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1. Association of Genes Related to Oxidative Stress with the Extent of Coronary Atherosclerosis

Author

Milena Racis, Anna Stanisławska-Sachadyn, Wojciech Sobiczewski, Marcin Wirtwein, Michał Krzemiński, Natalia Krawczyńska, Janusz Limon, Andrzej Rynkiewicz, and Marcin Gruchała

Subjects
oxidative stress, polymorphism, SNP, atherosclerosis, CAD, cardiovascular disease, Science
Abstract

Oxidative stress is believed to play a critical role in atherosclerosis initiation and progression. In line with this, in a group of 1099 subjects, we determined eight single nucleotide polymorphisms (SNPs) related to oxidative stress (PON1 c.575A>G, MPO c.−463G>A, SOD2 c.47T>C, GCLM c.−590C>T, NOS3 c.894G>T, NOS3 c.−786T>C, CYBA c.214C>T, and CYBA c.−932A>G) and assessed the extent of atherosclerosis in coronary arteries based on Gensini score. An increased risk of having a Gensini score in the higher half of the distribution was observed for the PON1 c.575G allele (odds ratio (OR) = 1.27, 95% confidence interval (CI): 1.004–1.617, p = 0.046). Next, the genetic risk score (GRS) for the additive effect of the total number of pro-oxidative alleles was assessed. We noted an increase in the risk of having a Gensini score above the median with the maximum number of risk alleles (OR = 2.47, 95% CI: 1.19–5.23, p = 0.014). A univariate Spearman’s test revealed significant correlation between the total number of pro-oxidant alleles (GRS) and the Gensini score (ρ = 0.068, p = 0.03). In conclusion, the PON1 c.575A>G variant and the high number of risk alleles (GRS) were independent risk factors for a high Gensini score. We suggest, however, that GRS might occur as a more valuable component in adding a predictive value to the genetic background of atherosclerosis.

Published
2020
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2. NADPH Oxidase Gene Polymorphism is Associated with Mortality and Cardiovascular Events in 7-Year Follow-Up

Author

Elżbieta Bluj, Andrzej Rynkiewicz, Milena Racis, Wojciech Sobiczewski, Marcin Gruchała, Michał Nedoszytko, Joanna Borzyszkowska, Anna Stanisławska-Sachadyn, Marcin Wirtwein, and Janusz Limon

Subjects
medicine.medical_specialty, medicine.medical_treatment, lcsh:Medicine, 030204 cardiovascular system & hematology, Lower risk, Article, CYBA, polymorphism, Coronary artery disease, 03 medical and health sciences, 0302 clinical medicine, cardiovascular disease, Internal medicine, medicine, CAD, cardiovascular diseases, Risk factor, Coronary atherosclerosis, 030304 developmental biology, 0303 health sciences, NADPH oxidase, business.industry, lcsh:R, Percutaneous coronary intervention, General Medicine, medicine.disease, Conventional PCI, Cardiology, Gene polymorphism, atherosclerosis, business, Mace
Abstract

The CYBA gene encodes the regulatory subunit of NADPH oxidase, which maintains the redox state within cells and in the blood vessels. That led us to investigate the course of coronary artery disease (CAD) with regards to CYBA polymorphisms. Thus, we recruited 1197 subjects with coronary atherosclerosis and observed them during 7-year follow-up. Three CYBA polymorphisms: c.214C&gt, T (rs4673), c.-932G&gt, A (rs9932581), and c.*24G&gt, A (1049255) were studied for an association with death, major adverse cardiovascular events (MACE) and an elective percutaneous coronary intervention or coronary artery bypass grafting (PCI/CABG). We found an association between the CYBA c.214C&gt, T polymorphism and two end points: death and PCI/CABG. CYBA c.214TT genotype was associated with a lower risk of death than C allele (9.5% vs. 21%, p &lt, 0.05) and a higher risk of PCI/CABG than C allele (69.3% vs. 51.7%, p &lt, 0.01). This suggests that the CYBA c.214TT genotype may be a protective factor against death OR = 0.47 (95%CI 0.28&ndash, 0.82, p &lt, 0.01), while also being a risk factor for an elective PCI/CABG OR = 2.36 (95%CI 1.15&ndash, 4.82, 0.05). Thus, we hypothesize that among patients with coronary atherosclerosis, the CYBA c.214TT genotype contributes to atherosclerotic plaque stability by altering the course of CAD towards chronic coronary syndrome, thereby lowering the incidence of fatal CAD-related events.

Published
2020

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