Absence of an interaction between the angiotensin-converting enzyme insertion-deletion polymorphism and pravastatin on cardiovascular disease in high-risk hypertensive patients: The Genetics of Hypertension-Associated Treatment (GenHAT) study

Zee, Anke‐Hilse Maitland‐van der; Boerwinkle, Eric; Arnett, Donna K.; Davis, Barry R.; Leiendecker–Foster, Catherine; Miller, Michael B.; Klungel, Olaf H.; Ford, Charles E.; Eckfeldt, John H.

doi:10.1016/j.ahj.2006.10.019

Cited by 19 publications

(7 citation statements)

References 22 publications

(18 reference statements)

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“…Recent pharmacogenetics data has contributed to better understanding statin pharmacokinetics and pharmacodynamic variability [ 44 ]. Pharmacogenetic and dynamic properties have been extensively studied, but only few studies included stroke as outcome ( Table 2 ) [ 22 – 25 ].…”

Section: Resultsmentioning

confidence: 99%

Gene-Drug Interaction in Stroke

Amici

Paciaroni

Agnelli

et al. 2011

Stroke Research and Treatment

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Stroke is the third cause of mortality and one of most frequent causes of long-term neurological disability, as well as a complex disease that results from the interaction of environmental and genetic factors. The focus on genetics has produced a large number of studies with the objective of revealing the genetic basis of cerebrovascular diseases. Furthermore, pharmacogenetic research has investigated the relation between genetic variability and drug effectiveness/toxicity. This review will examine the implications of pharmacogenetics of stroke; data on antihypertensives, statins, antiplatelets, anticoagulants, and recombinant tissue plasminogen activator will be illustrated. Several polymorphisms have been studied and some have been associated with positive drug-gene interaction on stroke, but the superiority of the genotype-guided approach over the clinical approach has not been proved yet; for this reason, it is not routinely recommended.

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Section: Resultsmentioning

confidence: 99%

Gene-Drug Interaction in Stroke

Amici

Paciaroni

Agnelli

et al. 2011

Stroke Research and Treatment

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“…There is also some evidence that ε2 carriers may more frequently achieve treatment goals than ε4 carriers [16]. Maitland-van der Zee et al [43] In a substudy of the Scandinavian Simvastatin Survival Study (4S) including patients with a prior myocardial infarction, the patients with ε4 benefited remarkably from simvastatin, as the treatment almost abolished the excess mortality risk related to the ε4 allele [17]. In a study using data from nearly 8000 patients in the Rotterdam Study, the protective effect of statins was independent of APOE ε2/ε3/ ε4 genotype [18].…”

Section: Apolipoprotein Ementioning

confidence: 97%

Statin Pharmacogenomics: Lipid Response and Cardiovascular Outcomes

Kerola

Lehtimäki

Kähönen

et al. 2010

Curr Cardio Risk Rep

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Use of lipid-lowering agents, mainly statins, is a proven strategy to prevent cardiovascular disease events. Because most of the beneficial effect of statins is accounted for by the improved lipid profile, more than 40 genes have been studied to ascertain whether variation therein modulates lipid response or prevention of cardiovascular disease during statin therapy. In addition, recent studies have also shown that genetic variation may stratify pleiotropic statin effects. Although this review briefly covers the pharmacogenetic implications on biochemical markers such as low-density lipoprotein cholesterol, it mainly focuses on recent findings (after 2005) on cardiovascular disease outcomes during statin therapy. Pharmacogenomic analysis of large trials of statin treatment is becoming a predominant trend. Another future direction is genome-wide analysis, which will reveal additional candidate genes to be further tested in prospective trials. The results so far are preliminary, and successful replication of the findings is needed in large unrelated populations before the evidence for any polymorphism is solid enough for clinical applications.

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“…A recent study in the Antihypertensive and LipidLowering Treatment to Prevent Heart Attack Trial (ALLHAT) showed that the ACE polymorphism had no effect on the cardiovascular outcome in pravastatintreated subjects [20]. In addition, in The Atorvastatin Comparative Cholesterol Efficacy and Safety Study (ACCESS) trial, G allele carriers of rs4341 (G allele corresponds with I allele as a result of high linkage disequilibrium with insertion/deletion polymorphism) exhibited greater total cholesterol reduction compared with CC carriers in response to pravastatin [21].…”

Section: Angiotensin-converting Enzymementioning

confidence: 99%

Pharmacogenomic Importance of Pravastatin

Peters

Zee

2008

Pharmacogenomics

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In developed countries, cardiovascular disease is one of the leading causes of death. Among other statins, pravastatin is abundantly prescribed to reduce risk of coronary artery disease by lowering cholesterol. Genetic factors are thought to be partly responsible for the interindividual variation in the response to pravastatin. This article reviews the most important studies conducted on the pharmacogenetics of pravastatin. Currently there is no evidence to advocate pharmacogenetic testing before initiating therapy.

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Absence of an interaction between the angiotensin-converting enzyme insertion-deletion polymorphism and pravastatin on cardiovascular disease in high-risk hypertensive patients: The Genetics of Hypertension-Associated Treatment (GenHAT) study

Cited by 19 publications

References 22 publications

Gene-Drug Interaction in Stroke

Gene-Drug Interaction in Stroke

Statin Pharmacogenomics: Lipid Response and Cardiovascular Outcomes

Pharmacogenomic Importance of Pravastatin

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