Platelet Survival Time in Coronary Artery Disease: Incidence and Significance

1975 ◽  
Author(s):  
P. Steele ◽  
E. Genton
Keyword(s):  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Survival Time ◽  
Saphenous Vein ◽  
Disease Incidence ◽  
Platelet Survival ◽  
Vein Bypass ◽  
History Of ◽  
Artery Disease ◽  
Or History

A role for platelets in the etiology of coronary artery disease (CAD) and its complications has been suggested. In 68 men with angiographically defined CAD platelet survival (SURV) (51Chromium) was shortened (3.2±.04 days; AVE±SEM; normal 3.7±.04 days; p < 0.001) and 41 (60%) had shortened SURV (< 3.3 days). SURV did not correlate with severity of CAD, angina, or history of infarction. Of 37 with hyperlipoproteinemia SURV was shortened (3.1 ±.12 days) in 27 (73%) and different from 31 with normal lipids (3.3±. 12 days; p < 0.05). SURV was performed in 35 following aorto-coronary saphenous vein bypass (ACB). Of 15 with all grafts open, SURV was normal (3.5±.11 days) in 10 (67%). Of 20 with one or more grafts occluded SURV was shortened (2.6±.08 days) in 19 (95%). In 11 with normal SURV, one of 23 (4%) grafts was occluded while in 24 with shortened SURV 26 of 46 (56%) grafts were occluded, Clofibrate prolonged shortened SURV (2.6 ±.09 to 3.4±14 days; p < 0.001) and altered lipids. Sulfinpyrazone prolonged shortened SURV (2.8 ±.12 to 3.6 ±.21 days; p < 0.001) and failed to alter lipids. Data suggest that shortened SURV is frequently present in CAD, can be altered by platelet suppressant agents and is associated with ACB occlusion.

Study on the Platelet Survival Time in the Patients with Coronary Artery Disease

1985 ◽  
Vol 15 (4) ◽  
pp. 625
Author(s):  
Hie Chull Son ◽  
Yeong Chun Lee ◽  
Yeong Sook Rha ◽  
Ja Cheon Kim ◽  
In Soon Kwon ◽  
...  
Keyword(s):  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Survival Time ◽  
Platelet Survival ◽  
Artery Disease

Platelet Survival in Patients with Angiographically Diseased and Normal Coronary Arteries

1984 ◽  
Vol 52 (02) ◽  
pp. 164-166 ◽  
Author(s):  
R Verhaeghe ◽  
J Piessens ◽  
R Suy ◽  
M Verstraete
Keyword(s):  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Survival Time ◽  
Coronary Arteries ◽  
Arterial Disease ◽  
High Serum ◽  
Normal Coronary Arteries ◽  
High Serum Cholesterol ◽  
Platelet Survival ◽  
Artery Disease

SummaryPlatelets may contribute to the pathogenesis of atherosclerosis and to the complications of coronary artery disease. Therefore, platelet kinetics were studied in 69 patients with angiographically documented coronary artery disease and in 16 patients with a normal coronary angiogram. Platelet survival time was calculated from the decay of radioactivity after injection of 51Cr-labeled autologous platelets. None of the mathematical models used was able to discriminate between the two patients groups. No correlation existed between survival time and extent of the arterial disease. Patients with a high serum cholesterol did not exhibit an enhanced platelet consumption. Thus, these studies do not support the idea that platelet turnover is enhanced in patients with coronary artery disease as compared to those with normal coronary arteries.

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

1981 ◽  
Author(s):  
A C de Boer ◽  
P Han ◽  
A G G Turpie ◽  
R Butt ◽  
M Gent ◽  
...  
Keyword(s):  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Survival Time ◽  
Crossover Trial ◽  
Exponential Model ◽  
Antiplatelet Drugs ◽  
Double Blind ◽  
Treatment Groups ◽  
Platelet Survival ◽  
Artery Disease

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.

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