Abstract
This study aimed to determine whether I/D polymorphism predispose to the development of MI in Tunisia. 50 patients with coronary artery disease complicated by MI and 70 healthy controls were analyzed. Quantitative analyses lipids are founded. DNA was isolated from blood samples. Polymorphisms were assessed by polymerase chain reaction method. Statistical differences between groups were determined by Chi-square test. Compared to controls, cases have significantly higher levels of total cholesterol, triglycerides and LDL-cholesterol and lower level of HDL-cholesterol. There are no significant differences between patients and controls in terms of allelic and genotypic frequencies. However, the frequency of the “I” allele is higher in cases which have 2 MI (p=0.0354). Additionally, a statistically significant association between diabetes, arterial high blood pressure, family history and cigarette smoking with MI was founded (p<0.01). I/D polymorphism of t-PA gene is not associated with MI in this sample of Tunisian population.
Highlights
Myocardial infarction (MI) is a coronary artery disease (CAD) caused by the degeneration of heart tissues as a result of blood clot formation in coronary arteries [1]
Tissue plasminogen activator (t-PA) produced by endothelial cells is involved in the breakdown of fibrin clot by converting plasminogen into plasmin, which leads to fibrinolysis [8]
The increased enzyme activity causes hyper-fibrinolysis which might leads to excessive bleeding whereas it's decreased activity result in thrombosis. t-PA-antigen might either play an important role in the development and progression of vascular disease, culminating in thromboembolic complications or death, or t-PA-antigen might just indicate the co-existence of confounders such as hypertension, insulin resistance, heart failure or ischemic heart disease, all of which can cause endothelial dysfunction and vascular injury [9]
Summary
Myocardial infarction (MI) is a coronary artery disease (CAD) caused by the degeneration of heart tissues as a result of blood clot formation in coronary arteries [1]. It represents one of the most important health problems in many nations worldwide [2]. MI is directly related to the thrombosis-fibrinolysis system which is regulated by factors involved either in clot formation and lysis [5]. Several gene polymorphisms of the fibrinolytic proteins and their cross regulators have been studied [6] and some studies founded that polymorphisms in genes encoding the components of thrombosis-fibrinolytic cascade may be a contributing factor in disease etiology by creating an imbalance between the two processes [7]. The presence of one I/D allele was associated with a 50% increase in risk of MI, whereas homozygous carriers had a two fold adjusted increase in risk, suggesting an association between the number of Alurepeats and arterial thrombosis [5,12]
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