Does Warfarin for Stroke Thromboprophylaxis Protect Against MI in Atrial Fibrillation Patients?

University of Birmingham Centre for Cardiovascular Sciences, Birmingham, UK.
The American journal of medicine (Impact Factor: 5.3). 09/2010; 123(9):785-9. DOI: 10.1016/j.amjmed.2010.01.031
Source: PubMed

ABSTRACT The Randomized Evaluation of Long-term anticoagulation therapY (RE-LY) study demonstrated a significant increase in myocardial infarction events with dabigatran compared with warfarin, provoking renewed interest in whether vitamin K antagonists are useful drugs for the prevention of myocardial infarction in high-risk patients with atrial fibrillation. Present analyses examined whether there was an increased risk of myocardial infarction associated with non-warfarin anticoagulants (Stroke Prevention with the ORal direct Thrombin Inhibitor ximelagatran compared with warfarin in patients with non-valvular atrial Fibrillation III and IV, RE-LY, Amadeus) or "anticoagulant equivalents" (Atrial fibrillation Clopidogrel Trial with Irbesartan for the prevention of Vascular Events) in patients with atrial fibrillation who are prescribed anticoagulation for stroke thromboprophylaxis. The overall annual event rate for those receiving warfarin was 0.98% compared with 1.32% for those receiving comparators. Warfarin was associated with a significant reduction in myocardial infarction (relative risk 0.77; 95% confidence interval (CI), 0.63-0.95), an effect largely driven by the RE-LY trial. Sensitivity analyses, excluding RE-LY, revealed a nonsignificant reduction in myocardial infarctions (relative risk 0.83; 95% CI, 0.62-1.10); an analogous analysis excluding the Atrial fibrillation Clopidogrel Trial with Irbesartan for the prevention of Vascular Events demonstrated a significant reduction in myocardial infarctions (relative risk 0.80; 95% CI, 0.64-1.00). Warfarin might provide a protective effect against myocardial infarction compared with non-warfarin anticoagulants or "anticoagulation equivalents" in patients with atrial fibrillation who are prescribed anticoagulation for stroke thromboprophylaxis.

  • [Show abstract] [Hide abstract]
    ABSTRACT: Direct thrombin inhibitor (anti-factor IIa) anticoagulants, now established for treatment and prevention of cardiac and venous thromboembolism, have been repeatedly associated with a significantly increased frequency of thrombosis on abnormal cardiac endothelium when compared head-to-head with indirectly-acting therapeutic anticoagulants in studies of sufficient patient number and duration. Although there is uncertainty as to mechanism, the weight of evidence as a class effect warrants prescribing effective anticoagulants other than direct thrombin inhibitors.
    Chest 09/2014; 147(1). DOI:10.1378/chest.14-2028 · 7.13 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: To compare key features of the new oral anticoagulants (NOACs)-dabigatran, rivaroxaban, and apixaban-and to address questions that arise when comparing the NOACs.
  • [Show abstract] [Hide abstract]
    ABSTRACT: Anticoagulant treatment can be currently instituted with two different classes of drugs: the vitamin K antagonists (VKAs) and the newer, "novel" or non-vitamin K antagonist oral anticoagulant drugs (NOACs). The NOACs have several practical advantages over VKAs, such as the rapid onset/offset of action, the lower potential for food and drug interactions, and the predictable anticoagulant response. However, the VKAs currently have a broader spectrum of indications, a standardized monitoring test, and established reversal strategies. The NOACs emerged as alternative options for the prevention and treatment of venous thromboembolism and for the prevention of stroke and systemic embolism in patients with nonvalvular atrial fibrillation. Nevertheless, there remain some populations for whom the VKAs remain the most appropriate anticoagulant drug. This article discusses the advantages and disadvantages of VKAs and NOACs. Thieme Medical Publishers 333 Seventh Avenue, New York, NY 10001, USA.
    Seminars in Thrombosis and Hemostasis 02/2015; DOI:10.1055/s-0035-1544231 · 3.69 Impact Factor