الفهرس 
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Abstract
Atherothrombosis, defined as atherosclerotic plaque disruption that leads to the development of thrombosis, is a leading cause of morbidity and mortality. It is the most common cause of acute coronary syndromes (including unstable angina and acute myocardial infarction), ischemic stroke, and peripheral occlusive disease.
Under physiological conditions, platelets do not interact with the vessel wall. Injury of vascular intima disrupts the antithrombotic properties of endothelium, and exposes the blood to adhesive molecules of the subendothelium. Platelet adhesion to the damaged vessel wall is the first step in development of thrombosis.
Arterial thrombosis is initiated by the spontaneous or mechanical rupture of atherosclerotic plaque, where circulating platelets act as a first line of defense to prevent blood loss. Beside platelet aggregation to occlude the lesion, platelets also release growth factors from their granules that contribute to the migration and proliferation of smooth muscle cells and monocytes. These processes are essential in developing atherothrombotic lesion.
Additionally, platelets may generate pro-coagulant rich particles, called micro-particles, a circulating cell fragments derived from the activated cells. Micro-particles contain negatively charged phospholipids essential for coagulation reaction, and express Tissue factor (TF) on their surface, and through this mechanism, they contribute to the pro-thrombotic state.
TF, formerly known as thromboplastin, is the key initiator of the coagulation cascade; it binds factor VIIa resulting in activation of factor IX, and factor X, ultimately leading to fibrin formation.
The aim of this study was to investigate the expression of tissue factor on platelet monocyte aggregates, and platelets as a participating factor in the pathogenesis of acute coronary syndrome.
The present study was conducted on 70 subjects divided into 3 groups:
group I (included 25 patients with AMI, 20 males, and 5 females, with age range from 48 to 70 Y/O, with a mean ± SD of 58.8±6.1Y/O.
group II (included 25 patients with SA, 15 males and 10 females, with age range from 47-68 Y/O, with a mean age ± SD of 59.1±6.7 Y/O.
group III (included 20 apparently healthy subjects served as a control group, 15 males and 5 females, with age range from 48- 68Y/O, with a mean ± SD of 57.8±6.3 Y/O.
Patients were selected following the exclusion criteria: Patients using drugs interfering with platelet functions except low dose aspirin were excluded from this study.
All patients and control groups subjected to the following: Full history taking (past history including history of DM, hypertension, smoking, dyslipidemia, recurrent chest pain, family history, and drug history), thorough clinical examination.
The following laboratory investigations were done: CBC, quantitative troponin I and CK MB mass, hs- CRP was measured in the serum using ELISA method, and flowcytometery analysis of tissue factor on platelet monocyte aggregates and platelets.
The results of this study revealed that:
There was no significant difference between the studied groups (AMI, SA and controls) regarding platelet count; a highly significant difference between the studied groups regarding hs-CRP; a significant difference between the studied groups regarding serum cholesterol, TG, LDL-c, and HDL-c and a highly significant difference between the studied groups regarding PTF%, absolute PTF and PMA TF.
Also, there was a highly significant difference between smokers and non smokers, as regards to PTF%, absolute PTF, and PMA TF being higher in smokers than non smokers; and a significant difference between diabetics, and non-diabetics, as regards to PTF%, absolute PTF, and PMA TF being higher in diabetics than non-diabetics.
There was a highly significant positive correlation between PMA TF and cholesterol, and no significant correlation between PTF%, absolute PTF and serum cholesterol.
There was a highly significant positive correlation between PMA TF and TG; a highly significant positive correlation between PTF% and TG; and a significant positive correlation between absolute PTF and TG.
There was a highly significant positive correlation between PMA TF, PTF%, and absolute PTF and LDL-c; and a highly significant negative correlation between PMA TF, PTF%, and absolute PTF and HDL-c.
There was no significant correlation between PMA TF and hs-CRP, but a highly significant positive correlation between PTF%, and absolute PTF and hs-CRP.
PTF (Absolute) was independent risk factor for cardiovascular diseases with odds ratio (3.5) and confidence interval (1.4-19.4) then followed by PMA TF with odds ratio (3.3) and confidence interval (1.7-13.9) then followed by PTF % with odds ratio (2.3) and confidence interval (2.9-16.9).
ROC curve shows that the PMA TF at cut off point of 2.35 predicts AMI with sensitivity 90%, specificity 92%, PPV 81.8%, and NPV 95.8%.
The PTF% at cut off point 1.85 predicts AMI with sensitivity 95%, specificity 68%, PPV 54.3% and NPV 97.1%.
Absolute PTF at cut off point 5272 predicts AMI with sensitivity 95%, specificity 54%, PPV 45.2%, and NPV 96.4%.