Coronary Artery Disease: Meade TW

Becker RC, Meade TW, Berger PB, Ezekowitz M, O'Connor CM, Vorchheimer DA, Guyatt GH, Mark DB, Harrington RA, Anonymous00140. · Duke Cardiovascular Thrombosis Center, Duke Clinical Research Institute, 2400 Pratt Street, Durham, NC 27705, USA. · Chest. · Pubmed #18574278 links to  free full text

Abstract: The following chapter devoted to antithrombotic therapy for chronic coronary artery disease (CAD) is part of the Antithrombotic and Thrombolytic Therapy: American College of Chest Physicians Evidence-Based Clinical Practice Guidelines (8th Edition). Grade 1 recommendations are strong and indicate that the benefits do or do not outweigh risks, burden, and costs. Grade 2 suggests that individual patient values may lead to different choices (for a full understanding of the grading see the "Grades of Recommendation" chapter by Guyatt et al in this supplement, CHEST 2008; 133[suppl]:123S-131S). Among the key recommendations in this chapter are the following: for patients with non-ST-segment elevation (NSTE)-acute coronary syndrome (ACS) we recommend daily oral aspirin (75-100 mg) [Grade 1A]. For patients with an aspirin allergy, we recommend clopidogrel, 75 mg/d (Grade 1A). For patients who have received clopidogrel and are scheduled for coronary bypass surgery, we suggest discontinuing clopidogrel for 5 days prior to the scheduled surgery (Grade 2A). For patients after myocardial infarction, after ACS, and those with stable CAD and patients after percutaneous coronary intervention (PCI), we recommend daily aspirin (75-100 mg) as indefinite therapy (Grade 1A). We recommend clopidogrel in combination with aspirin for patients experiencing ST-segment elevation (STE) and NSTE-ACS (Grade 1A). For patients with contraindications to aspirin, we recommend clopidogrel as monotherapy (Grade 1A). For long-term treatment after PCI in patients who receive antithrombotic agents such as clopidogrel or warfarin, we recommend aspirin (75 to 100 mg/d) [Grade 1B]. For patients who undergo bare metal stent placement, we recommend the combination of aspirin and clopidogrel for at least 4 weeks (Grade 1A). We recommend that patients receiving drug-eluting stents (DES) receive aspirin (325 mg/d for 3 months followed by 75-100 mg/d) and clopidogrel 75 mg/d for a minimum of 12 months (Grade 2B). For primary prevention in patients with moderate risk for a coronary event, we recommend aspirin, 75-100 mg/d, over either no antithrombotic therapy or vitamin K antagonist (Grade 1A).

Harrington RA, Becker RC, Ezekowitz M, Meade TW, O'Connor CM, Vorchheimer DA, Guyatt GH. · Duke Clinical Research Institute, 2400 Pratt St, Durham, NC 27705, USA. · Chest. · Pubmed #15383483 links to  free full text

Abstract: This chapter about antithrombotic therapy for coronary artery disease (CAD) is part of the Seventh ACCP Conference on Antithrombotic and Thrombolytic Therapy: Evidence Based Guidelines. Grade 1 recommendations are strong and indicate that the benefits do, or do not, outweigh risks, burden, and costs. Grade 2 suggests that individual patients' values may lead to different choices (for a full understanding of the grading see Guyatt et al, CHEST 2004; 126:179S-187S). Among the key recommendations in this chapter are the following: For patients presenting with non-ST-segment elevation (NSTE) acute coronary syndrome (ACS), we recommend immediate and then daily oral aspirin (Grade 1A). For patients with an aspirin allergy, we recommend immediate treatment with clopidogrel, 300-mg bolus po, followed by 75 mg/d indefinitely (Grade 1A). In all NSTE ACS patients in whom diagnostic catheterization will be delayed or when coronary bypass surgery will not occur until > 5 days, we recommend clopidogrel as bolus therapy (300 mg), followed by 75 mg/d for 9 to 12 months in addition to aspirin (Grade 1A). In NSTE ACS patients in whom angiography will take place within 24 h, we suggest beginning clopidogrel after the coronary anatomy has been determined (Grade 2A). For patients who have received clopidogrel and are scheduled for coronary bypass surgery, we recommend discontinuing clopidogrel for 5 days prior to the scheduled surgery (Grade 2A). In moderate- to high-risk patients presenting with NSTE ACS, we recommend either eptifibatide or tirofiban for initial (early) treatment in addition to treatment with aspirin and heparin (Grade 1A). For the acute treatment of NSTE ACS, we recommend low molecular weight heparins over unfractionated heparin (UFH) [Grade 1B] and UFH over no heparin therapy use with antiplatelet therapies (Grade 1A). We recommend against the direct thrombin inhibitors as routine initial antithrombin therapy (Grade 1B). For patients after myocardial infarction, after ACS, and with stable CAD, we recommend aspirin in doses from 75 to 325 mg as initial therapy and in doses of 75 to 162 mg as indefinite therapy (Grade 1A). For patients with contraindications to aspirin, we recommend long-term clopidogrel (Grade 1A). For primary prevention in patients with at least moderate risk for a coronary event, we recommend aspirin, 75 to 162 mg/d, over either no antithrombotic therapy or vitamin K antagonist (VKA) [Grade 2A]; for patients at particularly high risk of events in whom the international normalized ratio (INR) can be monitored without difficulty, we suggest low-dose VKA (target INR, 1.5) [Grade 2A].

Cairns JA, Théroux P, Lewis HD, Ezekowitz M, Meade TW. · Faculty of Medicine, University of British Columbia, Vancouver, Canada. · Chest. · Pubmed #11157652 links to  free full text

This publication has no abstract.

Meade TW. · MRC Epidemiology and Medical Care Unit, Wolfson Institute of Preventive Medicine, Charterhouse Square, London EC1M 6BQ, UK. · Int J Epidemiol. · Pubmed #11689542 links to  free full text

Abstract: BACKGROUND: Coronary heart disease (CHD) in the form of myocardial infarction first came to attention early in the 20th century. Mortality from CHD increased dramatically after the First World War and had assumed epidemic proportions, particularly in the USA, by 1945. The ensuing research stemmed almost exclusively from the lipid infiltration hypothesis for atheroma. METHODS: Using epidemiological methods, pathological evidence for the thrombotic component of CHD was demonstrated by Morris as early as 1951. Morris's main work was based, first, on routine autopsy records at the London (now Royal London) Hospital and, second, on the National Necropsy Survey relating physical activity at work to pathological findings. RESULTS: The indications from Morris's work that thrombosis contributes as much to clinical CHD as atheroma were in due course strengthened by the findings of clinical trials of aspirin, prospective studies incorporating measures of haemostatic function and further studies of pathology. CONCLUSIONS: Recognition of the thrombotic contribution to CHD does not materially alter approaches to prevention through lifestyle modifications but does have major implications for pharmacological measures. Thus, aspirin and thrombolytic therapy are mandatory in the acute stage of suspected myocardial infarction while aspirin is also part of accepted practice in the longer term in secondary prevention. The value of warfarin is being rediscovered, often at a lower and therefore safer intensity of anticoagulation than previously considered necessary. The effect that warfarin may have on the vessel wall as well as on occlusion of the lumen is helping to reconcile the two major hypotheses for the pathology of CHD. Much of our current knowledge about the origins, management and prevention of CHD stems from Morris's early studies linking pathology and epidemiology.