Dataset Information

An association of ABCG8: rs11887534 polymorphism and HDL-cholesterol response to statin treatment in the Polish population.

ABSTRACT:

Background

Variation in lipid changes in response to statin treatment is associated with genetic polymorphism. Sterolin-1, encoded by ABCG5, and sterolin-2, encoded by ABCG8, together form a sterol transporter. There are some reports indicating association of rs11887534 (ABCG8:c.55G > C) polymorphism with lipid concentrations, both prior to and after statin treatment. The aim of this study was to analyze both baseline plasma lipids and their concentrations in response to statin treatment with regard to ABCG8: rs11887534 polymorphism in Caucasian patients of Polish origin.

Methods

The study group consisted of 170 consecutive adult out-patients treated with atorvastatin or simvastatin for a minimum of 2 months. Concentrations of triglycerides (TG), total cholesterol (TC), LDL-cholesterol (LDL-C) and HDL-cholesterol (HDL-C) were measured before and after statin treatment. The ABCG8 polymorphism was identified by mini-sequencing genomic DNA extracted from peripheral blood leukocytes.

Results

There were no significant differences in regard to ABCG8 variants for baseline TG, TC, LDL-C and HDL-C as well as for TG, TC or LDL-C concentrations after statin treatment. However, patients carrying at least one C allele showed a decrease in post-statin HDL-C concentrations and the absolute and relative changes between post- and pre-statin HDL-C concentrations were negative in contrast to positive values in wild-type homozygotes.

Conclusions

Our results suggest that the c.55C allele of the ABCG8: rs11887534 polymorphism might be associated with decrease in HDL-cholesterol in response to statin treatment in Polish patients.

SUBMITTER: Salacka A

PROVIDER: S-EPMC8599229 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:Previous experimental studies showed that increasing high-density lipoprotein cholesterol (HDL) cholesterol shortens cardiac ventricular repolarization and the QT interval corrected for heart rate (QTc). However, little is known about the epidemiological relationship between HDL and QTc. The potential antiarrhythmic effect of HDL cholesterol remains a speculative hypothesis. In this cross-sectional population based study in adults living in the Italian-speaking part of Switzerland, we aimed to explore the association between HDL cholesterol and the QTc interval in the general population. A total of 1202 subjects were screened. electrocardiogram (ECG) recordings, measurements of lipid parameters and other laboratory tests were performed. QTc was corrected using Bazett's (QTcBaz) and Framingham (QTcFram) formulas. HDL was categorized according to percentile distributions: <25th (HDL-1; ?1.39 mmol/L); 25th-<50th (HDL-2; 1.40-1.69 mmol/L); 50th-<75th (HDL-3; 1.69-1.99 mmol/L); and ?75th (HDL-4; ?2.0 mmol/L). After exclusion procedures, data of 1085 subjects were analyzed. Compared with the HDL reference group (HDL-1), HDL-2 and HDL-3 were associated with a reduction of QTcBaz and QTcFram duration in crude (HDL-2, QTcBaz/QTcFram: ?-11.306/-10.186, SE 4.625/4.016; p = 0.016/0.012; HDL-3, ?-12.347/-12.048, SE 4.875/4.233, p = 0.012/<0.001) and adjusted (HDL-2: ?-11.697/-10.908, SE 4.333/4.151, p < 0.001/0.010; HDL-3 ?-11.786/-11.002, SE 4.719/4.521, p = 0.014/0.016) linear regression models in women. In adjusted logistic regression models higher HDL, were also associated with lower risk of prolonged QTcBaz/QTcFram (HDL-2: OR 0.16/0.17, CI 0.03-0.83/0.47-0.65; HDL-3: OR 0.10/0.14, CI 0.10-0.64/0.03-0.63) in women. Restricted cubic spline analysis confirmed a non linear association (p < 0.001). The present findings indicate an epidemiological association between HDL cholesterol and QTc duration. To draw firm conclusions, further investigations in other populations and with a prospective cohort design are needed.