الفهرس 
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Abstract
Thrombotic disorders represent a major cause of human morbidity and mortality worldwide. Acute myocardial infarction (AMI) and deep vein thrombosis (DVT) are of special concern because of their high frequency and fatality rates. The current concept of blood coagulation emphasizes the physiological role of tissue factor pathway in initiating the coagulation process in vivo. Since then, intensive and extensive studies have been carried out to address the role of TFPI in health and disease. The present study was designed to: • Assess the status of plasma TFPI in patients with acute myocardial infarction and deep vein thrombosis patients. • Assess the significance of G38123T polymorphism in patients with deep vein thrombosis To achieve this aim, a total of 95 subjects were enrolled in this study. They were categorized into the following groups: Group I: 20 controls, Group II: 10 ADVT patients, Group III: 35 RDVT patients, Group IV: 10 AMI patients, Group V: 20 old MI patients. All patients and controls were subjected to the following: • Screening tests of haemostasis, Measurement of plasma TFPI antigen levels, Analysis of TFPI gene for detection of G38123T polymorphism within intron 6 in 19 RDVT patients and 10 controls. The results could be summarized as follows: • There was non-significant increase in total plasma levels of TFPI in both ADVT and RDVT groups compared to controls. • There was highly significant decrease in post-heparin TFPI in both ADVT and RDVT groups compared to controls. • There was non-significant difference of total plasma levels of TFPI in AMI with mild significant increase in old MI group compared to controls. • There was significant decrease in the post-heparin TFPI levels in AMI with non-significant decrease in old MI groups compared to controls. • The cut off value for normal total TFPI level (40.39 ng/ml). Two out of 35 patients with RDVT had total plasma levels of TFPI below the cut off value. • There were 15 out of 35 patients with RDVT had post-heparin levels below the cut off value (237.12 ng/ml) and 9 out of 10 patients with ADVT had post-heparin levels below the cut off value. • Eleven out of 19 RDVT patients (57.9%), had post-heparin TFPI levels below the cut off value and 8 out 19 patients (42.1%) had post-heparin levels of TFPI above the cut off value. • There were 9 out of 10 patients with AMI had post-heparin levels of TFPI below the cut off value and 2 out of 20 patients with old MI had post-heparin levels of TFPI below the cut off value. • Three out of 10 cases (30%) in controls with G38123T polymorphism and 9 out of 19 cases (47.4%) with G38123T polymorphism in RDVT patients with non-significant difference between the frequency of polymorphism in RDVT patients compared to controls. • G38123T polymorphism was found in 30% (3 out of 10) RDVT patients with total plasma TFPI levels below the cut off value (62.97 ng/ml). And in 66.6% (6 out of 9) of RDVT patients above the cut off value. The estimated Odd’s ratio was 4.667 which was statistically insignificant. • Eight out of 11 cases (72.7%) with RDVT with post heparin levels below the cut off value had polymorphism and one out of 8 cases (12.5%) with RDVT above the cut off value had polymorphism. The estimated Odd’s ratio was 18.6, which was significant (P<0.021). Conclusions: • There are increased levels of total plasma TFPI in old MI patients that might have a protective role against recurrence of coronary thrombosis. • There are low heparin releasable plasma levels of TFPI in AMI patients. Whether this low level reflects a consumptive phenomenon or has a pathogenitic role in coronary thrombosis needs further elucidation. • There is no association between total plasma TFPI levels and venous thromboembolism. • There is association between low heparin releasable TFPI levels and venous thromboembolism. • G38123T polymorphism within intron 6 of TFPI gene could not be considered as an independent risk factor for DVT. • The combined association of G38123T polymorphism with total plasma TFPI levels is not considered as independent risk factor for DVT. • The combined association of G38123T polymorphism with low heparin releasable TFPI levels is considered a risk factor for DVT. Recommendations: Further studies are required to elucidate the underlining mechanism by which G38123T influences TFPI gene expression.