0
Letters |

Genetic Polymorphisms and Statin TherapyGenetic Polymorphisms and Statin Therapy

JAMA. 2004;292(11):1302-1303. doi:10.1001/jama.292.11.1302-b
Text Size: A A A
Published online

AUTHOR INFORMATION

Letters Section Editor: Robert M. Golub, MD, Senior Editor.

GENETIC POLYMORPHISMS AND STATIN THERAPY

To the Editor: Dr Chasman and colleagues1 recently reported the impact of genetic polymorphisms on variability in response to pravastatin using a candidate gene approach. While these findings are of considerable interest, their impact may be limited from a public policy perspective. For example, while AT heterozygotes at single-nucleotide polymorphism 12 (3-hydroxy-3-methylglutaryl-coenzyme A [HMG-CoA] reductase gene) had an attenuated response to pravastatin in lowering low-density lipoprotein (LDL) cholesterol, variant carriers represented only 6.7% of the population. Whether it is cost-effective to genotype 15 patients initiated on statin therapy to identify 1 patient who will have an attenuated LDL cholesterol response must be decided from a societal perspective. The fact that even those with an attenuated response had a 28-mg/dL (0.73-mmol/L) reduction in LDL cholesterol further challenges the usefulness of genotype-guided therapy in this scenario.

Pharmacogenomics of lipid-lowering therapy is further complicated in that the appropriate response phenotype is unclear. For example, pharmacogenetic studies investigating apolipoprotein E (APOE) polymorphisms suggest a gene-dose effect, with ∊2 carriers showing greater reductions in LDL cholesterol in response to statins, while ∊4 carriers are least responsive.2 3 In contrast, when adverse cardiovascular outcomes were examined in a substudy of the Scandinavian Simvastatin Survival Study, ∊4 carriers had the greatest reduction in death rates in response to simvastatin compared with non-∊4 carriers.4 Therefore, while ∊2 carriers may have a better response to statins using a surrogate outcome, ∊4 carriers have a better response using mortality as the outcome. Of note, these differences in risk reduction based on APOE genotype do not appear to be related to variable LDL cholesterol treatment responses.

This letter was shown to Dr Chasman, who declined to reply on behalf of the authors.—ED.

References
Chasman DI, Posada D, Subrahmanyan L, Cook NR, Stanton Jr VP, Ridker PM. Pharmacogenetic study of statin therapy and cholesterol reduction.  JAMA.2004;291:2821-2827.
PubMed
Ballantyne CM, Herd JA, Stein EA.  et al.  Apolipoprotein E genotypes and response of plasma lipids and progression-regression of coronary atherosclerosis to lipid-lowering drug therapy.  J Am Coll Cardiol.2000;36:1572-1578.
PubMed
Ordovas JM, Mooser V. The APOE locus and the pharmacogenetics of lipid response.  Curr Opin Lipidol.2002;13:113-117.
PubMed
Gerdes LU, Gerdes C, Kervinen K.  et al.  The apolipoprotein ∊4 allele determines prognosis and the effect on prognosis of simvastatin in survivors of myocardial infarction: a substudy of the Scandinavian Simvastatin Survival Study.  Circulation.2000;101:1366-1371.
PubMed

First Page Preview

First page PDF preview

Figures

Tables

Interactive Graphics

Video

Country-Specific Mortality and Growth Failure in Infancy and Yound Children and Association With Material Stature

Use interactive graphics and maps to view and sort country-specific infant and early dhildhood mortality and growth failure data and their association with maternal

Chasman DI, Posada D, Subrahmanyan L, Cook NR, Stanton Jr VP, Ridker PM. Pharmacogenetic study of statin therapy and cholesterol reduction.  JAMA.2004;291:2821-2827.
PubMed
Ballantyne CM, Herd JA, Stein EA.  et al.  Apolipoprotein E genotypes and response of plasma lipids and progression-regression of coronary atherosclerosis to lipid-lowering drug therapy.  J Am Coll Cardiol.2000;36:1572-1578.
PubMed
Ordovas JM, Mooser V. The APOE locus and the pharmacogenetics of lipid response.  Curr Opin Lipidol.2002;13:113-117.
PubMed
Gerdes LU, Gerdes C, Kervinen K.  et al.  The apolipoprotein ∊4 allele determines prognosis and the effect on prognosis of simvastatin in survivors of myocardial infarction: a substudy of the Scandinavian Simvastatin Survival Study.  Circulation.2000;101:1366-1371.
PubMed
CME Course for:


You need to register in order to view this quiz.


To understand the clinical management of acute heart failure syndromes.
Accreditation Information The American Medical Association is accredited by the Accreditation Council for Continuing Medical Education to provide continuing medical education for physicians.
The AMA designates this journal-based CME activity for a maximum of 1 AMA PRA Category 1 CreditTM per course. Physicians should claim only the credit commensurate with the extent of their participation in the activity.
Physicians who complete the CME course and score at least 80% correct on the quiz are eligible for AMA PRA Category 1 CreditTM.
Note: You must get at least of the answers correct to pass this quiz.
Note: You must get at least of the answers correct to pass this quiz.
You have not filled in all the answers to complete this quiz
The following questions were not answered:
Sorry, you have unsuccessfully completed this CME quiz with a score of
The following questions were not answered correctly:
For CME Course: A Proposed Model for Initial Assessment and Management of Acute Heart Failure Syndromes
Indicate what changes(s) you will implement in your practice, if any, based on this CME course.
To view and print your certificate and access a summary of your CME courses go to My CME.
NOTE:
Citing articles are presented as examples only. In non-demo SCM6 implementation, integration with CrossRef’s “Cited By” API will populate this tab (http://www.crossref.org/citedby.html).
Submit a Response

Some tools below are only available to our subscribers or users with an online account.

Related Content

Customize your page view by dragging & repositioning the boxes below.