الفهرس 
Introduction and aim of the workOnly 14 pages are availabe for public view
 |  | from | 120 |  |  |
| | | from | 120 | | |
Abstract
Atherosclerosis is by far the most frequent underlying cause of coronary artery disease, carotid artery disease, and peripheral arterial disease. Atherosclerosis alone is rarely fatal; it is thrombosis, superimposed on a ruptured or eroded atherosclerotic plaque that precipitates the life-threatening clinical events such as acute coronary syndromes and stroke (Naghavi et al., 2003and Spagnoli et al ., 2004)
Inflammation plays a major role in all phases of atherosclerosis. Stable plaques are characterized by a chronic inflammatory infiltrate, whereas vulnerable and ruptured plaques are characterized by an ‘‘active’’ inflammation involved in the thinning of the fibrous cap, predisposing the plaque to rupture (Spagnoli et al., 2007).
As many as 50% of patients with atherosclerosis lack currently identified risk factors (such as hypertension, smoking, hypercholesterolemia, and diabetes), an observation indicating that additional factors predisposing to atherosclerosis are as yet undetected.
Discovery of such factors, along with their accompanying mechanisms of action, would have profound implications for the development of new therapeutic strategies that could reduce the devastating impact this disease is having in the western world and is beginning to have in countries where the populations are adopting western lifestyles.
Recent studies suggest that certain chronic infections increase the risk for cardiovascular disease, and that such infections may be considered novel and potentially modifiable risk factors (Stephen et al., 1999).
Several previous studies have suggested a link between arteriosclerotic disease and persistent infection or seropositivity of certain microorganisms. There are very few data on the relationship between HCV infection and atherosclerosis, however very recent results indicate that seropositivity for HCV shows a positive association with carotid artery plaque and intima-media thickening, independent of other risk factors for atherosclerosis (Ishizaka, 2002).
In our study we tried to find if there is any association between HCV seropositivity and atherosclerotic CAD or not.
The study group consists of 526 patients who underwent clinically indicated coronary angiography due to chest pain or non-invasive tests compatible with myocardial ischemia.
All patients gave a complete history included cardiovascular risk factors such as smoking habits, hypertension, diabetes, family history of premature coronary artery disease and dyslipidemia.
All patient with coronary arteries intervened with percutaneous coronary intervention were excluded from the analysis to exclude neointima/restenosis also all patient with previous history of CABG, coronary ectasia, and HBV positive patient are also excluded.
All patients included to the study were subjected to quantitative coronary analysis
For each patient we calculate:
1. Number of lesions.
2. Average of minimum luminal diameter for all lesions (Colin Berry et al., 2007).
3. Modified reardon severity score (OmerAlyan et al., 2008).
4. Extent score.
The patients then divided into two groups:
1. HCV positive patients.
2. HCV negative patients.
Each group is then subdivided into two groups according to coronary angiography either normal or has atherosclerotic coronary artery disease.
Study group consists of 526patients; 153 with seropositive HCV (29.4%) (Mean age 54.9±9.1 and 64.7% males) vs 367 with seronegative HCV (70.6%) (Mean age 53.2±11.1 and 58% males with no significant difference between two groups regarding age, sex, DM, hypertension and family history of premature CAD.
In the group of HCV seropositivity (153 patients) 68 (44.4%) patients have normal coronary angiography, and 85 (55.6%) patients have atherosclerotic CAD (p=0.2), there is no significant difference between two groups in terms of diabetes mellitus, family history, hypertension, and dyslipidemia, however there was significant difference between two groups as regard age (p=0.01), sex (p=0.001), and smoking (p=.004) in the group of HVC seropositivity with atherosclerotic CAD.
In the group of HCV seronegativity (367 patients) 140 (38.1%) have normal coronary angiography, and 227 patients (62.9%) have atherosclerotic CAD (p=0.2) there was statistically significant differences between two groups as regard age, sex, family history, diabetes, and smoking, no difference as regard hypertension (p=.05) and dyslipidemia (p=0.3).
227 patients with seronegative HCV and have atherosclerotic CAD and 85 with seropositive HCV have atherosclerotic CAD. Baseline demographic characteristics of the patients in both groups there was no significant differences between the groups in terms of age, family history, diabetes and hypertension; but our study shows significant differences between two groups as regard sex (p=0.001), smoking (p=0.01)and dyslipidemia (p=.008)
In comparison of the angiographic parameters of the patients in both groups we found that there is no statistically significant difference between HCV seropositive patient and HCV seronegative patient regarding average of MELD (p=0.1), extent score (p=0.5), Reardone score (p=0.5), and lesion number (p=0.4).
Multivariate analysis showed that HCV is not considered as independent risk factor for atherosclerotic CAD odds ratio 1.2 (95% CI 0.7 to 1.9, p =0.3).