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J Am Coll Cardiol, 2001; 38:1307-1312 © 2001 by the American College of Cardiology Foundation |
* Cardiovascular Biology Research Laboratory, Zena and Michael A. Wiener Cardiovascular Institute, New York, New York, USA
Division of Endocrinology, Department of Medicine, Mount Sinai School of Medicine, New York, New York, USA
Manuscript received November 17, 2000; revised manuscript received July 10, 2001, accepted July 19, 2001.
* Reprint requests and correspondence: Dr. Juan Jose Badimon, Director, Cardiovascular Biology Research Laboratory, Zena and Michael A. Wiener Cardiovascular Institute, Box 1030, Mount Sinai School of Medicine, One Gustave L. Levy Place, New York, New York 10029 USA
juan.badimon{at}mssm.edu
OBJECTIVES
This study was designed to determine whether blood thrombogenicity is related to chronic glycemic control in type 2 diabetes mellitus (T2DM).
BACKGROUND
Type 2 diabetes mellitus is associated with accelerated atherosclerosis and a high rate of arterial thrombotic complications. Whether increased blood thrombogenicity is associated with glycemic control has not been properly tested.
METHODS
Forty patients with T2DM with hemoglobin A1c (HbA1c) 
7.5% were selected. Maintaining their current hypoglycemic therapies, patients were randomized into a conservative (diet modification plus placebo) or intensive (diet modification plus troglitazone) hypoglycemic regimen for three months. Blood thrombogenicity was measured at baseline and after three months with the Badimon ex vivo perfusion chamber and assessed as platelet-thrombus formation. The repeated measurements allowed every patient to be his/her own control.
RESULTS
Patients in both groups (48% and 74% of the conservative and intensive groups, respectively) improved glucose control (HbA1c reduction 0.5%), showing a significant decrease in blood thrombogenicity. A significant positive correlation was observed between the reduction in thrombus formation and the reduction in HbA1c (r = 0.47, p < 0.01). The reduction in HbA1c achieved by both treatments was comparable. Patients without glycemic improvement showed no change in blood thrombogenicity. Improved glycemic control was the only significant predictor of a decrease in blood thrombogenicity.
CONCLUSIONS
In T2DM, there is an association between improved glycemic control and blood thrombogenicity reduction. The effect of glycemic control on the thrombotic complications of T2DM patients deserves further investigation.
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