Thromb Haemost 1981; 46(01): 192
DOI: 10.1055/s-0038-1652553
Thrombosis, Clinical – VIII: Venous Thrombosis Treatment
Thrombosis, Clinical – IX: Arterial Disease, Platelet Survival
Schattauer GmbH Stuttgart

The Effect Of Antiplatelet Drugs On Platelet Survival Time And Betathromboglobulin In Coronary Artery Disease

A C de Boer
Departments of Medicine and Clinical Epidemiology and Biostatistics, McMaster University, Hamilton, Ontario, Canada
,
P Han
Departments of Medicine and Clinical Epidemiology and Biostatistics, McMaster University, Hamilton, Ontario, Canada
,
A G G Turpie
Departments of Medicine and Clinical Epidemiology and Biostatistics, McMaster University, Hamilton, Ontario, Canada
,
R Butt
Departments of Medicine and Clinical Epidemiology and Biostatistics, McMaster University, Hamilton, Ontario, Canada
,
M Gent
Departments of Medicine and Clinical Epidemiology and Biostatistics, McMaster University, Hamilton, Ontario, Canada
,
E Genton
Departments of Medicine and Clinical Epidemiology and Biostatistics, McMaster University, Hamilton, Ontario, Canada
› Author Affiliations
Further Information

Publication History

Publication Date:
24 July 2018 (online)

Platelets play a role in the development and complications of coronary artery disease (CAD). Abnormal platelet tests which can be corrected by antiplatelet drugs have been reported in CAD, including shortened platelet survival time (PST) and increased plasma betathromboglobulin (BTG) concentration. However, most of these reports were retrospective and unblinded. For these reasons we studied in a randomized double-blind crossover trial, the effect of sulphinpyrazone (800 mg) or aspirin (1200 mg)/dipyridamole (200 mg) on 51-Chromium PST calculated by an exponential model (normal 118±16 hrs; mean ± SD) and on plasma BTG measured by radioimmunoassay (28 ± 8 ng/ml) in 40 patients with angiographically documented CAD. Mean PST pretreatment (116 ± 16 hrs) was not different from normal; after 1 month’s treatment with placebo, sulphinpyrazone or aspirin/dipyridamole, mean PST was 123 ± 22, 123±17 and 128±26 respectively. Mean BTG pretreatment (52 ± 33) was elevated compared to normal (p<0.005) and abnormal in 21%; after treatment with placebo, sulphinpyrazone or aspirin/dipyridamole, mean BTG cone, was 59 ± 68, 51 ± 35 and 47 ± 33 respectively. Analysis of variance showed no significant differences between the various treatment groups for either PST or BTG. There was no correlation between PST and BTG (r= −0.04). In addition, there was no correlation of BTG or PST with the severity of CAD either clinically or angiographically. The data indicate that BTG levels were elevated in a proportion of patients with CAD and were not affected by the anti platelet drugs tested. The values of PST in CAD were usually within the range of normal, varied significantly between determinations and were not influenced by the anti platelet drugs.