(Circulation. 2007;115:1824-1826.)
© 2007 American Heart Association, Inc.
Editorial |
From the Division of Cardiology, Department of Medicine, University of Washington School of Medicine, Seattle, Wash.
Correspondence to B. Greg Brown, MD, PhD, Cardiology Division, University of Washington, Box 358855, 146 N. Canal St, Suite 200, Seattle, WA 98195-8855. E-mail bgbrown@u.washington.edu
Key Words: Editorials atherosclerosis imaging lipids lipoproteins
An extract of the first 250 words of the full text is provided, because this article has no abstract. |
Several established methods for the imaging of atherosclerosis (quantitative coronary arteriography [QCA],1,2 carotid intima-medial thickness,3,4 magnetic resonance imaging,5 and intravascular ultrasound [IVUS])6,7 have been used in clinical trials to determine whether defined therapeutic interventions slow the rate of progression of plaque size or composition, or reduce severity of luminal obstruction, and whether change in these measures predicts in-trial or future cardiovascular (CV) events. The report by Berry et al8 in this issue of Circulation, which compares simultaneously-obtained QCA measures of luminal obstruction with IVUS measures of plaque and luminal volume or percent plaque volume and their in-trial changes is a timely comparison between IVUS and QCA. The present editorial comment addresses the emerging evidence on the relative utility of measurements by these 2 techniques for use as surrogates for efficacy in clinical trials.
Article p 1851
Proponents of these atherosclerosis imaging methods seek to establish their role as reasonable surrogates for CV event end points. Success holds the promise of a substantial decrease in the size and duration (ie, cost) of the large, long, clinical trials needed to confirm significant therapeutic benefits. In this regard, results with these techniques have been encouraging. With carotid intima-medial thickness, single estimates of carotid plaque thickness have correlated with future CV event rates;3 furthermore, rates of plaque thickening over 1 year have tended to correlate with frequency of in-trial events.4 With QCA, progressive luminal obstruction has predicted in-trial event frequency and subsequent posttrial events.9,10 With magnetic resonance imaging, diminished plaque size5 and plaque
This article has been cited by other articles:
![]() |
P. Schoenhagen and I. Sipahi Arterial remodelling: an independent pathophysiological component of atherosclerotic disease progression and regression. Insights from serial pharmacological intervention trials Eur. Heart J., October 1, 2007; 28(19): 2299 - 2300. [Full Text] [PDF] |
||||
|
Circulation Home | Subscriptions | Archives | Feedback | Authors | Help | AHA Journals Home | Search Copyright © 2007 American Heart Association, Inc. All rights reserved. Unauthorized use prohibited. |