PubMed · 10608078
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R S Jack. 2000. Introduction: hunting devils.. https://pubmed.ncbi.nlm.nih.gov/10608078/
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Inflammation is involved in the initiation and progression of atherosclerosis and the development of atherosclerotic events. Understanding of the molecular basis of inflammation has led to the identification of markers that may be important new targets in atherothrombotic disease. Inflammatory markers, such as cell adhesion molecules, cytokines, and high-sensitivity C-reactive protein, have been shown to predict future cardiovascular events in individuals with and without established disease. 3-hydroxy-3-methylglutaryl coenzyme A (HMG CoA) reductase inhibitors, or statins, inhibit the synthesis of cholesterol and have been demonstrated to reduce cardiovascular morbidity and mortality. Recently, statins have been shown to modulate several of the mechanisms of inflammation in atherosclerosis in vitro and in vivo, including reduction of inflammatory markers in clinical trials. In this article, we briefly review the biology, epidemiology, and clinical trial data on the effects of statins on some of the more promising inflammatory markers.
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Many recent experimental and clinical studies have provided evidence for the presence of inflammation in atherosclerotic lesions. Ongoing inflammatory reactions within coronary atherosclerotic plaques are increasingly thought to be crucial determinants of the clinical course of patients with coronary artery disease (CAD). These facts lead to a search for reliable markers reflecting the inflammatory process in the atherosclerotic plaques. Circulating markers may consist of cytokines directly released from inflammatory cells present in the plaques and tissues exposed to recurrent ischemia as well as other reactants produced in response to these cytokines such as adhesion molecules and acute phase proteins. Recent studies suggest that markers of inflammation may reflect different aspects of the atherothrombotic process at different points in the continuum of acute coronary syndromes, have a potential role for the prediction of risk for developing CAD, and may correlate with severity and future risk for CAD. In spite of these findings, the clinical utility of measuring these markers is limited by the availability of reproducible diagnostic test assays. In addition, it remains to be determined whether markers of inflammation actually have a causal relation with cardiovascular disease, or simply reflect the underlying disease process. Such determination becomes important with the potential use of these markers in targeting preventive therapies. Therefore, further well-designed prospective evaluation of each of these markers is needed before their use in routine practice.