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(Circulation. 2003;108:1428.)
© 2003 American Heart Association, Inc.
Brief Rapid Communications |
From the Departments of Medicine I (W.J.J., M.N., B.J., J.S.), Cardiac Surgery (E.T., J.F.M.B., S.M., H.-H.S., C.B.), and Surgery (M.D.), University of Lübeck School of Medicine, Lübeck, Germany.
Correspondence to Wolfram J. Jabs, MD, Department of Medicine I, University of Lübeck School of Medicine, Ratzeburger Allee 160, 23538 Lübeck, Germany. E-mail wjabs{at}gmx.de
Received October 14, 2002; de novo received June 6, 2003; revision received August 1, 2003; accepted August 4, 2003.
Background Venous coronary artery bypass grafts (CABGs) are prone to accelerated atherosclerosis. In atherosclerotic diseases, serum C-reactive protein (CRP) levels have become an important diagnostic and prognostic marker. The origin of CRP in this setting remains to be elucidated.
Methods and Results Monoclonal anti-CRP identified CRP expression in medial and intimal
-actinpositive smooth muscle cells (SMCs) of diseased CABGs with type V and VI lesions and also of native saphenous veins of atherosclerotic individuals. In addition, patent coronary arteries with type IV and V but not with type I through III lesions exhibited intense SMC staining for CRP. Calcified desobliterates of occluded coronary arteries with end-stage disease did not show SMC staining for CRP and were consistently negative for CRP mRNA, as detected by means of real-time polymerase chain reaction. However, CRP mRNA was expressed in 11 of 15 diseased CABGs and also in 10 of 15 native veins. By contrast, only 3 of 18 internal mammary and 4 of 12 radial arteries with virtually no atherosclerosis were positive for CRP mRNA.
Conclusions CRP is produced by SMCs of atherosclerotic lesions with active disease but not in end-stage plaques. The role of CRP constitutively expressed by normal vascular tissue in vein graft disease has yet to be elucidated.
Key Words: atherosclerosis inflammation restenosis
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