Impact of Thrombomodulin Polymorphism -33G>A on Acute Myocardial Infarction Risk and Circulating Inflammatory Markers

Area of Science:

• Cardiovascular Genetics
• Molecular Cardiology
• Biomarkers of Cardiovascular Disease

Background:

• Thrombomodulin (THBD) gene polymorphisms and inflammatory markers like C-reactive protein (CRP), fibrinogen, and albumin are implicated in acute myocardial infarction (AMI) risk.
• The THBD -33G>A polymorphism (rs1042579) warrants investigation as a potential risk marker for AMI.

Purpose of the Study:

• To evaluate the THBD -33G>A polymorphism as a marker for acute myocardial infarction (AMI) risk.
• To correlate the THBD -33G>A polymorphism with serum levels of key inflammatory markers.

Main Methods:

• A case-control study involving 277 AMI patients and 329 healthy controls.
• Binary logistic regression analysis was employed to assess the association between studied parameters and AMI risk.
• A backward stepwise logistic regression model identified predictive risk factors for AMI.

Main Results:

• The AA genotype of the THBD -33G>A polymorphism was significantly associated with increased AMI risk (OR = 2.011, P < .001).
• The A allele also showed a significant association with higher AMI risk (OR = 1.725, P < .001).
• Smoking, hypertension, albumin, fibrinogen, CRP, ACE activity, cardiac troponin-I, and the THBD AA genotype were identified as significant predictors of AMI.

Conclusions:

• The THBD -33G>A polymorphism, particularly the AA genotype, is a significant risk factor for acute myocardial infarction (AMI).
• This genetic polymorphism should be incorporated into the risk stratification protocols for AMI.