Relationship between rs854560PON1Gene Polymorphism and Tobacco Smoking with Coronary Artery Disease

Paraoxonase-1 (PON1) is the antioxidant marker of high-density lipoproteins protecting against atherosclerosis and coronary artery disease (CAD) phenotype. The purpose of the present study was to determine whether thePON1gene rs854560 polymorphism (163T>A) is associated with CAD in Polish population. rs854560 was genotyped in 494 subjects: 248 patients with premature CAD and 246 blood donors as a control. We found that the risk of CAD was significantly higher in TT homozygotes than in A allele carriers (OR = 1.87,p=0.041). The synergistic effect between the TT genotype and cigarette smoking was observed (SIM = 9.81; SI = 14.70). The relative increase in risk from interaction between factors was over 37 (RERI = 36.13). ThePON1polymorphism did not modulate the risk of CAD in response to exposure to other traditional risk factors. In conclusion, the rs854560 polymorphism may modulate the risk of CAD in response to cigarette smoking in Polish population. Carriers of TT genotype seem to be particularly at risk of CAD, when exposed to cigarette smoking.

Download Full-text

Paraoxonase-1 and Simvastatin Treatment in Patients with Stable Coronary Artery Disease

International Journal of Vascular Medicine ◽

10.1155/2016/6312478 ◽

2016 ◽

Vol 2016 ◽

pp. 1-10

Author(s):

Rafał Januszek

Keyword(s):

Coronary Artery Disease ◽

Coronary Artery ◽

Stable Coronary Artery Disease ◽

Paraoxonase 1 ◽

High Density Lipoproteins ◽

Pon1 Activity ◽

Control Group ◽

Simvastatin Treatment ◽

Simvastatin Therapy ◽

Artery Disease

Background.Paraoxonase-1 (PON1) is the crucial antioxidant marker of high-density lipoproteins. The present study is aimed at assessing the effect of simvastatin treatment on PON1 activity and its relationship to Q192R and M55L polymorphisms in subjects with stable coronary artery disease (CAD).Methods.The patient group was composed of 53 individuals with stable CAD, and the control group included 53 sex-matched police officers without CAD. CAD patients were treated with simvastatin 40mg/day for 12 months. Respectively, flow mediated dilatation (FMD), serum hs-CRP and TNF-αlevels, urinary 8-iso-PGF2αconcentrations, and PON1 activity were evaluated in definitive intervals.Results.There was no effect of simvastatin treatment on urinary 8-iso-PGF2α. Simvastatin treatment significantly increased FMD value, decreased CRP and TNF-αconcentration. After adjusting for PON1 genotypes, significantly higher PON1 activity was noted in the 192R allele carriers, in both groups. Regardless of genotype, PON1 activity remained stable after simvastatin treatment.Conclusions.The present study confirms a positive effect of simvastatin therapy on endothelial function and inflammatory markers in secondary prevention. Simvastatin treatment shows no effects on PON1 activity and 8-isoprostanes level. The effect of simvastatin therapy on PON1 activity is not modulated by Q192R and M55L polymorphisms.

Download Full-text

The TT Genotype of the MTHFR 677C>T Polymorphism Increases Susceptibility to Premature Coronary Artery Disease in Interaction with Some of the Traditional Risk Factors

Acta Medica (Hradec Kralove Czech Republic) ◽

10.14712/18059694.2015.42 ◽

2012 ◽

Vol 55 (4) ◽

pp. 172-179 ◽

Cited By ~ 3

Author(s):

Beata Sarecka-Hujar ◽

Iwona Zak ◽

Jolanta Krauze

Keyword(s):

Risk Factors ◽

Coronary Artery Disease ◽

Coronary Artery ◽

Premature Coronary Artery Disease ◽

Environment Interaction ◽

Increased Risk ◽

Premature Cad ◽

Traditional Risk Factors ◽

Artery Disease ◽

Chol Level

Background: The presence of several risk factors (genetic and non-genetic) has greater impact on the risk of premature coronary artery disease (CAD) than single risk factor. Objective: The aim of the study was to establish possible relations between genotypes and alleles of 677C>T polymorphism ofMTHFRgene and some traditional risk factors e.g. elevated levels of lipid parameters and smoking in development of premature CAD. Methods: The groups comprised 152 patients with angiographically documented premature CAD (aged 42.9 ± 5.5) and 121 age-matched blood donors (aged 42.3 ± 6.5) were studied. TheMTHFR677C>T polymorphism was genotyped with Polymerase Chain Reaction-Restriction Fragment Length Polymorphism (PCR-RFLP) method. Results: Patients with TT genotype who simultaneously smoked had increased risk of premature CAD compared to non-smoking cases with CC genotype (OR = 24.62). We also found that individuals with TT genotype and elevated LDL-cholesterol (LDL-chol.) level had significantly higher risk of CAD (OR = 9.92) than individuals with normal LDL-chol. level and CC genotype. Conclusions: The present study shows that simultaneous presence ofMTHFRTT genotype and smoking or elevated levels of LDL-chol. influences the risk of premature CAD. This findings give interesting contribution to gene-environment interaction problem that may have clinical implications in the future.

Download Full-text