Role of inflammation in the pathogenesis of unstable coronary artery diseases

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Abstract
Inflammation has been shown to play a pivotal role in ischemic heart disease, in particular unstable angina. The instability that characterizes this syndrome is related to the waxing and waning of ischemic stimuli, especially thrombotic ones. Angiographically and autoptically the severity of the atherosclerotic background in unstable angina does not differ from that in chronic stable angina, but in the former mural thrombi are often found and coronary atherosclerotic plaques are characterized by an inflammatory infiltrate, mostly consisting of activated lymphocytes, macrophages and mast-cells. In addition to these local findings, systemic evidence also suggests the importance of the role of inflammation in unstable angina as platelets, neutrophils and monocytes are activated, and elevated levels of serum markers of inflammation, e.g. C-Reactive Protein, have been consistently found. CRP has been demonstrated to be a reliable marker of prognosis in coronary heart disease. The consequenses of inflammation are a disruption in the dynamic balance between antithrombotic and prothrombotic activities, an altered extracellular matrix metabolism, hyper-reactivity of cells such as monocytes and smooth muscle cells, all important features of unstable angina. These findings have important prognostic implications, since markers of inflammation are associated to a worse prognosis, and may also have therapeutic implications in the near future

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