Abstract
The complications of atherosclerosis are associated with a high incidence of morbidity and mortality in Western societies [1]. Coronary atherosclerosis is now considered a complex inflammatory process in response to the retention of specific atherogenic lipoproteins in the arterial wall. In addition to the localized immune response, there is emerging evidence that systemic inflammatory markers may have a diagnostic value in predicting acute cardiac events. Among the many risk factors for atherosclerosis, hyperlipidemia is thought the most influential on inflammatory processes along with specific immunological factors. Recent animal studies suggest that the induction of atherosclerosis is closely linked to lipoprotein abnormalities since genetic derangements of systemic or localized immunity alone do not initiate the disease. Although genetically engineered animals have furthered the understanding of the role of inflammation in atherosclerosis, the relevance of these findings to disease progression in humans are not as clear. This chapter will discuss the role of inflammation in the evolution of varying coronary lesions, particularly those associated with acute coronary syndromes. In addition, potential systemic factors that may influence inflammation in the vessel wall in relation to plaque instability will also be addressed.
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Virmani, R., Kolodgie, F.D., Burke, A.P., Farb, A., Gold, H.K., Finn, A.V. (2003). Inflammation and coronary artery disease. In: Feuerstein, G.Z., Libby, P., Mann, D.L. (eds) Inflammation and Cardiac Diseases. Progress in Inflammation Research. Birkhäuser, Basel. https://doi.org/10.1007/978-3-0348-8047-3_3
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DOI: https://doi.org/10.1007/978-3-0348-8047-3_3
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