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Circulating Thrombotic Risk Factors in Young Patients with Coronary Artery Disease Who Are on Statins and
Reema George1, Harikrishnan Sivadasanpillai1, Narayani Jayakumari2
1Department of Cardiology, Sree Chitra Tirunal Institute for Medical Sciences and Technology, Thiruvananthapuram, 695011 Kerala India.
Insights
This study found that low antithrombin-III, high fibrinogen, and high lipoprotein(a) are key thrombotic risk factors for premature coronary artery disease (CAD) in Indian patients. Managing these alongside conventional factors may aid CAD prevention.
Area of Science:
- Cardiovascular Medicine
- Thrombosis and Hemostasis
- Preventive Cardiology
Background:
- Premature coronary artery disease (CAD) is influenced by thrombotic factors beyond conventional risks.
- Limited data exists on thrombotic factors in young Indian patients with premature CAD.
- This study investigates thrombotic and atherogenic factors in young Indian CAD patients on statins and anti-platelet therapy.
Purpose of the Study:
- To evaluate the role of thrombotic and atherogenic factors in young, angiographically proven CAD patients.
- To assess these factors in Indian patients undergoing treatment with statins and anti-platelet drugs.
Main Methods:
- A case-control study involving 152 patients (≤55 years) with CAD and 102 asymptomatic controls.
- Analysis of clinical and biochemical data, including blood levels of fibrinogen, antithrombin-III, t-PA, PAI-1, v-WF, Lp(a), and homocysteine.
- Logistic regression analysis to identify independent risk factors.
Main Results:
- Patients exhibited higher conventional CAD risk factors (diabetes, smoking, hypertension, dyslipidemia, family history).
- Independent risk factors identified: low antithrombin-III (OR 11.2), high fibrinogen (OR 6.04), and high Lp(a) (OR 4.54).
- Plasminogen activator inhibitor-1 (PAI-1) levels were significantly lower in patients (OR 0.15); t-PA, v-WF, and homocysteine showed no significant difference.
Conclusions:
- Low antithrombin-III, high fibrinogen, and high Lp(a) are significant independent risk factors for premature CAD in this Indian cohort.
- Current treatments (statins, anti-platelets) may influence some thrombotic factor levels.
- Targeting thrombotic factors alongside conventional risk factors is recommended for primary and secondary CAD prevention.
Abstract:
Thrombotic risk factors may contribute to premature coronary artery disease (CAD), in addition to the conventional risk factors. There is paucity of data on studies evaluating the role of thrombotic factors in premature CAD in Indian patients. Thus a case-control study was performed to evaluate the role of thrombotic and atherogenic factors in young patients with angiographically proven CAD who are on treatment with statins and anti-platelet drugs. 152 patients (≤55 years) with angiographically proven CAD and 102 asymptomatic controls were recruited. Clinical and biochemical data were obtained in both groups. Blood levels of thrombotic factors-fibrinogen, antithrombin-III, tissue-plasminogen activator (t-PA), plasminogen activator inhibitor-1 (PAI-1), von-Willebrand factor (v-WF), lipoprotein(a) [Lp(a)] and homocysteine were analyzed. Patients had high levels of conventional CAD risk factors (diabetes mellitus, smoking, hypertension, dyslipidemia and positive family history) compared to controls. Logistic regression analysis revealed that low antithrombin-III (odds ratio/OR 11.2; 95 % confidence interval/CI 2.29-54.01), high fibrinogen (OR 6.04; 95 % CI 1.09-33.21) and high Lp(a) (OR 4.54; 95 % CI 0.92-22.56), as important, independent risk factors in patients. PAI-1(OR 0.15; 95 % CI 0.03-0.69) levels were significantly lower in patients. But other thrombotic risk factors studied (t-PA, v-WF and homocysteine) were comparable among patients and controls. The treatment using statins and anti-platelet drugs might be contributing to the control of some of the thrombotic risk factors. The strategies aiming at lowering the levels of thrombotic risk factors along with conventional risk factors may be useful in primary and secondary prevention of CAD.
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