الفهرس 
CORONARY ARTERY DISEASEOnly 14 pages are availabe for public view
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Abstract
C
oronary artery disease (CAD) is a leading cause of mortality, morbidity and disability worldwide. It includes stable angina and acute coronary syndrome which ranges from unstable angina to acute myocardial infarction. Atherosclerosis is a chronic inflammatory disease which is considered the underlying pathogenic process in CAD.The pathogenesis of atherosclerosis results from the interaction between biology of arterial wall and various stress stimuli present in circulating blood as oxidized low density lipoprotein, tobacco toxins and hyperglycemia.
CXCL16 is a protein with both scavenger and inflammatory chemokine like action. There are three forms of CXCL16 a membrane bound form, a soluble form and a cellular form. It is expressed in macrophages and aortic smooth muscles but not found in normal arteries. CXCL16 has been implicated in a variety of inflammatory diseases such as hepatitis and encephalitis. The receptor of CXCL16 has been identified as CXCR6 which is abundant in inflammatory cells as natural killer cells and T-helper cells. The binding between CXCL16 and CXCR6 increases nuclear factor kappa B and tumor necrosis factor which attracts NK cells and TH1 that induces the immune response. The aim of our study is to evaluate the role of serum CXCL16 in coronary disease through studying its relationship to the severity of coronary artery occlusion.
This study was conducted on 65 patients with CAD and 20 apparently healthy subjects from cardiology and emergency department in Ain Shams University Hospital and Nasr Insurance hospital. The patients groups were divided into 3 groups 25 patients with SA who have stable effort angina for more than 6 months, 15 patients with UA who have ischemic chest pain at rest in the preceding 48h with no evidence of necrosis, and 25 patients with AMI who have ischemic chest pain at rest in the preceding 48h with elevated biomarkers of necrosis. A number of clinical conditions which could interfere with CXCL16 levels were excluded as peripheral vascular disease, fever, liver disease, renal dysfunction, autoimmune disease and malignancy. All patients in our study underwent coronary angiography and our marker was correlated to the degree of vessel disease either single, two or multivessel disease and within different patients groups in comparison to control group.
Statistical comparison of serum CXCL16 in different studied groups revealed that CXCL16 was significantly higher in CAD patients collectively compared to control group (t=2.653 and p<0.001). This agreed with Smith et al., 2008 and was explained by the fact that CXCL16 is expressed in macrophages and atherosclerotic plaques in response to inflammation and not present in normal arteries.
However, no significant difference in CXCL16 level was observed between SA, UA and AMI (p<0.05) and these results were in accordance with those of Sheikine et al., 2009 and Lehrhe et al., 2007.The possible explanation to this is that CXCL16 is related to the atherosclerotic burden rather than the clinical presentation which is related to the vulnerability of the plaques to complicate further more it may to be related to other factor such as hypercoagulable blood and myocardium without efficient collaterals.
Also there are statistical significance between CXCL16 and the degree of vessel disease as it showed higher level in multivessel than in single vessel disease (p value<0.05) and the best diagnostic cut off was 1.6 ng/ml. This cut off provides both sensitivity, specificity, PPV and NPV of 79.8%, 84.4%, 64% and 90% respectively. This was explained by the fact that atherosclerotic plaques exerts more burden hence more inflammation and more CXCL16 is released in response to inflammatory cytokines.
Also there was positive correlation between CXCL16 and levels of cholesterol, triglycerides and LDL cholesterol (r values were 0.8, 0.9, and 0.6 respectively). This emphasized the effect of dyslipidemia on atherosclerosis.
And so the value of CXCL16 is to identify high risk patients with multivessel disease regardless of their clinical presentations with accepted sensitivity, specificity and NPV.
It is recommended to measure CXCL 16 in patient with CAD as one of risk stratification methods to detect not only its presence but also to predict the disease severity (mutivessel disease).