Uric acid level and its association with carotid Intima-media thickness in patients with cardiac syndrome X

The aim of our study was to evaluate serum uric acid level and its relationship with carotid intima-media thickness [CIMT] in patients with cardiac syndrome X [CSX]. A total of 50 patients with CSX [28 females/22 males, 51.0 +/- 10.9 years] and 40 controls [27 females/13 males, 53.0 +/- 10.2 years] were included in the study. All subjects underwent a noninvasive stress test and conventional coronary angiography. Serum uric acid levels were measured and B mode ultrasonography was performed to assess CIMT in all subjects. Serum uric acid levels were higher in patients with CSX than in the control subjects [5.1 +/- 1.8 vs. 3.9 +/- 1.3 mg/dl; p = 0.002]. The CIMT was higher in patients with CSX than in the control subjects [0.75 +/- 0.18 vs. 0.63 +/- 0.09 mm; p < 0.001]. A significant correlation was found between serum uric acid values and CIMT measurements in patients with CSX [r = 0.666, p < 0.001]. Serum uric acid levels were higher in patients with CSX and elevated serum uric acid levels were associated with carotid atherosclerosis, thereby indicating that elevated serum uric acid levels might contribute to the development of subclinical atherosclerosis in CSX patients

Factor VLeiden and Prothrombin G20210A Gene Polymorphisms in Patients with Coronary Artery Disease

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.