Heart disease and the inflammatory response

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Abstract
Papers pp 199, 204, 208 Inflammation in the vessel wall plays an essential part not only in the initiation and progression of atherosclerosis but also in the erosion or fissure of plaques and, eventually, in the rupture of plaques.1 Moreover, recent investigations have shown that various markers of systemic inflammation can predict future cardiovascular events including non-fatal and fatal myocardial infarction, stroke, and the progression of peripheral arterial occlusive disease in men and women regardless of whether they are known to have atherosclerosis. Most of the data available are on the role of fibrinogen, an acute phase protein, in coronary heart disease.2 Other acute phase reactants, including leucocyte count, have also been consistently linked to the future risk of cardiovascular events.3 C reactive protein, the classic acute phase protein, was first associated with cardiovascular events in patients with coronary heart disease after analysis of prospective data from the European concerted action on thrombosis (ECAT) angina pectoris study.4 Although the epidemiological evidence for such an association is consistent, it is not clear whether it reflects a causal relation. Firstly, residual confounding cannot be excluded from the studies. Secondly, although various mechanisms have been suggested that would link the protein directly to atherogenesis—for example, that it binds low density lipoproteins, stimulates tissue factor production, or mediates tissue damage through activation of the …