Inflammation markers and coronary heart disease

Abstract

Evidence supports the position that the chronic atherothrombotic process is intimately associated with what has classically been called ‘inflammation'. Proteins that are part of the acute phase response (e.g. fibrinogen, C-reactive protein) are sensitive markers of low-level inflammation, and in population studies, inflammation marker levels at the upper end of the healthy reference range are associated with the presence of subclinical atherothrombotic disease (e.g. carotid wall thickness) and, prospectively, with future cardiovascular disease events. While there are plausible mechanisms for most of these markers, it remains to be demonstrated whether the markers actually participate in cardiovascular disease, or simply reflect the underlying disease process. This point is important, since marker-specific interventions might be useful if the former position is correct. Recent work suggests that inflammation markers may represent different aspects of the atherothrombotic process at different points in the natural history of the disease. This has implications for the interpretation of marker levels and the timing of the future events that they predict.