This study indicates that low activity of GPx, SOD and Zn concentration are associated with CHD patients. We hypothesize that hyperhomocysteinaemia and low antioxidant enzyme activities may increase the extent of CHD.

BACKGROUND AND OBJECTIVES:A state of low-grade inflammation accompanies the pathogenesis of atherosclerotic events. Interleukin-6 (IL-6) is a pleotropic pro-inflammatory cytokine that modulates the development of acute coronary syndromes (ACSs), partly by destabilizing coronary atherosclerotic plaques. We have examined the contribution of the -174G>C IL-6 promoter variant on the risk of coronary artery disease (CAD) among Tunisians.PATIENTS AND METHODS:Study subjects included 418 CAD patients and 406 age- and sex-matched controls. IL-6 genotyping was done by PCR–restriction fragment length polymorphism.RESULTSThe frequency of the -174C allele (mutant) was lower in Tunisians than in Europeans, and the distribution of -174 G>C genotypes was similar between CAD patients and control subjects. Moreover, compared to GG genotype carriers, -174C allele carriage did not increase the CAD relative risk (odds ratio and 95% confidence interval=1.09 and 0.80-1.49), which remained nonsignificant after adjusting for traditional risk factors for CAD (age, smoking, hypertension, diabetes and obesity).CONCLUSIONThe -174G>C IL-6 promoter variant is not associated with an increased risk of CAD among Tunisians.

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The contribution of human platelet antigen (HPA)-1 (GPIIb/IIIa), HPA-2 (GPIb/IX), and HPA-3 (GPIIb/IIIa) polymorphisms to the risk of coronary artery disease (CAD) was investigated in 341 CAD patients and 316 matched control subjects. HPA genotyping was performed by PCR-SSP. Regression analysis was employed in assessing the contribution of these variants to CAD risk. The frequency of HPA-1b (P = .009) and HPA-3b (P = .004) alleles, and HPA-1a/1b (P = .045), HPA-1b/1b (P = .007), and HPA-3b/3b (P = .008) genotypes were higher in patients than control subjects. No significant association was demonstrated between the HPA variants and 1-, 2- and 3-vessel disease. HPA-1b/2a/3b (Pc = .021) and HPA-1b/2b/3a (Pc = .002) haplotypes were positively associated with CAD, thereby conferring a disease susceptibility nature to these haplotypes. Multivariate analysis confirmed the positive association of HPA-1b/2a/3b (aOR = 3.72; 95% CI = 1.49-9.28), and in addition identified HPA-1b/2a/3a (aOR = 2.49; 95% CI = 1.06-5.86) to be positively associated with CAD, after adjusting for a number of covariates. Our results demonstrate positive association of HPA variants and specific HPA-1/HPA-2/HPA-3 haplotypes with CAD in Tunisians.

BackgroundThe effects of Ramadan fasting (RF) on clopidogrel antiplatelet inhibition were not previously investigated. The present study evaluated the influence of RF on platelet reactivity in patients with high cardiovascular risk (CVR) in particular those with type 2 diabetes mellitus (DM).MethodsA total of 98 stable patients with ≥2 CVR factors were recruited. All patients observed RF and were taking clopidogrel at a maintenance dose of 75 mg. Clinical findings and serum lipids data were recorded before Ramadan (Pre-R), at the last week of Ramadan (R) and 4 weeks after the end of Ramadan (Post-R). During each patient visit, nutrients intakes were calculated and platelet reactivity assessment using Verify Now P2Y12 assay was performed.ResultsIn DM patients, the absolute PRU changes from baseline were +27 (p = 0.01) and +16 (p = 0.02) respectively at R and Post-R. In addition, there was a significant increase of glycemia and triglycerides levels with a significant decrease of high-density lipoprotein. In non DM patients there was no significant change in absolute PRU values and metabolic parameters. Clopidogrel resistance rate using 2 cut-off PRU values (235 and 208) did not change significantly in DM and non DM patients.ConclusionsRF significantly decreased platelet sensitivity to clopidogrel in DM patients during and after Ramadan. This effect is possibly related to an increase of glycemia and serum lipids levels induced by fasting.Trial registrationClinical Trials.gov NCT02720133. Registered 24 July 2014.Retrospectively registered.