasonography, Doppler
• ISSN: 0039-2499; 1524-4628
• DOI: 10.1161/01.str.30.1.66

The present study investigated the influence of the antiplatelet agent acetylsalicylic acid (ASA) on cerebral microembolism as detected by transcranial Doppler sonography (TCD). Nine patients with recent transient ischemic attack or minor stroke of arterial origin were investigated. Eight had not received an antiplatelet or anticoagulant medication before TCD, and in 1 patient a preexisting ASA medication (100 mg/d) had not been changed since the onset of stroke symptoms. An initial 1-hour TCD monitoring was extended for an additional 2.5 hours after an intravenous bolus injection of 500 mg ASA and was repeated for 1 hour on the following day. Microembolic signals (MES) were detected in all patients only on the symptomatic side. After the ASA bolus injection, a significant drop of the MES rate was found in 7 patients, all without previous medication, starting 30 minutes after the application (mean per hour=25.1 [range, 6 to 66] versus mean per hour=6.4 [range, 0 to 14]). In 3 of these patients, platelet aggregation tests were performed that demonstrated normal aggregation before bolus injection and inhibited aggregability as early as 30 minutes after bolus injection. The rate of MES remained unchanged in 1 patient without antiplatelet medication. The ninth patient, who had suffered an ischemic event on ASA, showed only a transient decrease of MES frequency. In patients with recent stroke of arterial origin, intravenous ASA can rapidly reduce cerebral microemboli as detected by TCD. Microemboli might be a useful parameter to monitor early effects of antiplatelet therapy.