Aims In patients recovering from acute coronary syndromes (ACS) the role of oral anticoagulation (and its intensity) in addition to aspirin remains controversial. We conducted a specific meta-analysis of randomized trials comparing aspirin plus warfarin (A+W) with aspirin alone in such patients. Methods and results MEDLINE and Cochrane databases yielded 14 (of 148 potentially relevant) articles enrolling 25 307 patients. Follow-up ranged from 3 months to 5 years. Irrespective of International normalized ratio (INR), A+W did not significantly affect the risk of major adverse events (MAE: all cause death, non-fatal myocardial infarction, and non-fatal thrombo-embolic stroke) when compared with aspirin alone [OR 0.96 (0.90–1.03), P=0.30], but increased the risk of major bleeds (MB): OR 1.77 (1.47–2.13), P<0.00001. However, in studies with INR of 2–3, A+W was associated with a significant reduction of MAE [OR 0.73 (0.63–0.84), P<0.0001, number needed to treat to avoid one MAE=33], albeit at an increased risk of MB [OR 2.32 (1.63–3.29), P<0.00001; number needed to harm by causing one MB=100]. In both analyses, intracranial bleeding was not significantly increased by A+W when compared with aspirin alone. Conclusion For patients recovering from ACS, a combined strategy of A+W at INR values of 2–3 doubles the risk of MB, but is nonetheless superior to aspirin alone in preventing MAE. Whether this combined regimen is also superior to a ‘double’ anti-platelet strategy or to newer evolving treatments warrants further investigation.

Contemporary medicine is shifting towards person rather than disease-oriented care.¹ With increasing life expectancy and the ageing of baby boomers, the proportion over 60 years is growing faster than the overall population, with worldwide estimates reaching 2 billion by 2050 (http://www.un.org/esa/population/publications/worldageing19502050).² In parallel, acute coronary syndromes (ACS) and atrial fibrillation (AF)—the most frequent indications for dual platelet inhibition or anticoagulation—occur mostly in older patients.^2–6 There is general agreement that people ≥75 years can be defined ‘elderly’; however, cutoffs as low as 65 years have been applied to important clinical datasets and risk scores.^3,7–10 Moreover, ageing is a continuous process and life-span expansion is deflating (http://www.nber.org/papers/w18407). For these reasons, a threshold to define ‘elderly’ has been intentionally avoided in this document. Of note, over one third of patients admitted with acute myocardial infarction (MI) and two thirds dying from MI are over 75 years, but <7% of patients in ACS trials are reported ≥75 years.¹¹ Older patients have multi-organ changes, increased risk of both bleeding and ischaemic events,^3,5,12 frequent comorbidities/comedication, and reduced adherence to prescriptions. Given the challenges of antithrombotic treatment in the elderly, the European Society of Cardiology (ESC) Working Group on Thrombosis gathered a task group to address the topic.

Inflammation and genetics are both prominent mechanisms in the pathogenesis of atherosclerosis and arterial thrombosis. Accordingly, a number of population studies have explored the association of ischaemic heart disease with gene polymorphisms of the inflammatory molecules tumour necrosis factors (TNF) α and β, transforming growth factors (TGF) β1 and 2, interleukin (IL) 1 and its receptor antagonist (IL 1ra), CD14 (the receptor for lipopolysaccharide), P and E selectins, and platelet endothelial cell adhesion molecule (PECAM) 1. Although they are very preliminary and partly conflicting, the data provide some evidence that alterations in the genetics of the inflammatory system may modify the risk of ischaemic heart disease.