Evidence map›Paper›PMID 19255811›Full record

ArticleJournal of general internal medicine2009

Should we test for CYP2C9 before initiating anticoagulant therapy in patients with atrial fibrillation?

Mark H Eckman, Steven M Greenberg, Jonathan Rosand

Open access · bronzeAbstract readCase Reports
In one paragraph

Article in Journal of general internal medicine, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed, 1 pooled it
0.9field-weighted citation impact, top 22% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

6 citing papers in PubMed, 1 synthesis or guideline pooled it, 11 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Debating clinical utility.Public health genomics · 2010
    Article
  5. Testing for CYP2C9 before initiating anticoagulant therapy.Journal of general internal medicine · 2009
    Article
  6. Personalizing health care--is this the right time for warfarin?Journal of general internal medicine · 2009
    Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

3 authors at 2 institutions in 1 country.

Mark H EckmanDivision of General Internal Medicine and Center for Clinical Effectiveness, University of Cincinnati Medical Center, University of Cincinnati (MHE), PO Box 670535, Cincinnati, OH 45267-0535, USA. mark.eckman@uc.edu
Steven M Greenberg
Jonathan Rosand
Massachusetts General Hospital · USUniversity of Cincinnati Medical Center · US

Funding

Gene Discovery for Warfarin-Related Intracerebral HemorrhageR01NS059727 · NINDS · MASSACHUSETTS GENERAL HOSPITAL · PI ROSAND, JONATHAN · 2008 to 2012
$4.2M
A Patient-Specific Decision Support Tool for Bariatric SurgeryK23DK075599 · NIDDK · UNIVERSITY OF CINCINNATI · PI SCHAUER, DANIEL P · 2007 to 2011
$666k
NHLBI NIH HHS K30 HL078581-01NIDDK NIH HHS K23 DK075599NINDS NIH HHS R01 NS059727
6 · The paper itself

Abstract

backgroundGenetic variants of the warfarin sensitivity gene CYP2C9 have been associated with increased bleeding risk during warfarin initiation. Studies also suggest that such patients remain at risk throughout treatment.

objectiveWould testing patients with non-valvular atrial fibrillation (AF) for CYP2C9 before initiating warfarin improve outcomes?

designMarkov state transition decision model.

settingAmbulatory or inpatient settings necessitating new initiation of anticoagulation. PATIENTS: The base case was a 69-year-old man with newly diagnosed non-valvular AF. Interventions included: (1) warfarin, (2) aspirin, or (3) no antithrombotic therapy without genetic testing; and genetic testing followed by (4) aspirin or (5) no antithrombotic therapy in those with culprit CYP2C9 alleles. MEASURES: Quality-adjusted life years (QALYs).

resultsIn the base case, testing and treating patients with CYP2C9*2 and/or CYP2C9*3 with aspirin rather than warfarin was best (8.97 QALYs). However, warfarin without genetic testing was a close second (8.96 QALYs), a difference of roughly 5 days. Sensitivity analyses demonstrated that genetic testing followed by aspirin was best for patients at lower risk of embolic events. Warfarin without testing was preferred if the rate of embolic events was greater than 5% per year, or the risk of major bleeding while receiving warfarin was lower.

conclusionFor patients at average risk for ischemic stroke due to AF and at average risk for major hemorrhage, treatment based on genetic testing offers no benefit compared to warfarin initiation without testing. The gain from testing may be larger in patients at lower risk of embolic events or at greater risk of bleeding.

Indexed as

AgedAnticoagulantsAryl Hydrocarbon HydroxylasesAtrial FibrillationCytochrome P-450 CYP2C9HemorrhageHumansMaleMarkov ChainsQuality-Adjusted Life YearsAnticoagulantsAryl Hydrocarbon HydroxylasesCYP2C9 protein, humanCytochrome P-450 CYP2C9

Identifiers

PMID19255811
PMCPMC2669861
OpenAlexW2094989706

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.