Fitzgerald, P.J. (Peter)

Herity, N.A. (Niall)

Jaegere, P.P.T. (Peter) de

Jeremias, A.

Pasterkamp, G. (Gerard)

Serruys, P.W.J.C. (Patrick)

Smits, P.C. (Pieter)

Ward, M.R.

Yeung, A.C. (Alan)

Erasmus University Digital Repository

ISSN: 1524-4636 Copyright © 2001 American Heart Association. All rights reserved. Print ISSN: 1079-5642. Online7272 Greenville Avenue, Dallas, TX 72514Arteriosclerosis, Thrombosis, and Vascular Biology is published by the American Heart Association. 2001;21;1383- Arterioscler. Thromb. Vasc. Biol.Alan C. Yeung, Peter de Jaegere, Patrick W. Serruys and Gerard Pasterkamp Michael R. Ward, Peter Smits, Niall A. Herity, Allen Jeremias, Peter J. Fitzgerald, Arterial Segment InvolvedRemodeling of Focal Stenotic Atherosclerotic Lesions and Tortuosity of the Letter to the Editor: No Relationship Between Compensatory Arterial http://atvb.ahajournals.org/cgi/content/full/21/8/1383located on the World Wide Web at: The online version of this article, along with updated information and services, is http://www.lww.com/static/html/reprints.htmlReprints: Information about reprints can be found online at    journalpermissions@lww.comStreet, Baltimore, MD 21202-2436. Phone 410-5280-4050. Fax: 410-528-8550. Email: Permissions: Permissions & Rights Desk, Lippincott Williams & Wilkins, 351 West Camden   http://atvb.ahajournals.org/subsriptions/Biology is online at Subscriptions: Information about subscribing to Arteriosclerosis, Thrombosis, and Vascular at SWETS SUBS SERVICE on October 17, 2006 atvb.ahajournals.orgDownloaded from No Relationship Between CompensatoryArterial Remodeling of Focal StenoticAtherosclerotic Lesions and Tortuosity of theArterial Segment InvolvedTo the Editor:Arterial remodeling (change in vessel size) is an important yetpoorly understood component of coronary atherosclerotic disease: itis a stronger predictor of stenosis than plaque burden and has alsobeen linked to plaque rupture and acute coronary syndromes.1Extracellular matrix (ECM) protein turnover is necessary for flow-dependent physiological remodeling and postangioplasty remodel-ing, and recent studies have shown a correlation between de novoatherosclerotic remodeling patterns and local expression of matrixmetalloproteinases (MMPs).2 However, heightened local MMP ac-tivity and ECM turnover with atherosclerotic remodeling may haveother effects on the vessel. Breakdown or deficiency of elastin notonly is associated with radial vessel enlargement but also leads toaxial vessel enlargement and tortuosity.3 It therefore seems intuitivethat tortuosity and remodeling might be interrelated: if tortuositydevelops before atherosclerotic plaque build-up, then the alreadyweakened vessel wall may have a lower threshold for compensatoryenlargement; conversely, compensatory enlargement may weakenthe wall and promote tortuosity. To examine this hypothesis, weassessed whether tortuosity is associated with enhanced compensa-tory enlargement at the site of focal de novo atherosclerotic lesions.We retrospectively examined our combined intravascular ultra-sound (IVUS) databases to identify de novo coronary lesions(excluding ostial, bifurcation, and calcified lesions and those patientswho had undergone previous coronary artery bypass grafting). Fromthe angiographic plane in which the lesion-containing segment wasmaximally elongated, the tortuosity ratio (TR) was defined as thelength of the segment in diastole along the midline of the lumendivided by the direct length between the ends of the vessel segment(measured by quantitative angiography with the guiding catheter asa reference, where the vessel segment is defined as that betweensignificant [.1.0-mm diameter] side branches). Offline IVUS mea-surements of vessel area (VA: area within the external elastic lamina)and plaque area (PA: VA minus lumen area) were used to calculatenormalized vessel area (NVA: VAlesion/VAreference) and the remodelingcompensation index (RCI: [VAlesion 2 VAreference]/[PAlesion 2 PAreference]),where the reference site is the site proximal to the lesion within the samesegment with the least PA (mostly ,10 mm proximal). Simple linearregression and multiple linear regression were used to try to ascertainany relationship between TR and either NVA or RI, with coronary riskfactors (smoking, hypertension, hypercholesterolemia, family history,and diabetes), age, sex, and vessel segment as independent covariates inthe multivariate model.In 86 patients, there was no relationship between TR and NVA orRCI by either simple linear (R50.09, P50.47; R50.01, P50.96,respectively) or multiple linear (P50.18, P50.68, respectively)regression. When the analysis was confined to the proximal leftanterior descending coronary artery (n544), where there is minimalnatural curvature of the vessel, there was also no relationship(P50.77, 0.41, 0.90, and 0.99, respectively).Tortuosity is frequently associated with generalized vessel en-largement, which in turn is frequently seen in normal segments ofotherwise diseased vessels where compensatory enlargement hasalso taken place.4 However, we found no relationship betweentortuosity and focal compensatory enlargement, possibly for anumber of reasons. The most likely reason is that generalized vesselenlargement, both axial (tortuosity) and radial, has completelydifferent mechanisms from the localized compensatory enlargementthat occurs as a response to atherosclerosis. Generalized enlargementis frequently seen as an active response to impaired flow-mediateddilatation5 or as an aging response.4 Localized enlargement may bemore of a passive response to atheroinflammation-induced MMPinduction.1 Alternatively, localized compensatory enlargement mayonly be associated with very localized tortuosity. Because the latteris very difficult to measure, it would be almost impossible to confirmor refute this possibility. Last, it may be that compensatory enlarge-ment has a limit, as first suggested by Glagov et al,6 and thatgeneralized enlargement thus limits additional localized enlarge-ment. However, tortuosity would then be inversely related tolocalized remodeling, not unrelated. Our findings, though negative,add to the limited observational data characterizing de novo athero-sclerotic remodeling, which are important starting points whenconducting interventional studies in the newly identified animalmodels of atherosclerotic remodeling, such as in genetically manip-ulated mice, and Watanabe rabbits.Michael R. Ward, MBBS, PhDPeter Smits, MD, PhDNiall A. Herity, MDAllen Jeremias, MDPeter J. Fitzgerald, MD, PhDAlan C. Yeung, MDPeter de Jaegere, MD, PhDPatrick W. Serruys, MD, PhDGerard Pasterkamp, MD, PhDStanford University, Stanford, California (M.R.W., N.A.H., A.J.,P.J.F., A.C.Y.); Thoraxcenter, Rotterdam, The Netherlands (P.S.,P.W.S.); Utrecht University, Utrecht,The Netherlands (P.d.J., G.P.)1. Ward MR, Pasterkamp G, Yeung AC, Borst C. Arterial remodeling:mechanisms and clinical implications. Circulation. 2000;102:1186–1191.2. Pasterkamp G, Schoneveld AH, Hijnen DJ, de Kleijn DP, Teepen H, vander Wal AC, Borst C. Atherosclerotic arterial remodeling and the local-ization of macrophages and matrix metalloproteases 1, 2 and 9 in thehuman coronary artery. Atherosclerosis. 2000;150:245–253.3. Dobrin PB, Schwarcz TH, Baker WH. Mechanisms of arterial and aneu-rysmal tortuosity. Surgery. 1988;104:568–571.4. Kiechl S, Willeit J. The natural course of atherosclerosis, part II: vascularremodeling: Bruneck Study Group. Arterioscler Thromb Vasc Biol. 1999;19:1491–1498.5. Lerman A, Cannan CR, Higano SH, Nishimura RA, Holmes DR Jr.Coronary vascular remodeling in association with endothelial dys-function. Am J Cardiol. 1998;81:1105–1109.6. Glagov S, Weisenberg E, Zarins CK, Stankunavicius R, KolettisGJ. Compensatory enlargement of human atherosclerotic coronaryarteries. N Engl J Med. 1987;316:1371–1375.1383Letter to the Editor

No relationship between compensatory arterial remodeling of focal stenotic atherosclerotic lesions and tortuosity of the arterial segment involved

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No relationship between compensatory arterial remodeling of focal stenotic atherosclerotic lesions and tortuosity of the arterial segment involved

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