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• W2000250960 abstract "Coronary artery disease (CAD) is the leading cause of death in the Western world, and atherosclerosis is responsible for virtually all of the cases. An understanding of atherosclerosis as an inflammatory process, rather than just a disease of lipid accumulation, has evolved over the recent years. There is compelling evidence that elevated levels of inflammatory mediators (interleukin-6, tumor necrosis factor [TNF]), cell adhesion molecules (intercellular adhesion molecule-1, P-selectin, E-selectin), and acute phase reactants (Creactive protein, fibrinogen, serum amyloid A) correlate with increased vascular risk. Oxidized lipoproteins, components of the renin-angiotensin system, high serum glucose, and obesity serve as potential triggers for inflammation in atherogenesis. These triggers are instantly recognizable as components of such risk factors for atherosclerosis as dyslipidemia, hypertension, and diabetes mellitus. However, while epidemiologic evidence for these and other “traditional” risk factors, such as age, gender, smoking, and family history of CAD is well established, a significant proportion of patients with symptomatic atherosclerosis fail to demonstrate any of them. An exploration of potential novel risk factors for CAD has been advocated, and the influence of infection as a contributor to atherogenic inflammation has since emerged as one of the attractive targets for basic scientific and clinical investigation." @default.
• W2000250960 created "2016-06-24" @default.
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• W2000250960 date "2004-02-01" @default.
• W2000250960 modified "2023-09-26" @default.
• W2000250960 title "Antibiotics for secondary prevention of coronary artery disease: an ACES hypothesis but we need to PROVE IT" @default.
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• W2000250960 doi "https://doi.org/10.1016/j.ahj.2003.09.011" @default.
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