Oral Anticoagulants Versus Antiplatelet Therapy for Preventing Further Vascular Events After Transient Ischemic Attack or Minor Stroke of Presumed Arterial Origin
2003; Lippincott Williams & Wilkins; Volume: 34; Issue: 1 Linguagem: Inglês
10.1161/01.str.0000047035.04395.ed
ISSN1524-4628
AutoresAle Algra, E.L.L.M. De Schryver, J. van Gijn, L. Jaap Kappelle, Peter J. Koudstaal,
Tópico(s)Antiplatelet Therapy and Cardiovascular Diseases
ResumoHomeStrokeVol. 34, No. 1Oral Anticoagulants Versus Antiplatelet Therapy for Preventing Further Vascular Events After Transient Ischemic Attack or Minor Stroke of Presumed Arterial Origin Free AccessReview ArticlePDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessReview ArticlePDF/EPUBOral Anticoagulants Versus Antiplatelet Therapy for Preventing Further Vascular Events After Transient Ischemic Attack or Minor Stroke of Presumed Arterial Origin A. Algra, MD, E.L.L.M. De Schryver, MD, J. van Gijn, MD, FRCP, FRCPE, L.J. Kappelle, MD and P.J. Koudstaal, MD A. AlgraA. Algra From the Department of Neurology (A.A., E.L.L.M.D.S., J.v.G., L.J.K.) and the Julius Center for Health Sciences and Primary Care (A.A.), University Medical Center Utrecht, the Netherlands; and the Department of Neurology (P.J.K.), Erasmus Medical Center Rotterdam, the Netherlands. , E.L.L.M. De SchryverE.L.L.M. De Schryver From the Department of Neurology (A.A., E.L.L.M.D.S., J.v.G., L.J.K.) and the Julius Center for Health Sciences and Primary Care (A.A.), University Medical Center Utrecht, the Netherlands; and the Department of Neurology (P.J.K.), Erasmus Medical Center Rotterdam, the Netherlands. , J. van GijnJ. van Gijn From the Department of Neurology (A.A., E.L.L.M.D.S., J.v.G., L.J.K.) and the Julius Center for Health Sciences and Primary Care (A.A.), University Medical Center Utrecht, the Netherlands; and the Department of Neurology (P.J.K.), Erasmus Medical Center Rotterdam, the Netherlands. , L.J. KappelleL.J. Kappelle From the Department of Neurology (A.A., E.L.L.M.D.S., J.v.G., L.J.K.) and the Julius Center for Health Sciences and Primary Care (A.A.), University Medical Center Utrecht, the Netherlands; and the Department of Neurology (P.J.K.), Erasmus Medical Center Rotterdam, the Netherlands. and P.J. KoudstaalP.J. Koudstaal From the Department of Neurology (A.A., E.L.L.M.D.S., J.v.G., L.J.K.) and the Julius Center for Health Sciences and Primary Care (A.A.), University Medical Center Utrecht, the Netherlands; and the Department of Neurology (P.J.K.), Erasmus Medical Center Rotterdam, the Netherlands. Originally published12 Dec 2002https://doi.org/10.1161/01.STR.0000047035.04395.EDStroke. 2003;34:234–235Other version(s) of this articleYou are viewing the most recent version of this article. Previous versions: December 12, 2002: Previous Version 1 BackgroundPatients who are entered in clinical trials after a transient ischemic attack or nondisabling ischemic stroke have an annual risk of important vascular events (death from all vascular causes, nonfatal stroke, or nonfatal myocardial infarction) of between 4% and 11%.1,2 Aspirin, in a daily dose of 30 mg or more, offers only modest protection after cerebral ischemia: it reduces the incidence of major vascular events by 20% at most.1–3 Secondary prevention trials after myocardial infarction indicate that treatment with oral anticoagulants is associated with a risk reduction approximately twice that of treatment with antiplatelet therapy.1,4–7ObjectivesThis review aimed to (1) compare the efficacy of oral anticoagulants and antiplatelet therapy in the secondary prevention of vascular events after cerebral ischemia of presumed arterial origin and (2) compare the safety of oral anticoagulants and antiplatelet therapy in the secondary prevention of vascular events after cerebral ischemia of presumed arterial origin.Search StrategyThis review draws on the search strategy developed for the Cochrane Stroke Review Group as a whole. Relevant trials were identified in the Specialized Register of Controlled Trials. Authors of published trials were contacted for further information and unpublished data.Selection CriteriaRandomized trials with concealed treatment allocation on long-term (>6 months) secondary prevention after recent (<6 months) transient ischemic attack or minor ischemic stroke of presumed arterial origin were selected. The oral anticoagulant therapy was to be of specified intensity (by means of the International Normalized Ratio [INR]) with warfarin, phenprocoumon, or acenocoumarol versus a single antiplatelet drug (or combination of antiplatelet agents).Data Collection and AnalysisTwo reviewers selected trials meeting the inclusion criteria and extracted details of randomization methods, blinding of treatments and assessments, whether intention-to-treat analysis is possible from the published data, whether treatment groups are comparable with regard to major prognostic risk factors for outcomes, the number of patients who are excluded or lost to follow-up, definition of outcomes, and entry and exclusion criteria. The methodological quality of each trial was assessed by the 2 reviewers using these extracted data. In addition, target INR for anticoagulant treatment and dose and type of antiplatelet drug, duration of follow-up, and the numbers of defined outcome events were recorded.The data were analyzed according to the intention-to-treat principle. Subgroup analyses with treatment INR 1.4 to 2.8 (low intensity), INR 2.1 to 3.6 (medium intensity), and INR 3.0 to 4.5 (high intensity) were performed. Relative and absolute risk reductions were calculated by means of the statistical software provided by the Cochrane Collaboration.Main ResultsFive trials, with a total of 4076 patients, were selected.8-12In the prevention of ischemic stroke after cerebral ischemia of presumed arterial origin, the available data do not allow a robust conclusion on whether anticoagulants (in any intensity) are more efficacious in the prevention of vascular events than antiplatelet therapy (medium-intensity anticoagulation relative risk [RR] 0.96, 95% CI 0.38 to 2.42; high-intensity anticoagulation RR 1.02, 95% CI 0.49 to 2.13) (Figure 1). The (primary) outcome event of WARSS12 (target INR 1.4 to 2.8) did not contain myocardial infarction of bleeding complications. Recently, the optimal level of anticoagulation for similar patients in an observational study was between INR 2.5 and 3.5.13Download figureDownload PowerPointFigure 1. Outcome recurrent ischemic stroke. (Figure 01.06.00. Algra A, De Schryver ELLM, van Gijn J, Kappelle LJ, Koudstaal PJ. Oral anticoagulants versus antiplatelet therapy for preventing further vascular events after transient ischaemic attack or minor stroke of presumed arterial origin [Cochrane Review]. In: The Cochrane Library, Issue 3, 2002. Oxford: Update Software. MetaView © Update Software, Oxford.)There is no evidence that treatment with low- or medium-intensity anticoagulation gives a higher bleeding risk than treatment with antiplatelet agents. The RR for major bleeding complications for low-intensity anticoagulation was 1.27 (95% CI 0.79 to 2.03) and for medium-intensity anticoagulation 1.19 (95% CI 0.59 to 2.41). However, it was clear that high-intensity oral anticoagulants with INR 3.0 to 4.5 were not safe, because they yielded a higher risk of major bleeding complications (RR 9.0, 95% CI 3.9 to 21) (Figure 2). Download figureDownload PowerPointFigure 2. Outcome major bleeding complication. (Figure 01.09.00. Algra A, De Schryver ELLM, van Gijn J, Kappelle LJ, Koudstaal PJ. Oral anticoagulants versus antiplatelet therapy for preventing further vascular events after transient ischaemic attack or minor stroke of presumed arterial origin [Cochrane Review]. In: The Cochrane Library, Issue 3, 2002. Oxford: Update Software. MetaView © Update Software, Oxford.)Reviewers' ConclusionsFor the secondary prevention of further vascular events after transient ischemic attack or minor stroke of presumed arterial origin, there is insufficient evidence to justify the routine use of medium-intensity oral anticoagulants (INR 2.0 to 3.6); such treatment preferably should be used only as part of a clinical trial. More intense anticoagulation (INR 3.0 to 4.5) is not safe and should not be used in this setting. Low-intensity anticoagulation (INR 1.4 to 2.8) is not likely to be more efficacious than aspirin.Note: Cochrane Reviews are regularly updated as new information becomes available and in response to comments and criticisms. Readers should consult The Cochrane Library for the latest version of a Cochrane Review. Information on The Cochrane Library can be found at www.update-software.com.Section Editor: Graeme J. Hankey, MD, FRACPFootnotesCorrespondence to Ale Algra, University Medical Centre Utrecht, Julius Center for Health Sciences and Primary Care, Room D.01.335, PO Box 85500, 3508 GA Utrecht, Netherlands. E-mail [email protected] References 1 Antiplatelet Trialists' Collaboration. Collaborative overview of randomised trials of antiplatelet therapy, I: prevention of death, myocardial infarction, and stroke by prolonged antiplatelet therapy in various categories of patients. BMJ. 1994; 308: 81–106.CrossrefMedlineGoogle Scholar2 Algra A, van Gijn J. Aspirin at any dose above 30 mg offers only modest protection after cerebral ischaemia. J Neurol Neurosurg Psychiatry. 1996; 60: 197–199.CrossrefMedlineGoogle Scholar3 Algra A, van Gijn J. Cumulative meta-analysis of aspirin efficacy after cerebral ischaemia of arterial origin. J Neurol Neurosurg Psychiatry. 1999; 66: 255.Letter.CrossrefGoogle Scholar4 The Sixty Plus Reinfarction Study Research Group. A double-blind trial to assess long-term oral anticoagulant therapy in elderly patients after myocardial infarction. Lancet. 1980; 2: 989–994.MedlineGoogle Scholar5 Smith P, Arnesen H, Holme I. The effect of warfarin on mortality and reinfarction after myocardial infarction. N Engl J Med. 1990; 323: 147–152.CrossrefMedlineGoogle Scholar6 Anticoagulants in the Secondary Prevention of Events in Coronary Thrombosis (ASPECT) Research Group. Effect of long-term oral anticoagulant treatment on mortality and cardiovascular morbidity after myocardial infarction. Lancet. 1994; 343: 499–503.MedlineGoogle Scholar7 The EPSIM Research Group. A controlled comparison of aspirin and oral anticoagulants in prevention of death after myocardial infarction. N Engl J Med. 1982; 307: 701–708.CrossrefMedlineGoogle Scholar8 The Stroke Prevention in Reversible Ischemia Trial (SPIRIT) Study Group. A randomized trial of anticoagulants versus aspirin after cerebral ischemia of presumed arterial origin. Ann Neurol. 1997; 42: 857–865.CrossrefMedlineGoogle Scholar9 Garde A, Samuelsson K, Fahlgren H, Hedberg E, Hjerne LG, Ostman J. Treatment after transient ischemic attacks: a comparison between anticoagulant drug and inhibition of platelet aggregation. Stroke. 1983; 14: 677–681.CrossrefMedlineGoogle Scholar10 Olsson JE, Brechter C, Backlund H, Krook H, Muller R, Nitelius E, Olsson O, Tornberg A. Anticoagulant vs anti-platelet therapy as prophylactic against cerebral infarction in transient ischemic attacks. Stroke. 1980; 11: 4–9.CrossrefMedlineGoogle Scholar11 Stewart B, Shuaib A, Veloso F, for the SWAT Investigators. Stroke prevention with warfarin or aspirin trial (SWAT). Stroke. 1998; 29: 304.Abstract.Google Scholar12 Mohr JP, Thompson JL, Lazar RM, Levin B, Sacco RL, Furie KL, Kistler JP, Albers GW, Pettigrew LC, Adams HP Jr, et al. A comparison of warfarin and aspirin for the prevention of recurrent ischemic stroke. N Engl J Med. 2001; 345: 1444–1451.CrossrefMedlineGoogle Scholar13 Torn M, Algra A, Rosendaal FR. Oral anticoagulation for cerebral ischemia of arterial origin: high initial bleeding risk. 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January 2003Vol 34, Issue 1 Advertisement Article InformationMetrics https://doi.org/10.1161/01.STR.0000047035.04395.EDPMID: 12511782 Manuscript receivedOctober 28, 2002Manuscript acceptedOctober 28, 2002Originally publishedDecember 12, 2002 Keywordsantiplatelet therapyanticoagulantscerebral ischemiarandomized controlled trialsPDF download Advertisement
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