Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
9101437 | Seminars in Arthritis and Rheumatism | 2005 | 10 Pages |
Abstract
The increased prevalence of CV mortality rate in RA cannot only be explained by the presence of traditional atherosclerotic risk factors. A chronic inflammatory response may promote the development of accelerated atherogenesis in these patients. Active treatment of the disease is required to reduce the risk of developing CV complications in individuals with RA.
Keywords
TNFFFAiNOSDASeNOSIMTESREDVMTXDMARDssICAM-1AtherogenesisLp(a)inducible NO synthaseRheumatoid arthritisHuman leukocyte antigenHLAapolipoproteinEndothelial dysfunctionFree fatty acidsendothelial NO synthaseinterleukinDisease-modifying antirheumatic drugerythrocyte sedimentation ratebody mass indexBMICarotid intima-media thicknessIntima-media thicknessrheumatoid factorCardiovascular complicationstumor necrosis factorcardiovascularLipoproteinLipoprotein(a)MethotrexateMortalityDisease activity scoreNitric oxideEndothelium-dependent vasodilatationInflammatory responseC-reactive proteinCRP
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Authors
Miguel A. MD, PhD, Carlos MD, Javier MD, PhD,