Inflammation and Atherosclerosis Export

@article{citeulike:809569, abstract = {Atherosclerosis, formerly considered a bland lipid storage disease, actually involves an ongoing inflammatory response. Recent advances in basic science have established a fundamental role for inflammation in mediating all stages of this disease from initiation through progression and, ultimately, the thrombotic complications of atherosclerosis. These new findings provide important links between risk factors and the mechanisms of atherogenesis. Clinical studies have shown that this emerging biology of inflammation in atherosclerosis applies directly to human patients. Elevation in markers of inflammation predicts outcomes of patients with acute coronary syndromes, independently of myocardial damage. In addition, low-grade chronic inflammation, as indicated by levels of the inflammatory marker C-reactive protein, prospectively defines risk of atherosclerotic complications, thus adding to prognostic information provided by traditional risk factors. Moreover, certain treatments that reduce coronary risk also limit inflammation. In the case of lipid lowering with statins, this anti-inflammatory effect does not appear to correlate with reduction in low-density lipoprotein levels. These new insights into inflammation in atherosclerosis not only increase our understanding of this disease, but also have practical clinical applications in risk stratification and targeting of therapy for this scourge of growing worldwide importance. 10.1161/hc0902.104353}, author = {Libby, Peter and Ridker, Paul M. and Maseri, Attilio}, citeulike-article-id = {809569}, citeulike-linkout-0 = {http://dx.doi.org/10.1161/hc0902.104353}, citeulike-linkout-1 = {http://circ.ahajournals.org/cgi/content/abstract/105/9/1135}, citeulike-linkout-2 = {http://view.ncbi.nlm.nih.gov/pubmed/11877368}, citeulike-linkout-3 = {http://www.hubmed.org/display.cgi?uids=11877368}, day = {5}, doi = {10.1161/hc0902.104353}, journal = {Circulation}, keywords = {atherosclerosis, inflammation, inflammatory, review}, month = {March}, number = {9}, pages = {1135--1143}, posted-at = {2008-06-02 10:36:51}, priority = {3}, title = {Inflammation and Atherosclerosis}, url = {http://dx.doi.org/10.1161/hc0902.104353}, volume = {105}, year = {2002} }

TY - JOUR ID - citeulike:809569 L3 - citeulike-article-id:809569 N2 - Atherosclerosis, formerly considered a bland lipid storage disease, actually involves an ongoing inflammatory response. Recent advances in basic science have established a fundamental role for inflammation in mediating all stages of this disease from initiation through progression and, ultimately, the thrombotic complications of atherosclerosis. These new findings provide important links between risk factors and the mechanisms of atherogenesis. Clinical studies have shown that this emerging biology of inflammation in atherosclerosis applies directly to human patients. Elevation in markers of inflammation predicts outcomes of patients with acute coronary syndromes, independently of myocardial damage. In addition, low-grade chronic inflammation, as indicated by levels of the inflammatory marker C-reactive protein, prospectively defines risk of atherosclerotic complications, thus adding to prognostic information provided by traditional risk factors. Moreover, certain treatments that reduce coronary risk also limit inflammation. In the case of lipid lowering with statins, this anti-inflammatory effect does not appear to correlate with reduction in low-density lipoprotein levels. These new insights into inflammation in atherosclerosis not only increase our understanding of this disease, but also have practical clinical applications in risk stratification and targeting of therapy for this scourge of growing worldwide importance. 10.1161/hc0902.104353 IS - 9 JF - Circulation EP - 1143 TI - Inflammation and Atherosclerosis VL - 105 SP - 1135 KW - atherosclerosis KW - inflammation KW - inflammatory KW - review AU - Libby, Peter AU - Ridker, Paul AU - Maseri, Attilio PY - 2002/03/05/ UR - http://dx.doi.org/10.1161/hc0902.104353 ER -