Published Online
on September 15, 2003

A more recent version of this article appeared on September 23, 2003

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Submitted on October 14, 2002
Revised on August 1, 2003
Accepted on August 4, 2003

Local Generation of C-Reactive Protein in Diseased Coronary Artery Venous Bypass Grafts and Normal Vascular Tissue

Wolfram J. Jabs MD^*, Elisabeth Theissing , Martin Nitschke MD, J.F. Matthias Bechtel MD, Michael Duchrow PhD, Salah Mohamed PhD, Bernhard Jahrbeck MD, Hans-Hinrich Sievers MD, Jürgen Steinhoff MD, and Claus Bartels MD

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.

^* To whom correspondence should be addressed. E-mail: wjabs{at}gmx.de.

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 -actin-positive 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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