ABSTRACT
Activation of inflammation and coagulation are closely related and mutually interdependent in myocardial infarction [MI]. The acute-phase protein, plasminogen activator inhibitor-1 [PAI-1], is a key element in the inhibition of fibrinolysis. Elevated levels of PAI-1 have been related to MI. There are controversial data regarding the impact of 4G/5G polymorphism of the PAI-1 gene in the pathogenesis of MI. Patients with MI exhibited significantly higher plasma PAI-1 levels than controls. Significant changes in PAI-1 levels were found in homozygous PAI-1 4G/4G carriers compared with other 4G/5G genotype carriers in patients with MI. The allelic frequency of 4G among the patients was 83.3%; that of 5G was 16.7%. In the control group, the allelic frequencies of 4G and 5G were 62.0% and 38.0% respectively. The difference in genotype distribution between the two groups was significant. There were significant associations between MI and the 4G allele, hypertension, smoking, and family history of coronary heart disease. Our findings suggest that the 4G allele of the PAI-1 promoter polymorphism is an independent risk factor for MI. The emerging evidence that circulating levels of PAI-1 relate to genotype at a common polymorphism in the promoter of the PAI-1 gene has opened the possibility of using PAI-1 genotype as a surrogate measure of pre-morbid PAI-1 levels to tease apart the cause and effect limbs of the PAI-1-coronary disease relationship. The detection of this allele along with other risk factors may therefore be useful in primary prevention