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Acute respiratory infections (ARIs) are increasingly recognized as triggers of acute cardiovascular events [1]. Observational studies using large electronic healthcare databases have shown an approximately 2–5-fold transient increase in the risk of acute myocardial infarction (AMI), stroke, and other thrombotic events such as deep venous thrombosis after ARI [2–4]. Although the definition of ARI in these studies is frequently based on clinical, rather than microbiological, criteria evidence that some specific infections trigger vascular events comes indirectly from vaccine trials. One meta-analysis of randomized controlled trials of influenza vaccine in patients with existing cardiovascular disease showed a reduced risk of major adverse cardiovascular outcomes at 1 year [5]. For pneumococcal vaccine, meta-analyses of observational studies suggest a small protective effect against cardiovascular events in people aged >65 years [6, 7], but controlled trial evidence is lacking. In people who develop ARI, unanswered questions about how different ARI treatments might modulate vascular risk remain. Nonsteroidal anti-inflammatory drugs (NSAIDs) are widely used to reduce pain, fever, and inflammation associated with acute infections as well as symptoms of chronic musculoskeletal and other inflammatory conditions. Although the risk of gastrointestinal hemorrhage associated with these drugs has long been recognized, in recent years attention has focussed on adverse cardiovascular effects. Initially, concerns about increased risk of acute cardiovascular events arose when the new class-selective cyclooxygenase 2 (COX-2) inhibitors, with lower risks of gastrointestinal bleeding, were introduced [8–10]. However, a growing body of evidence has now established that risks of vascular events are increased by traditional nonselective NSAIDs, notably diclofenac [11]. The US Food and Drug Administration recommended that the selective COX-2 inhibitors rofecoxib and valdecoxib be removed from the market in 2004 and 2005 [12] and recently issued a black-box warning that NSAIDs can cause heart attacks [13]. In the United Kingdom, the National Institute for Health and Care Excellence recommends cautious prescription of NSAIDs based on assessing an individual’s risk factors such as history of cardiovascular and gastrointestinal illness, using the lowest effective dose for the shortest duration necessary to control symptoms, and opting for naproxen or low-dose ibuprofen for their more favorable thrombotic cardiovascular safety profile [14]. Nevertheless, some NSAIDs such as ibuprofen are widely available over the counter, and in the United States, NSAIDS are reportedly taken at least once per week by 50% of people aged >65 years [15]. In this issue of the Journal of Infectious Diseases, Wen and colleagues provide evidence for a dual effect of acute respiratory infection and NSAIDs on myocardial infarction risk in a case crossover study of 9793 patients from Taiwan [16]. Using comprehensive claims data over a 7-year period from the National Health Research Insurance Database, which covers approximately 99% of the population, they showed that acute respiratory infections treated with NSAIDs had a stronger association with AMI than ARIs not treated with NSAIDs or NSAID treatment alone. A series of sensitivity analyses strengthened the validity of the results and reduced the risk of bias due to inappropriate control time-window selection. This study represents an important step toward understanding the interaction between transient, nontraditional AMI risk factors. E D I T O R I A L C O M M E N T A R Y

the journal of infectious diseases (online. university of chicago press)/the journal of infectious diseases

Respiratory Tract Infections, Nonsteroidal Anti-inflammatory Drugs and Acute Myocardial Infarction: Is Understanding Interaction Between Risk Factors the Key to Personalizing Prevention?