Published Online
on June 9, 2008

A more recent version of this article appeared on June 17, 2008

This Article Full Text (PDF) CME: Take the course for this article: Circulation: June 17, 2008, Volume 117, Number 24 All Versions of this Article: 117/24/3126    most recent CIRCULATIONAHA.108.778472v1 Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Vita, J. A. Articles by Shapira, O. M. Search for Related Content PubMed PubMed Citation Articles by Vita, J. A. Articles by Shapira, O. M. Pubmed/NCBI databases Medline Plus Health Information Coronary Artery Bypass Surgery Related Collections Remodeling Pathophysiology Endothelium/vascular type/nitric oxide Related Article

Submitted on November 4, 2007
Accepted on April 22, 2008

Flow-Induced Arterial Remodeling Relates to Endothelial Function in the Human Forearm

Joseph A. Vita MD^*, Monika Holbrook MS, Joseph Palmisano MPH, Sherene M. Shenouda PhD, William B. Chung MD, Naomi M. Hamburg MD, Benjamin R. Eskenazi BA, Lija Joseph MD, and Oz M. Shapira MD

From the Evans Department of Medicine (J.A.V., M.H., J.P., S.M.S., W.B.C., N.M.H.), Department of Cardiothoracic Surgery (B.R.E., O.M.S.), and Mallory Institute of Pathology (L.J.), Boston University School of Medicine, Boston, Mass.

^* To whom correspondence should be addressed. E-mail: jvita{at}bu.edu.

Background—Chronic changes in blood flow stimulate arterial remodeling, which contributes to the maintenance of vascular homeostasis. Experimental studies suggest that remodeling represents a response to local changes in endothelial shear stress and is nitric oxide–dependent.

Methods and Results—To investigate determinants of outward arterial remodeling in humans, we measured ulnar artery flow, diameter, and flow-mediated dilation before and after removal of the adjacent radial artery in 53 patients who were undergoing coronary bypass surgery (age 60±11 years; 13% female). Removal of the radial artery increased ulnar artery blood flow by 35% (P=0.009) and increased ulnar artery diameter by 9% (P<0.001) 4 to 8 weeks after surgery. At 1 week, ulnar artery shear stress was increased by 58% (P<0.001), but it was no longer different from baseline at longer-term follow-up. The contralateral ulnar artery was unaffected, which suggests that these findings were not attributable to the systemic effects of medications or the postoperative state. Extent of outward remodeling correlated with the increase in blood flow (r=0.50, P=0.001) and with flow-mediated dilation at baseline (r=0.50, P=0.001). Remodeling correlated inversely with baseline endothelial expression of P-selectin in the radial artery (r=-0.76, P=0.004, n=14).

Conclusions—A sustained increase in blood flow in the ulnar artery induced outward arterial remodeling despite the presence of risk factors and coronary artery disease. The remodeling response was related to endothelial phenotype, as reflected by flow-mediated dilation and expression of P-selectin. These findings provide evidence that the endothelium plays an important role in the regulation of vascular structure in humans.

Key words: remodeling • endothelium • shear stress • blood flow • P-selectin

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Clinical Summaries
Circulation 2008 117: 3055-3056. [Extract] [Full Text]

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