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Published on: April 1, 2015
Good metabolic control is associated with decreased circulating factor VIIa- antithrombin complexes in type 2
Joanna Gastoł1,2, Elżbieta Paszek3,4, Agata Bryk-Wiązania5,6
1Metabolic Diseases and Diabetology Clinical Department, University Hospital, Kraków, Poland.
Insights
In type 2 diabetes, higher activated factor VIIa-antithrombin complexes correlate with poor blood sugar and cholesterol control. Achieving treatment targets may help suppress tissue factor-induced coagulation activation.
Area of Science:
- Cardiovascular Medicine
- Endocrinology
- Hematology
Background:
- Type 2 diabetes (T2DM) is linked to a prothrombotic state, increasing cardiovascular event risk.
- Activated factor VIIa-antithrombin (FVIIa-AT) complexes indicate tissue factor (TF) exposure and are associated with thromboembolic risk.
- Previous research has not explored FVIIa-AT complexes in T2DM.
Purpose of the Study:
- To investigate factors influencing FVIIa-AT complexes in T2DM patients.
- To assess the impact of elevated FVIIa-AT complexes on the prothrombotic state in T2DM.
- To establish the relationship between glycemic control, lipid profiles, and FVIIa-AT complexes.
Main Methods:
- Compared FVIIa-AT complexes in 108 T2DM patients and 83 non-diabetic controls.
- Assessed metabolic control using fasting glucose, HbA1c, albumin/creatinine ratio (ACR), and lipid levels.
- Evaluated prothrombotic state via thrombin generation, fibrinolysis markers, and plasma fibrin clot properties.
Main Results:
- FVIIa-AT complexes were similar between T2DM patients and controls.
- Higher FVIIa-AT complexes in T2DM patients correlated with active smoking, insulin use, and elevated fasting glucose, HbA1c, ACR, total cholesterol, and LDL-cholesterol.
- FVIIa-AT complexes did not associate with thrombin generation, fibrin clot properties, or fibrinolysis markers.
- HbA1c, ACR, and total cholesterol were independently associated with FVIIa-AT complexes in T2DM.
Conclusions:
- This study is the first to link higher FVIIa-AT complexes in T2DM to markers of dyslipidemia and glycemic control.
- Findings suggest that TF-induced coagulation activation in T2DM may be mitigated by optimizing treatment targets.
- Improved management of diabetes and associated metabolic factors could reduce thrombotic risk.
Background:
Diabetes is associated with a prothrombotic state that contributes to cardiovascular (CV) events in type 2 diabetes (T2DM). Activated factor VII (FVIIa)- antithrombin (AT) complexes are indicative of tissue factor (TF) exposure and have been associated with thromboembolic risk in coronary artery disease. To our knowledge there have been no reports on FVIIa-AT complexes in T2DM, therefore we assessed factors that determine FVIIa-AT complexes in this disease and the impact of higher complexes on a prothrombotic state.
Methods:
In 108 T2DM patients (mean age 63.8 years, 52.8% men, median HbA1c of 6.9 [interquartile range 6.1-8.2] %) and 83 age- and sex-matched non-diabetic subjects, we measured FVIIa-AT complexes. Metabolic control of T2DM involved fasting glucose, glycated hemoglobin (HbA1c), albumin/creatinine ratio (ACR), and lipid levels. To characterize a prothrombotic state, we determined thrombin generation parameters, fibrinolysis markers, and plasma fibrin clot properties.
Results:
FVII-AT complexes in T2DM patients were similar to controls (73.6 [59.4-91.7] vs. 79.6 [59.2-97.1]pM, respectively, p = 0.30). The T2DM patients with FVIIa-AT in the top vs. the bottom quartile had a larger prevalence of active smoking and insulin use, along with higher fasting glucose (+ 36.4%), HbA1c (+ 27.4%), ACR (+ 72.8%), total cholesterol (+ 34.5%), and LDL-cholesterol (+ 80%). FVIIa-AT complexes showed no associations with in vitro thrombin generation potential, plasma fibrin clot properties, or fibrinolysis variables. On multivariable analysis HbA1c, ACR, and total cholesterol remained independently associated with FVIIa-AT complexes in T2DM.
Conclusions:
This is the first study to show that in T2DM higher FVIIa-AT complexes are associated with markers of dyslipidemia and glycemia control, indicating that TF-induced coagulation activation could be suppressed by achieving treatment targets.
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