Genetic testing could improve warfarin dosing
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American Heart Association Late-Breaking Clinical Trial Report LBCT 5/Abstract: 19658 (Hall E)
- In a study conducted in Europe, genetic testing before beginning warfarin therapy helped patients increase their time in therapeutic range by 7 percent while reducing the need for warfarin dose adjustments.
Embargoed until 10:45 a.m. CT/11:45 a.m. ET Tuesday, Nov.19, 2013
This release is featured in an embargoed media briefing at 8:30 a.m. CT, Tuesday, Nov. 19.
DALLAS, Nov. 19, 2013 — Obtaining genetic information before starting warfarin therapy helped patients increase the effectiveness of treatment while reducing the risk of over-anticoagulation and improper dosing in a late-breaking clinical trial presented at the American Heart Association’s Scientific Sessions 2013.
“We found that genotyping before starting warfarin increased the time in therapeutic range by approximately 7 percent, reduced over-anticoagulation, reduced the time required to reach therapeutic range, improved the time required to reach stable dose and reduced the number of warfarin dose adjustments,” said Munir Pirmohamed, M.D., Ph.D., lead author of the study and NHS Chair of Pharmacogenetics at the University of Liverpool in the United Kingdom.
The EU Pharmacogenetics of Anticoagulant Therapy (EU-PACT) Warfarin Study of 454 patients in Europe compared using genetic tests to guide warfarin dosing with traditional methods, which involves patients undergoing frequent blood testing to gauge whether their warfarin levels are too high or too low.
The majority of patients were white, average age 67 years, 61 percent were male, 72 percent had atrial fibrillation and the other patients had venous thromboembolism. All patients were followed for three months, and were checked at days four, six, eight, 15, 22, 57 and 85 of the study. Adjustments to the patients’ warfarin doses were either based on genetic results or standard blood testing to decide whether warfarin levels were too high, too low or just right.
Although warfarin has been approved for decades, there is a lot of variability as to how patients will respond to warfarin. Additionally, finding the right dosage can be difficult — too little warfarin can lead to blood clots and too much can cause bleeding.
Researchers specifically looked for two genes associated with the clotting process.
“Our study very much fits in with the concept of personalized medicine, which aims to get the right drug, at the right dose to the right patient,” Pirmohamed said.
“There is huge potential in the cardiovascular field for personalizing therapy on the basis of genetic or non-genetic tests,” he said. “For genetic testing, in some cases it may be possible to undertake the testing at the bedside or in surgery, so called point-of-care tests as we did in this trial. We need evidence from randomized controlled trials to show the utility of genetic testing.”
Co-authors are Girvan Burnside; Jenni Stoddern; Clare Prince; Cheng Hok Toh; Toby Nicholson; Patrick. Kesteven; Andrea Jorgensen; Anne Daly; Anke-Hilse Maitland-van der Zee; Paula Williamson; Niclas Eriksson; Peter Avery; Farhad Kamali and Mia Wadelius for the EU-PACT Investigators, Disclosures
EU-FP7 Programme funded the study.
For more news from AHA Scientific Sessions 2013, follow @HeartNews #AHA13 on Twitter.
Statements and conclusions of study authors that are presented at American Heart Association scientific meetings are solely those of the study authors and do not necessarily reflect association policy or position. The association makes no representation or warranty as to their accuracy or reliability. The association receives funding primarily from individuals; foundations and corporations (including pharmaceutical, device manufacturers and other companies) also make donations and fund specific association programs and events. The association has strict policies to prevent these relationships from influencing the science content. Revenues from pharmaceutical and device corporations are available at www.heart.org/corporatefunding.
Note: Actual presentation is 11:07 a.m. CT/12:07 p.m. ET, Tuesday, Nov. 19, 2013 in Hall E.
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