@article {8571, title = {Rooted in risk: genetic predisposition for low-density lipoprotein cholesterol level associates with diminished low-density lipoprotein cholesterol response to statin treatment.}, journal = {Pharmacogenomics}, volume = {17}, year = {2016}, month = {2016 10}, pages = {1621-1628}, abstract = {

AIMS: To utilize previously reported lead SNPs for low-density lipoprotein cholesterol (LDL-c) levels to find additional loci of importance to statin response, and examine whether genetic predisposition to LDL-c levels associates with differential statin response.

METHODS: We investigated effects on statin response of 59 LDL-c SNPs, by combining summary level statistics from the Global Lipids Genetics and Genomic Investigation of Statin Therapy consortia.

RESULTS: Lead SNPs for APOE, SORT1 and NPC1L1 were associated with a decreased LDL-c response to statin treatment, as was overall genetic predisposition for increased LDL-c levels as quantified with 59 SNPs, with a 5.4\% smaller statin response per standard deviation increase in genetically raised LDL-c levels.

CONCLUSION: Genetic predisposition for increased LDL-c level may decrease efficacy of statin therapy.

}, keywords = {Cholesterol, LDL, Genetic Predisposition to Disease, Humans, Hydroxymethylglutaryl-CoA Reductase Inhibitors, Pharmacogenetics, Polymorphism, Single Nucleotide, Triglycerides}, issn = {1744-8042}, doi = {10.2217/pgs-2016-0091}, author = {Smit, Roelof Aj and Postmus, Iris and Trompet, Stella and Barnes, Michael R and Warren, Helen and Arsenault, Benoit J and Chasman, Daniel I and Cupples, L Adrienne and Hitman, Graham A and Krauss, Ronald M and Li, Xiaohui and Psaty, Bruce M and Stein, Charles M and Rotter, Jerome I and Jukema, J Wouter} }