Inflammation and acute coronary syndromes

The presence of inflammatory infiltrates in unstable coronary plaques sugge sts that inflammatory processes may contribute to the pathogenesis of these syndromes In patients with unstable angina, coronary atherosclerotic plaqu es are characterized by the presence of macrophages, and to a lesser extent , T-lymphocytes at the immediate site of either plaque rupture or superfici al erosion: moreover, the rupture-related inflammatory cells an activated, indicating ongoing inflammation at the site of plaque disruption. These obs ervations are confirmed by clinical studies demonstrating activated circula ting neutrophils lymphocytes and monocytes, and increased concentrations of pro-inflammatory cytokines, such as interleukin (IL) 1 and 6, and of acute phase reactants in patients with unstable angina and myocardial infarction . In particular elevated levels of C-reactive protein are associated with a n increased risk of in-hospital and 1 to 2 years new coronary events in pat ients with unstable angina, but are also associated with an increased long- term risk of death and myocardial infarction in apparently normal subjects. Thus, accumulating evidence suggests that inflammation may cause local end othelial activation and, possibly plaque fissure, leading to unstable angin a and infarction. Although no information is yet available on the causes of inflammation and on its localization, these novel lines of research may op en the way to a different approach to the patient with acute coronary syndr omes.