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(Arteriosclerosis, Thrombosis, and Vascular Biology. 2001;21:1383.)
© 2001 American Heart Association, Inc.

Letters to the Editor

Letter to the Editor

No Relationship Between Compensatory Arterial Remodeling of Focal Stenotic Atherosclerotic Lesions and Tortuosity of the Arterial Segment Involved

Michael R. Ward, MBBS, PhD; Peter Smits, MD, PhD; Niall A. Herity, MD; Allen Jeremias, MD; Peter J. Fitzgerald, MD, PhD; Alan C. Yeung, MD; Peter de Jaegere, MD, PhD; Patrick W. Serruys, MD, PhD; Gerard Pasterkamp, MD, PhD

Stanford 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.)

To the Editor:

Arterial remodeling (change in vessel size) is an important yet poorly understood component of coronary atherosclerotic disease: it is a stronger predictor of stenosis than plaque burden and has also been linked to plaque rupture and acute coronary syndromes.¹ Extracellular matrix (ECM) protein turnover is necessary for flow-dependent physiological remodeling and postangioplasty remodeling, and recent studies have shown a correlation between de novo atherosclerotic remodeling patterns and local expression of matrix metalloproteinases (MMPs).² However, heightened local MMP activity and ECM turnover with atherosclerotic remodeling may have other effects on the vessel. Breakdown or deficiency of elastin not only is associated with radial vessel enlargement but also leads to axial vessel enlargement and tortuosity.³ It therefore seems intuitive that tortuosity and remodeling might be interrelated: if tortuosity develops before atherosclerotic plaque build-up, then the already weakened vessel wall may have a lower threshold for compensatory enlargement; conversely, compensatory enlargement may weaken the wall and promote tortuosity. To examine this hypothesis, we assessed whether tortuosity is associated with enhanced compensatory enlargement at the site of focal de novo atherosclerotic lesions.

We retrospectively examined our combined intravascular ultrasound (IVUS) databases to identify de novo coronary lesions (excluding ostial, bifurcation, and calcified lesions and those patients who had undergone previous coronary artery bypass grafting). From the angiographic plane in which the lesion-containing segment was maximally elongated, the tortuosity ratio (TR) was defined as the length of the segment in diastole along the midline of the lumen divided by the direct length between the ends . . . [Full Text of this Article]