Role of inflammation in the pathogenesis of unstable coronary artery diseases

Inflammation has been shown to play a pivotal role in ischemic heart diseas e, in particular unstable angina. The instability that characterizes this s yndrome is related to the waxing and waning of ischemic stimuli, especially thrombotic ones. Angiographically and autoptically the severity of the ath erosclerotic background in unstable angina does not differ from that in chr onic stable angina, but in the former mural thrombi are often found and cor onary atherosclerotic plaques are characterized by an inflammatory infiltra te, mostly consisting of activated lymphocytes, macrophages and mast-cells. In addition to these local findings, systemic evidence also suggests the i mportance of the role of inflammation in unstable angina as platelets, neut rophils and monocytes are activated, and elevated levels of serum markers o f inflammation, e.g. C-Reactive Protein, have been consistently found. CRP has been demonstrated to be a reliable marker of prognosis in coronary hear t disease. The consequenses of inflammation are a disruption in the dynamic balance between antithrombotic and prothrombotic activities, an altered ex tracellular matrix metabolism, hyper-reactivity of cells such as monocytes and smooth muscle cells, all important features of unstable angina. These f indings have important prognostic implications, since markers of inflammati on are associated to a worse prognosis, and may also have therapeutic impli cations in the near future.