Association between Endothelial Nitric Oxide Synthase Gene Polymorphism (Glu298Asp) and Coronary No-Reflow Phenomenon in Acute Myocardial Infarction

WOS: 000490553700005Aim: No-reflow phenomenon is an important complication of primary percutaneous coronary intervention. Several variants in the endothelial nitric oxide synthase gene, which reduce endothelial nitric oxide synthase activity, are a risk factor for coronary heart disease. However, its role in no-reflow phenomenon has not yet been revealed. This study aimed to investigate whether there is a relationship between endothelial nitric oxide synthase Glu298Asp gene variant and the development of coronary no-reflow phenomenon in patients with ST elevation myocardial infarction. Material/Methods: The study was conducted among 116 patients undergoing primary percutaneous coronary intervention for ST elevation myocardial infarction. Group 1 included 52 ST elevation myocardial infarction patients undergoing no-reflow phenomenon as a study group. Group 2 comprised 64 ST elevation myocardial infarction patients without no-reflow phenomenon as a control group. Endothelial nitric oxide synthase was tested using polymerase chain reaction-restriction fragment length variant. Results: The prevalence of TT genotype of endothelial nitric oxide synthase Glu298Asp gene variant was found to be significantly higher in patients developing coronary no-reflow when compared to those without no-reflow (p = 0.016; 11.54% vs. 1.56%) (OR = 10.85, 95% CI = 1.22-96.39). However, a similar association for the heterozygous GT genotype of endothelial nitric oxide synthase Glu298Asp gene variant was not observed between the two groups. Conclusions: The results of this preliminary study indicate that there is an association between Glu298Asp variant in endothelial nitric oxide synthase gene and the development of no-reflow phenomenon in ST elevation myocardial infarction. The presence of homozygous TT allele may contribute to tendency to the development of no-reflow phenomenon

Association between serum vitamin D levels and subclinical coronary atherosclerosis and plaque burden/composition in young adult population

Evidence suggests that low 25-OH vitamin D 25(OH)D concentrations may increase the risk of several cardiovascular diseases such as hypertension, peripheral vascular disease, diabetes mellitus, obesity, myocardial infarction, heart failure and cardiovascular mortality. Recent studies suggested a possible relationship between vitamin D deficiency and increased carotid intima-media wall thickness and vascular calcification. We hypothesized that low 25(OH)D may be associated with coronary atherosclerosis and coronary plaque burden and composition, and investigated the relationship between serum vitamin D levels and coronary atherosclerosis, plaque burden or structure, in young adult patients by using dual-source 128x2 slice coronary computed tomography angiography (CCTA). We included 98 patients with coronary atherosclerosis and 110, age and gender matched, subjects with normal findings on CCTA examinations. Patients with subclinical atherosclerosis had significantly higher serum total cholesterol, triglycerides, hs-CRP, uric acid, HbA1c and creatinine levels and lower serum 25(OH)D levels in comparison with controls. There was no significant correlation between 25(OH)D and plaque morphology. There was also a positive relationship between 25(OH)D and plaque burden of coronary atherosclerosis. In multivariate analysis, coronary atherosclerosis was associated high hs-CRP (adjusted OR: 2.832), uric acid (adjusted OR: 3.671) and low 25(OH)D (adjusted OR: 0.689). Low levels of 25(OH)D were associated with coronary atherosclerosis and plaque burden, but there was no significant correlation between 25(OH)D and plaque morphology

A study of the combination of oxaliplatin, capecitabine, and herceptin (trastuzumab) and chemoradiotherapy in the adjuvant setting in operated patients with HER2+gastric or gastro-esophageal junction cancer (TOXAG study).

Gastrointestinal Cancers Symposium -- JAN 21-23, 2016 -- San Francisco, CAWOS: 00037810960017