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Aspirin in the primary prevention of cardiovascular disease and cancer

Frederick A Spencer, MD
Gordon Guyatt, MD
Charles H Hennekens, MD, DrPH
Section Editors
Joann G Elmore, MD, MPH
Christopher P Cannon, MD
Deputy Editors
Howard Libman, MD, FACP
Gordon M Saperia, MD, FACC


Cardiovascular disease (CVD) and cancer are the leading causes of morbidity and mortality worldwide, representing 24 and 13 percent of all deaths, respectively [1,2]. Aspirin produces statistically significant and important reductions in CVD morbidity and mortality among survivors of a wide range of occlusive CVD events, including subsequent coronary heart disease, especially myocardial infarction, stroke, and CVD death. In secondary prevention, the absolute benefits on occlusive events are far greater than the absolute risks of major bleeding. In primary prevention, however, among apparently healthy people, the benefit-to-risk ratio is less clear due, at least in part, to the paucity of randomized evidence among the moderate- to high-risk subjects most likely to achieve a net benefit.  

While the benefits of aspirin on CVD have been known for decades, more recent randomized evidence has suggested a benefit on colorectal cancer and possibly total cancer deaths as well as on the development of other cancers. These findings may impact the threshold for the prescription of aspirin by health care professionals and the wishes of primary prevention subjects.  

This topic summarizes the evidence regarding the benefits and risks of aspirin for primary prevention of CVD and cancer. We believe the utilization of aspirin, as for any over-the-counter drug used long term, should be an individual clinical and shared decision between the health care professional and each of his or her patients that carefully weighs all the absolute benefits against all the absolute risks [3-5].

Discussion of the role of aspirin in secondary prevention of CVD is presented separately. The role of nonsteroidal anti-inflammatory drugs and aspirin in the prevention of colorectal cancer (exclusive of CVD) is discussed separately as well. (See "NSAIDs (including aspirin): Role in prevention of colorectal cancer" and "Aspirin for the secondary prevention of atherosclerotic cardiovascular disease".)


Cardiovascular disease — Aspirin at all clinically relevant doses produces a clinically relevant antiplatelet effect by irreversibly acetylating the active site of cyclooxygenase-1 (COX-1), which is required for the production of thromboxane A2, a powerful promoter of aggregation. These findings are achieved by daily doses of 75 mg (and higher) or perhaps doses as low as 30 mg. Higher doses of aspirin also inhibit COX-2, which blocks prostaglandin production leading to analgesic and antipyretic effects. Although other mechanisms have been proposed (eg, an antiinflammatory effect), the antiplatelet effect seems sufficient to explain the observed statistically significant and clinically important benefits of aspirin on CVD. (See "Aspirin: Mechanism of action, major toxicities, and use in rheumatic diseases" and "Platelet biology" and "The role of the vulnerable plaque in acute coronary syndromes".)

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Literature review current through: Nov 2017. | This topic last updated: Jul 19, 2017.
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