When I was a medical student, atherosclerosis was seen as a process resembling the deposition of calcium deposits in pipes in an old house with gradual accumulation of precipitated minerals on the inner walls of these pipes. Basic science and clinical research over the last 40 years have made it clear that the process that actually leads to atherosclerosis involves inflammatory changes within the arterial wall that begin after some form of injury to the vascular endothelium that lines the arteries.
Macrophages in atherosclerotic lesions are highly active, producing a variety of inflammatory cytokines (eg, interleukins), as well as a number of other enzymes, for example, collagenase, a molecule that can dissolve structural components within the atherosclerotic plaque itself, thereby weakening the structural integrity of the plaque. Current thinking supports the concept that these inflammatory mediators are involved in the transition from a stable plaque to an unstable, fissured, ruptured, or dissected plaque with exposure of underlying thrombogenic material to the flowing blood in the artery with resultant thrombus formation.
What factors contribute to this inflammatory atherosclerotic process, and how might these be curtailed? A number of circulating inflammatory biomarkers have been identified in the blood of patients with ischemic heart disease. Higher levels of these molecules in the blood are associated with a markedly increased risk that the patient will develop an acute coronary syndrome, such as unstable angina or acute myocardial infarction. One of the most carefully studied of these inflammatory biomarkers is high-sensitivity C-reactive protein (hsCRP).(1, 2)
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— Joseph S. Alpert, MD
This article was originally published in the May 2009 issue of The American Journal of Medicine.
