Inflammation in coronary artery disease: Which biomarker and which treatment?

As early as 1856, Richard Virchow used the term coronaritis in his pathology book. More than a century later, in 1994, Liuzzo et al. published the first clinical evidence of the important role of inflammation in ischemic heart disease, showing that among patients with an acute coronary syndrome, those with C-reactive protein (CRP) > 3 mg/l had a worse outcome than those with normal CRP levels.1 In 1999, Ross published in New England Journal of Medicine a review paper titled “Atherosclerosis: An inflammatory disease.”2 Thus, after more than one and a half centuries from Virchow’s observation, there is now solid experimental, clinical and epidemiological evidence of a close association between inflammation and short- and long-term cardiovascular outcomes.3 Also, the increased risk of myocardial infarction after infections has been recognized for decades.4 As this risk is constant for a wide variety of etiologic agents and sites of infection, it is probably reasonable to assume that the systemic inflammatory reaction, and not the specific pathogen or location, is the major determinant of this relationship. Possible contributing mechanisms are the increased inflammatory activity in atheromatous plaques and the pro-thrombotic state induced by the systemic inflammatory reaction.