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Published Online First: 10 October 2005. doi:10.1136/hrt.2005.069161
Heart 2006;92:3-4
Copyright © 2006 BMJ Publishing Group Ltd & British Cardiovascular Society

EDITORIAL

Antiplatelet therapy and the vascular tree

A Blann

Correspondence to:
Dr Andrew Blann
University Department of Medicine, City Hospital NHS Trust, Birmingham B18 7QH, UK; a.blann@bham.ac.uk


While treatment with aspirin plus clopidogrel may be valid as an adjunct to percutaneous coronary intervention, other issues remain to be addressed before routine combination therapy is recommended for any level of atherosclerosis

Abbreviations: CAMPER, clopidogrel and aspirin in the management of peripheral endovascular revascularisation; CAPRIE, clopidogrel versus aspirin in patients at risk of ischaemic events; CASPAR:, clopidogrel and acetylsalicylic acid in bypass surgery for peripheral arterial disease; CLASSICS, clopidogrel aspirin stent international cooperative study; CURE, clopidogrel in unstable angina to prevent recurrent events; CREDO, clopidogrel for the reduction of events during observation; HOT, hypertension optimal treatment; MATCH:, management of atherothrombosis with clopidogrel in high-risk patients with recent transient ischemic attack or ischemic stroke; PCI, percutaneous coronary intervention; RRR, relative risk reduction

Keywords: antiplatelet therapy; aspirin; clopidrel; percutaneous coronary intervention

The first 150 words of the full text of this article appear below.

Aspirin is effective in reducing the risk of primary and secondary cardiovascular events, such as myocardial infarction and stroke, and is a mainstay of both the adjuvant treatment of acute coronary syndromes and other cardiovascular disease, with a minor effect on reducing the risk of venous thromboembolism. While this impact is widely believed to be caused by suppression of the platelet, aspirin also has likely desirable non-platelet effects—for example, in inhibiting nuclear transcription initiators such as NF{kappa}b (implicated in the promotion of various genes with pro-inflammatory activity), in protecting low density lipoprotein cholesterol from oxidative modification, and in modulating endothelial dysfunction in atherosclerosis. However, the precise value of these latter mechanisms in vivo and any possible contribution to a reduction in thrombotic events is speculative.

Although low to medium dose aspirin (32.5–75 mg daily) is well tolerated in the majority of patients, the principle adverse effects are gastrointestinal bleeding . . . [Full text of this article]


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