TY - JOUR
T1 - Association between single nucleotide polymorphism SLCO1B1 gene and simvastatin pleiotropic effects measured through flow-mediated dilation endothelial function parameters
AU - Andrianto,
AU - Puspitasari, Mia
AU - Ardiana, Meity
AU - Dewi, Ivana Purnama
AU - Shonafi, Khubay Alvia
AU - Kusuma Wardhani, Louisa Fadjri
AU - Nugraha, Ricardo Adrian
N1 - Publisher Copyright:
© The Author(s), 2022.
PY - 2022
Y1 - 2022
N2 - Background: Atherosclerosis is a condition in which the medium to large arteries become inflamed over time. The cornerstone to the atherosclerosis process is endothelial dysfunction. Simvastatin is a cholesterol-lowering drug known for its endothelial cell pleiotropic properties. The role of genetic polymorphisms in simvastatin-resistance difficulties has recently piqued people’s interest. This problem is thought to be linked to the pleiotropic action of simvastatin, particularly in terms of restoring endothelial function. The goal of this study is to see if there is a link between the single nucleotide polymorphism (SNP) c.521T>C and the pleiotropic effect of simvastatin as determined by the endothelial function parameter, flow-mediated dilation (FMD). Methods: This research was a multicentre cross-sectional study including 71 hypercholesterolemia patients who have been on simvastatin for at least 3 months. The real-time polymerase chain reaction identified SNP c.521T>C. The right brachial artery ultrasonography was used to measure FMD. Results: In 71 hypercholesterolemia patients, the SNP c.521T>C was found in 9.9% of them. On χ2 analysis, there was no significant association between SNP c.521T>C (TC genotype) and FMD (p = 0.973). On logistic regression analysis, the duration of simvastatin medication was linked with an increased incidence (Adj. OR (adjusted odds ratio) = 2.424; confidence interval (CI) = 1.117–5.260, p = 0.025) and a reduction in systolic blood pressure (Adj. OR = 0.92; CI = 0.025–0.333, p = 0.001). Conclusion: There was no association between FMD and the SNP c.521T>C (TC genotype). The duration of simvastatin medication and systolic blood pressure were both associated to FMD.
AB - Background: Atherosclerosis is a condition in which the medium to large arteries become inflamed over time. The cornerstone to the atherosclerosis process is endothelial dysfunction. Simvastatin is a cholesterol-lowering drug known for its endothelial cell pleiotropic properties. The role of genetic polymorphisms in simvastatin-resistance difficulties has recently piqued people’s interest. This problem is thought to be linked to the pleiotropic action of simvastatin, particularly in terms of restoring endothelial function. The goal of this study is to see if there is a link between the single nucleotide polymorphism (SNP) c.521T>C and the pleiotropic effect of simvastatin as determined by the endothelial function parameter, flow-mediated dilation (FMD). Methods: This research was a multicentre cross-sectional study including 71 hypercholesterolemia patients who have been on simvastatin for at least 3 months. The real-time polymerase chain reaction identified SNP c.521T>C. The right brachial artery ultrasonography was used to measure FMD. Results: In 71 hypercholesterolemia patients, the SNP c.521T>C was found in 9.9% of them. On χ2 analysis, there was no significant association between SNP c.521T>C (TC genotype) and FMD (p = 0.973). On logistic regression analysis, the duration of simvastatin medication was linked with an increased incidence (Adj. OR (adjusted odds ratio) = 2.424; confidence interval (CI) = 1.117–5.260, p = 0.025) and a reduction in systolic blood pressure (Adj. OR = 0.92; CI = 0.025–0.333, p = 0.001). Conclusion: There was no association between FMD and the SNP c.521T>C (TC genotype). The duration of simvastatin medication and systolic blood pressure were both associated to FMD.
KW - SLCO1B1 gene
KW - flow-mediated dilation
KW - simvastatin
KW - single nucleotide polymorphism
UR - http://www.scopus.com/inward/record.url?scp=85141003701&partnerID=8YFLogxK
U2 - 10.1177/17539447221132367
DO - 10.1177/17539447221132367
M3 - Article
C2 - 36314075
AN - SCOPUS:85141003701
SN - 1753-9447
VL - 16
JO - Therapeutic Advances in Cardiovascular Disease
JF - Therapeutic Advances in Cardiovascular Disease
ER -