REGULAR ARTICLEShear-Induced Platelet Adhesion and Aggregation on Subendothelium Are Increased in Diabetic Patients
Section snippets
Patients
The study population consisted of 82 NIDDM patients who were being followed at a diabetes clinic. All patients had been managed by diet and/or treatment with oral hypoglycemic agents for at least 1 year after diabetes was diagnosed and were not ketosis-prone. The diabetics were outpatients and had not been hospitalized during the 6 months prior to the study. The control group consisted of 71 healthy volunteers who came from a nearby community and showed no evidence of cardiovascular diseases or
Patient Characteristics
The mean duration of diabetes among the 82 NIDDM patients in this study was 12.4+8.5 (range 1–27) years. Forty-five patients (55%) were receiving treatment with the oral hypoglycemic agents glyburide (12 patients) or metformin (9 patients) or both (24 patients). Thirty patients (37%) were being treated with insulin, six (7%) with glyburide, metformin and insulin, and one patient by diet alone. All patients were evaluated for diabetic complications; the results are shown in Table 1. Of the 29
Discussion
The results obtained with the CPA method for evaluating platelet function in vitro show that the platelets of patients with NIDDM have an increased interaction with the ECM compared to those of nondiabetic controls. This increased platelet activity and interaction with the ECM is manifested as a significant increase in SC and AS of the adhered particles. These data confirm the results of previous studies showing an increased aggregation response in diabetic patients 13, 14, 15. However, they
Acknowledgements
This research was supported by a grant from the National Council for Research and Development, Israel and Deutsche Forschungsanstalt Luft and Raumfahrt. We thank Dr. Rima Dardik and Dr. Ilia Tamarin for their help in the analysis of platelet activity, and Ilana Gelernter for her help with the statistical analysis of the data.
References (41)
- et al.
Can restenosis after coronary angioplasty be predicted from clinical variables?
J Am Coll Cardiol
(1993) - et al.
Potential mechanisms promoting restenosis in diabetic patients
J Am Coll Cardiol
(1996) - et al.
Platelet and shear stress
Blood
(1996) - et al.
A new method for quantitative analysis of whole blood platelet interaction with extracellular matrix under flow conditions
Thromb Res
(1997) - et al.
Abnormalities of erythrocyte deformability and platelet aggregation in insulin-dependent diabetics corrected by insulin in vivo and in vitro
Lancet
(1982) - et al.
Lovastatin decreases plasma and platelet cholesterol levels and normalizes elevated platelet fluidity and aggregation in hypercholesterolemic patients
Metabolism
(1994) Lipoprotein metabolism in diabetes mellitus
J Lipid Res
(1987)- et al.
Rapidity and duration of platelet suppression by entric-coated aspirin in healthy young men
Am J Cardiol
(1992) - et al.
Diabetes, other risk factors, and 12-yr cardiovascular mortality for men screened in the Multiple Risk Factor Intervention Trial
Diabetes Care
(1993) - et al.
Platelets in diabetesThe role in the hemostatic regulation in atherosclerosis
Semin Thromb Hemost
(1993)
Platelet abnormalities in diabetes mellitus
Diabetes
The pathogenesis of coronary disease and the acute coronary syndrome
N Eng J Med
Ischemic heart disease and platelet aggregationThe Caerphilly collaborative heart disease study
Circulation
Platelet hyperreactivity and prognosis in survivors of myocardial infarction
N Eng J Med
Collaborative overview of randomised trials of antiplatelet. I. Prevention of death, myocardial infarction and stroke by prolonged antiplatelet therapy in various categories of patients
Br Med J
The role of platelets, thrombin, and hyperplasia in restenosis after coronary angiography
J Am Coll Cardiol
Use of a monoclonal antibody directed against the platelet glycoprotein IIb/IIIa receptor in high-risk coronary angioplasty
N Eng J Med
Restenosis after arterial injury caused by coronary stenting in patients with diabetes mellitus
Ann Intern Med
Increased platelet aggregation in diabetes mellitus
Ann Intern Med
Platelet function in diabetes mellitus
Br J Haematol
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