C-reactive protein and coronary artery disease—what is the link?

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Abstract
Inflammation of the vessel wall is now considered to play an essential role in the initiation and progression of atherosclerosis [1], and also in its final steps, i.e. plaque erosion or fissure, and eventually plaque rupture [2]. This notion is based on classical pathological studies showing the presence of inflammatory cells, such as monocyte-derived macrophages, T-lymphocytes, and mast cells not only at the site of rupture or superficial erosion [3] but rather at every stage of the disease, even in the very early lesions, the so-called fatty streaks. These morphologic changes are preceded by dysfunction of activated endothelial cells that produce so called adhesion molecules (ICAM-1, E-selectin) that interact with inflammatory cells [4]. The ability of monocyte-derived macrophages to secrete various cytokines (IL-1, IL-6, TNF-α), chemokines (MCP-1), and growth-factors (PDGF, bFGF, VEGF), further leads to activation and proliferation of smooth muscle cells, progression of the lesion, and finally weakening of vulnerable plaques by degradation of the fibrous cap. Yet atherosclerosis and its clinical complications are not only characterized by local inflammation. Recent prospective studies have shown that several markers of systemic inflammation may be used to predict future cardiovascular events [5].