PURPOSE: The precise molecular mechanisms culminating in coronary artery disease (CAD) are not well understood, despite a wealth of knowledge on predisposing risk factors and pathomechanisms. CAD and myocardial infarction (MI) are complex genetic diseases; neither the environment alone, nor a single gene, cause disease, rather, a mix of environmental and genetic factors lead to atherosclerosis of the coronary arteries. MATERIALS AND METHODS: In the present study, our aim was to investigate the roles of prothrombin G20210A mutation and Factor VLeiden mutation in atherosclerotic coronary artery disease. 287 subjects (106 control subjects, who were angiographically normal, and 181 angiographically documented coronary atherosclerotic patients who exhibited coronary artery narrowing to a degree of > or = 50%) were included in this study. The mutations were assessed with LightCycler Real-Time PCR mutation detection kits (Roche Diagnostics, GmbH, Germany). RESULTS: 6.6% of control subjects, and 6.1% of patients with (50% coronary artery narrowing were determined to have the Factor VLeiden heterozygote mutation. 6.6% of control subjects had the Prothrombin G20210A heterozygote mutation, while 7.7% of patients with (50% coronary artery narrowing had this mutation. The OR for Factor VLeiden was 1.52 (CI: 0.240-9.602) and for Prothrombin G20210A mutation, the OR was 1.415 (CI: 0.287-6.962). CONCLUSION: Although both the heterozygote Factor VLeiden and Prothrombin gene mutations were more frequent in patients with CAD than in control subjects, there was no statistical relationship found to exist between coronary artery disease and the Factor VLeiden and Prothrombin G20210A mutations.
Aged ; Coronary Artery Disease/*genetics ; Factor V/*genetics ; Female ; Gene Frequency ; Genotype ; Humans ; Male ; Middle Aged ; *Polymorphism, Single Nucleotide ; Prothrombin/*genetics

Cardiovascular disease (CVD) is still the major cause of the morbidity and mortality in hemodialysis (HD) patients. The characteristics of major arterial changes, atherosclerosis and related risk factors in HD patients remain unclear. We aimed to evaluate the atherosclerotic process in asymptomatic HD patients and healthy volunteers, and to determine the association between the risk factor (s) and the atherosclerotic process in these groups. 92 HD patients (female: 43, male: 49) and 62 age and sex matched healthy volunteers (female: 27, male: 35) were enrolled in this study. Diabetics, smokers, and patients with symptomatic CVD were excluded. The right and left carotid intima-media thicknesses (CIMTs) were measured and plaque structures were studied by B-mode ultrasound. The mean CIMT in patients and control group were 0.79 +/- 0.16 mm and 0.54 +/- 0.09 mm, respectively. Mean CIMT in HD patients was thicker (p < 0.001) and the presence ratio of plaque was higher in patients group (n=38, %61.2 vs n=9, %17.3) (p < 0.001). Calcified type of plaque was more frequent in HD patients than control group. Age (r=0.48, p < 0.001), left ventricular mass (r=0.42, p < 0.05), and homocysteine (r=0.46, p < 0.01), mean hematocrit (r=-0.36, p < 0.05), plasma CRP (r=0.50, p < 0.001), ESR (r=0.43, p < 0.01) and albumin (r= -0.34, p < 0.05) levels were correlated with the CIMT measurements and plaque presence, significantly. -CIMT as an atherosclerotic process indicator is thicker in asymptomatic HD patients than healthy subjects. We concluded that in addition to various classical risk factors, uremic environment may also contribute to acceleration of the atherosclerotic process.
Adult ; Aged ; Carotid Artery Diseases/*epidemiology/*pathology ; Female ; Human ; Incidence ; Kidney Failure, Chronic/*epidemiology/therapy ; Male ; Middle Aged ; *Renal Dialysis ; Risk Factors