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(Circulation. 1999;99:2976-2978.)
© 1999 American Heart Association, Inc.

Brief Rapid Communications

Intravascular Ultrasound Evidence for Coarctation Causing Symptomatic Renal Artery Stenosis

Trude C. Leertouwer, MSc; Elma J. Gussenhoven, MD; Lukas C. van Dijk, MD; Jeroen A. van Essen, MD; Jan Honkoop, BSc; Jaap Deinum, MD; Peter M. T. Pattynama, MD

From the Departments of Radiology (T.C.L., L.C.v.D., P.M.T.P.), Internal Medicine (T.C.L., J.D.), and Cardiology (E.J.G., J.A.v.E., J.H.), the Erasmus University Medical Center, Rotterdam, and the Interuniversity Cardiology Institute (E.J.G., J.A.v.E.), The Netherlands.

Correspondence to Elma J. Gussenhoven, MD, Erasmus University Rotterdam (Ee 2312), Dr. Molewaterplein 50, 3000 DR Rotterdam, The Netherlands. E-mail leertouwer{at}tch.fgg.eur.nl

Background—A recent study of human cadaveric renal arteries revealed that renal artery narrowing could be due not only to atherosclerotic plaque compensated for by adaptive remodeling, but also to hitherto undescribed focal narrowing of an otherwise normal renal arterial wall (ie, coarctation). The present study investigated whether vessel coarctation could be identified in patients with symptomatic renal artery stenosis (RAS).

Methods and Results—Consecutive symptomatic patients with angiographically proven atherosclerotic RAS who were referred for stent placement were studied by 30-MHz intravascular ultrasound before intervention (n=18) or after predilatation (n=18). Analysis included assessment of the media-bounded area and plaque area (PLA) at the most stenotic site and at a distal reference site (most distal cross-section in the main renal artery with normal appearance). Coarctation was considered present whenever the target/reference media-bounded area was 85%. Before intervention, coarctation was observed in 9 of 18 patients and adaptive remodeling in 9 of 18 patients. Coarctation lesions had a significantly smaller PLA than adaptive remodeled lesions (P=0.001). Similarly, despite predilatation, coarctation was seen in 8 of 18 patients who had significantly smaller PLAs (P=0.008) when compared with those patients who had adaptive remodeled lesions. No differences in severity of RAS or angiographic or clinical parameters were observed.

Conclusions—Low-plaque coarctation may cause a considerable proportion of symptomatic RAS, which is angiographically and clinically indistinguishable from plaque-rich RAS.

Key Words: renal artery • stenosis • hypertension • ultrasonography, interventional

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