J Thorac Cardiovasc Surg 2007;134:277-279
© 2007 The American Association for Thoracic Surgery
Division of Cardiac Surgery and Keenan Research Centre, Li Ka Shing Knowledge Institute, St Michaels Hospital, University of Toronto, Toronto, Ontario, Canada.
Received for publication March 10, 2007; accepted for publication March 15, 2007. * Address for reprints: Subodh Verma, MD, PhD, Division of Cardiac Surgery, Suite 8-003F, Bond Wing, St Michaels Hospital, 30 Bond St, Toronto, Ontario, Canada M5B 1W8. (Email: firstname.lastname@example.org).
|The first 20% of the full text of this article appears below.|
In this issue, Momin and colleagues1 present timely translational evidence that preoperative C-reactive protein (CRP) levels may predict the functionality and patency of saphenous vein grafts (SVGs) after coronary artery bypass graft (CABG) procedures. Endothelial function was examined in saphenous vein segments from patients undergoing CABG who had been treated with simvastatin preoperatively. CRP levels emerged as the only independent (negative) correlate of endothelial function, and they consequently open the window to the possibility that patients with elevated CRP may be predisposed to postoperative SVG occlusions among other de novo atherosclerosis-related complications.
Although the immediate procedural success with SVGs is comparable with that of arterial grafts, the greater susceptibility of SVGs to accelerated intimal hyperplasia and atherosclerosis remains a limiting factor. Improving endothelial function is an important therapeutic approach in limiting aberrant saphenous vein remodeling.
Notwithstanding the small cohort size of 76 subjects and some interpretational limitations, Momin and colleagues1 are to be congratulated for evaluating how CRP (a critical player in inflammatory processes and a biomarker of atherosclerosis) alters SVG vasoresponsiveness and how this, in turn, may influence the efficacy of SVGs. Insight on the interplay between serum CRP concentrations and SVG longevity are unfortunately lacking and would have greatly strengthened this work. Inasmuch as inflammation is increasingly recognized as the crux of atherosclerosis, it would have been prudent for the authors to also monitor CRP values perioperatively and postoperatively. Concurrent expansion of the inflammatory marker panel studied to include serum amyloid A and fibrinogen (among others) that are closely associated with the pathogenesis of atherosclerosis would also have been of great interest. Accordingly, a prospective study encompassing angiographic follow-ups coupled with measurements of serum CRP and other endogenous inflammatory agents in
J. Thorac. Cardiovasc. Surg. 2007 134: 335-341.
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