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Extensive research in recent decades has established a critical role for cellular and humoral inflammation in the initiation and progression of atherosclerosis and its acute clinical presentations.1 Although atherosclerotic disease has a slow progression over many years, several intrinsic and extrinsic factors may trigger latent stable atherosclerotic plaques to become inflamed, unstable plaques that often rupture and start a cascade leading to thrombus formation and acute coronary syndromes or sudden cardiac death. Respiratory infections are among the known triggers for such acute cardiovascular events.
In the past 2 decades, many basic and epidemiologic studies have suggested a role for chronic indolent infections, such as Chlamydia pneumoniae, in the chronic progression of atherosclerotic lesions over years. Failure of clinical trials using antibiotics against C. pneumoniae to prevent cardiovascular events has led to a decreased interest in the role of infections in cardiovascular disease. However, in contrast to chronic infections, acute infections may cause acute coronary syndromes by triggering severe and abrupt inflammatory changes in high-risk coronary plaques over a few days or weeks. Prevention or treatment of these infections may offer new targets for coronary prevention.2
In this issue of CMAJ, Lamontagne and colleagues3 present their findings from a large hospital-based database study. The authors studied the incidence of myocardial infarctions among those who had or had not received a pneumococcal vaccine before admission to hospital. They include patients who were free of known atherosclerotic disease but who were at risk of myocardial infarction based on age (men aged 45 years or older, women aged 50 years or older) and who had at least 1 cardiovascular disease risk factor (hypertension, diabetes or hyperlipidemia). The authors report that people who had a myocardial infarction were less likely than those who did not have a myocardial infarction to have received a pneumococcal polysaccharide vaccine (7.1% v. 11.6%; adjusted odds ratio 0.53, 95% confidence interval 0.40-0.70).
The study by Lamontagne and colleagues does not include data on the incidence of pneumonia and its relation to myocardial infarction in cases and controls. However, it is reasonable to hypothesize that pneumococcal vaccination may protect against cardiovascular events by preventing pneumonia, as the latter has been shown to trigger myocardial infarction. Musher and colleagues4 reviewed a series of 170 patients admitted to...