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Effect of Ginkgo biloba (EGb 761) and aspirin on platelet aggregation and platelet function analysis among older adults at risk of cardiovascular disease: a randomized clinical trial

Gardner, Christopher Da; Zehnder, James Lb; Rigby, Alison Ja; Nicholus, Joel Ra; Farquhar, John Wa

Blood Coagulation & Fibrinolysis: December 2007 - Volume 18 - Issue 8 - p 787–793
doi: 10.1097/MBC.0b013e3282f102b1
Original Articles

Several case reports have implicated Ginkgo biloba in clinically adverse bleeding disorders. Ginkgo biloba has been reported to increase pain-free walking distance among patients with peripheral artery disease (PAD). Standard PAD therapy includes 325 mg/day aspirin. The objective of this study was to examine potential adverse effects of concomitant aspirin and Ginkgo biloba on platelet function. Ginkgo biloba (EGb 761, 300 mg/day) was compared with placebo for effects on measures of platelet aggregation among adults consuming 325 mg/day aspirin in a randomized, double-blind, placebo-controlled, parallel design trial of 4-week duration. Participants were adults, age 69 ± 10 years, with PAD or risk factors for cardiovascular disease. Outcome measures included platelet function analysis (PFA-100 analyzer) using ADP as an agonist (n = 26 placebo; n = 29 ginkgo), and platelet aggregation using ADP, epinephrine, collagen and ristocetin as agonists (n = 21 placebo; n = 23 ginkgo). Participants kept daily logs of bleeding or bruising episodes. There were no clinically or statistically significant differences between treatment groups for any agonists, for either PFA-100 analysis or platelet aggregation. Reports of bleeding or bruising were infrequent and similar for both study groups. In conclusion, in older adults with PAD or cardiovascular disease risk, a relatively high dose of Ginkgo biloba combined with 325 mg/day daily aspirin did not have a clinically or statistically detectable impact on indices of coagulation examined over 4 weeks, compared with the effect of aspirin alone. No adverse bleeding events were observed, although the trial was limited to a small sample size.

aStanford Prevention Research Center and the Department of Medicine, USA

bDepartment of Pathology, Stanford University Medical School, Stanford, California, USA

Received 17 February, 2007

Revised 29 June, 2007

Accepted 8 August, 2007

Correspondence to Christopher D. Gardner, PhD, Stanford Prevention Research Center, Stanford University School of Medicine, 211 Quarry Road, Room N229, Stanford, CA 94305-5705, USA Tel: +1 650 725 2751; fax: +1 650 498 7623; e-mail:

© 2007 Lippincott Williams & Wilkins, Inc.