الفهرس 
Introduction and RationaleOnly 14 pages are availabe for public view
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Abstract
Coronary artery disease (CAD) is considered as the principal cause of death, affecting nearly every nation, ethnicity, and economic stratum. CAD is partially inherited; great efforts have been devoted to explore the genetic basis of CAD. Genetic studies led to the emergence of many challenges related to understanding how DNA variants are connected to function, and in translation of genetics to the clinic, as promising opportunities to elucidate new target therapies.
Tissue factor pathway inhibitor (TFPI) is a multivalent, Kunitz-type, serine protease inhibitor, the TFPI inhibits both tissue factor-activated factor VII and activation of factor X, thereby downregulating the tissue factor (TF)-dependent pathway, consequently limiting clot growth and preventing prothrombin to thrombin conversion. TFPI is an anticoagulant protein that is expressed primarily in the vascular endothelium, megakaryocytes, platelets and plasma.
In recent years, considerable progress has been made in discovering the genetic variants of TFPI and understanding of their implications on molecular function, and published data remains controversial. The present study was designed to explore whether TFPI-rs7586970 genetic variant, could influence the TFPI plasma level, with subsequent potential modification of the risk of myocardial infarction (MI), which may give rise to a new biomarker of MI risk, and novel treatment targets; so preventive measures can be implemented to reduce its health and economic burden of MI.
The present descriptive case control study aimed to assess the TFPI plasma level in conjunction with TFPI: rs7586970 genetic variant in patients with MI