Dataset Information

SCARB1 Gene Polymorphisms and HDL Subfractions in Coronary Artery Disease.

ABSTRACT: BACKGROUND/AIM:Cardiovascular diseases are a leading cause of mortality and morbidity worldwide. Polymorphisms in the SCARB1 gene are known to be related to plasma lipids. PATIENTS AND METHODS:Real time-polymerase chain reaction (RT-PCR) was used for identification of SCARB1 polymorphisms and the Lipoprint Quantimetrix System was employed in identification of HDL subfractions. RESULTS:According to allelic distribution, in both groups SCARB1 AA genotype led to a two-fold decrease in the risk of developing cardiovascular disease (p=0.04), while the GA genotype increased the risk two-fold (p=0.03). According to the HDL subfraction analysis results, the AA genotype had higher levels of big-sized HDL subfraction (p=0.02). CONCLUSION:The SCARB1AA genotype decreased cardiovascular risk and carrying GA genotype and G allele increased the risk of CAD. AA genotype carriers had higher levels of big-sized HDL subfraction.

SUBMITTER: Ayhan H

PROVIDER: S-EPMC5656860 | biostudies-literature | 2017 Sep-Oct

REPOSITORIES: biostudies-literature

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<i>SCARB1</i> Gene Polymorphisms and HDL Subfractions in Coronary Artery Disease.

Ayhan Huseyin H Gormus Uzay U Isbir Selim S Yilmaz Seda Gulec SG Isbir Turgay T

In vivo (Athens, Greece) 20170901 5

<h4>Background/aim</h4>Cardiovascular diseases are a leading cause of mortality and morbidity worldwide. Polymorphisms in the SCARB1 gene are known to be related to plasma lipids.<h4>Patients and methods</h4>Real time-polymerase chain reaction (RT-PCR) was used for identification of SCARB1 polymorphisms and the Lipoprint Quantimetrix System was employed in identification of HDL subfractions.<h4>Results</h4>According to allelic distribution, in both groups SCARB1 AA genotype led to a two-fold dec ...[more]

PMID: 28882953

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Project description:Background Although acute coronary syndromes (ACS) are a major cause of morbidity and mortality, relationships with biologically active lipid species potentially associated with plaque disruption/erosion in the context of their lipoprotein carriers are indeterminate. The aim was to characterize lipid species within lipoprotein particles which differentiate ACS from stable coronary artery disease. Methods and Results Venous blood was obtained from 130 individuals with de novo presentation of an ACS (n=47) or stable coronary artery disease (n=83) before coronary catheterization. Lipidomic measurements (533 lipid species; liquid chromatography electrospray ionization/tandem mass spectrometry) were performed on whole plasma as well as 2 lipoprotein subfractions: apolipoprotein A1 (apolipoprotein A, high-density lipoprotein) and apolipoprotein B. Compared with stable coronary artery disease, ACS plasma was lower in phospholipids including lyso species and plasmalogens, with the majority of lipid species differing in abundance located within high-density lipoprotein (high-density lipoprotein, 113 lipids; plasma, 73 lipids). Models including plasma lipid species alone improved discrimination between the stable and ACS groups by 0.16 (C-statistic) compared with conventional risk factors. Models utilizing lipid species either in plasma or within lipoprotein fractions had a similar ability to discriminate groups, though the C-statistic was highest for plasma lipid species (0.80; 95% CI, 0.75-0.86). Conclusions Multiple lysophospholipids, but not cholesterol, featured among the lipids which were present at low concentration within high-density lipoprotein of those presenting with ACS. Lipidomics, when applied to either whole plasma or lipoprotein fractions, was superior to conventional risk factors in discriminating ACS from stable coronary artery disease. These associative mechanistic insights elucidate potential new preventive, prognostic, and therapeutic avenues for ACS which require investigation in prospective analyses.

Dataset Information

SCARB1 Gene Polymorphisms and HDL Subfractions in Coronary Artery Disease.

Publications

<i>SCARB1</i> Gene Polymorphisms and HDL Subfractions in Coronary Artery Disease.

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