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      Contemporary Clinical Use of Aspirin: Mechanisms of Action, Current Concepts, Unresolved Questions, and Future Perspectives

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          Abstract

          The ability of aspirin to inhibit platelet aggregation has positioned this agent within the most frequently used drugs worldwide. The aim of this article is to review the contemporary clinical use of aspirin and also to discuss unresolved issues not yet translated into clinical practice. Results from several clinical trials have led to strong guideline recommendations for aspirin use in the acute management and secondary prevention of cardiovascular disease. On the contrary, guidelines regarding aspirin use as primary prevention of cardiovascular disease are almost conservative, supported by recent trials reporting that the bleeding risk outweighs the potential benefits in most patients. In pregnancy, aspirin has proved efficient in preventing preeclampsia and small-for-gestational-age births in women at high risk, and is hence widely recommended in clinical guidelines. Despite the vast amount of clinical data on aspirin, several unresolved questions remain. Randomized trials have reported that aspirin reduces the risk of recurrent venous thromboembolism, but the clinical relevance remains limited, because direct oral anticoagulants are more effective. Laboratory studies suggest that a twice-daily dosing regimen or evening intake may lead to more efficient platelet inhibition, and the potential clinical benefit of such strategies is currently being explored in ongoing clinical trials. Enteric-coated formulations of aspirin are frequently used, but it remains unclear if they are safer and as efficient as plain aspirin. In the future, aspirin use after percutaneous coronary interventions might not be mandatory in patients who also need anticoagulant therapy, as several trials support shorter aspirin duration strategies. On the other hand, new treatment indications for aspirin will likely arise, as there is growing evidence that aspirin may reduce the risk of colorectal cancer and other types of cancer.

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          Most cited references148

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          2019 ESC Guidelines for the diagnosis and management of chronic coronary syndromes

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            Is Open Access

            Global causes of maternal death: a WHO systematic analysis.

            Data for the causes of maternal deaths are needed to inform policies to improve maternal health. We developed and analysed global, regional, and subregional estimates of the causes of maternal death during 2003-09, with a novel method, updating the previous WHO systematic review. We searched specialised and general bibliographic databases for articles published between between Jan 1, 2003, and Dec 31, 2012, for research data, with no language restrictions, and the WHO mortality database for vital registration data. On the basis of prespecified inclusion criteria, we analysed causes of maternal death from datasets. We aggregated country level estimates to report estimates of causes of death by Millennium Development Goal regions and worldwide, for main and subcauses of death categories with a Bayesian hierarchical model. We identified 23 eligible studies (published 2003-12). We included 417 datasets from 115 countries comprising 60 799 deaths in the analysis. About 73% (1 771 000 of 2 443 000) of all maternal deaths between 2003 and 2009 were due to direct obstetric causes and deaths due to indirect causes accounted for 27·5% (672 000, 95% UI 19·7-37·5) of all deaths. Haemorrhage accounted for 27·1% (661 000, 19·9-36·2), hypertensive disorders 14·0% (343 000, 11·1-17·4), and sepsis 10·7% (261 000, 5·9-18·6) of maternal deaths. The rest of deaths were due to abortion (7·9% [193 000], 4·7-13·2), embolism (3·2% [78 000], 1·8-5·5), and all other direct causes of death (9·6% [235 000], 6·5-14·3). Regional estimates varied substantially. Between 2003 and 2009, haemorrhage, hypertensive disorders, and sepsis were responsible for more than half of maternal deaths worldwide. More than a quarter of deaths were attributable to indirect causes. These analyses should inform the prioritisation of health policies, programmes, and funding to reduce maternal deaths at regional and global levels. Further efforts are needed to improve the availability and quality of data related to maternal mortality. © 2014 World Health Organization; licensee Elsevier. This is an Open Access article published without any waiver of WHO's privileges and immunities under international law, convention, or agreement. This article should not be reproduced for use in association with the promotion of commercial products, services, or any legal entity. There should be no suggestion that WHO endorses any specific organisation or products. The use of the WHO logo is not permitted. This notice should be preserved along with the article's original URL.
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              Diabetes mellitus, fasting blood glucose concentration, and risk of vascular disease: a collaborative meta-analysis of 102 prospective studies

              Summary Background Uncertainties persist about the magnitude of associations of diabetes mellitus and fasting glucose concentration with risk of coronary heart disease and major stroke subtypes. We aimed to quantify these associations for a wide range of circumstances. Methods We undertook a meta-analysis of individual records of diabetes, fasting blood glucose concentration, and other risk factors in people without initial vascular disease from studies in the Emerging Risk Factors Collaboration. We combined within-study regressions that were adjusted for age, sex, smoking, systolic blood pressure, and body-mass index to calculate hazard ratios (HRs) for vascular disease. Findings Analyses included data for 698 782 people (52 765 non-fatal or fatal vascular outcomes; 8·49 million person-years at risk) from 102 prospective studies. Adjusted HRs with diabetes were: 2·00 (95% CI 1·83–2·19) for coronary heart disease; 2·27 (1·95–2·65) for ischaemic stroke; 1·56 (1·19–2·05) for haemorrhagic stroke; 1·84 (1·59–2·13) for unclassified stroke; and 1·73 (1·51–1·98) for the aggregate of other vascular deaths. HRs did not change appreciably after further adjustment for lipid, inflammatory, or renal markers. HRs for coronary heart disease were higher in women than in men, at 40–59 years than at 70 years and older, and with fatal than with non-fatal disease. At an adult population-wide prevalence of 10%, diabetes was estimated to account for 11% (10–12%) of vascular deaths. Fasting blood glucose concentration was non-linearly related to vascular risk, with no significant associations between 3·90 mmol/L and 5·59 mmol/L. Compared with fasting blood glucose concentrations of 3·90–5·59 mmol/L, HRs for coronary heart disease were: 1·07 (0·97–1·18) for lower than 3·90 mmol/L; 1·11 (1·04–1·18) for 5·60–6·09 mmol/L; and 1·17 (1·08–1·26) for 6·10–6·99 mmol/L. In people without a history of diabetes, information about fasting blood glucose concentration or impaired fasting glucose status did not significantly improve metrics of vascular disease prediction when added to information about several conventional risk factors. Interpretation Diabetes confers about a two-fold excess risk for a wide range of vascular diseases, independently from other conventional risk factors. In people without diabetes, fasting blood glucose concentration is modestly and non-linearly associated with risk of vascular disease. Funding British Heart Foundation, UK Medical Research Council, and Pfizer.
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                Author and article information

                Journal
                Seminars in Thrombosis and Hemostasis
                Semin Thromb Hemost
                Georg Thieme Verlag KG
                0094-6176
                1098-9064
                June 15 2021
                Affiliations
                [1 ]Department of Clinical Biochemistry, Regional Hospital in Horsens, Horsens, Denmark
                [2 ]Department of Cardiology, Aarhus University Hospital, Aarhus, Denmark
                [3 ]Department of Clinical Medicine, Faculty of Health, Aarhus University, Aarhus, Denmark
                [4 ]Department of Clinical Biochemistry, Aarhus University Hospital, Aarhus, Denmark
                Article
                10.1055/s-0041-1726096
                34130339
                6178864b-68af-4c14-b761-acb0018cd966
                © 2021
                History

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