CONTRIBUTION OF INADEQUATE ARTERIAL REMODELING TO THE DEVELOPMENT OF FOCAL CORONARY-ARTERY STENOSES - AN INTRAVASCULAR ULTRASOUND STUDY

Citation
Gs. Mintz et al., CONTRIBUTION OF INADEQUATE ARTERIAL REMODELING TO THE DEVELOPMENT OF FOCAL CORONARY-ARTERY STENOSES - AN INTRAVASCULAR ULTRASOUND STUDY, Circulation, 95(7), 1997, pp. 1791-1798
Citations number
54
Categorie Soggetti
Peripheal Vascular Diseas",Hematology
Journal title
ISSN journal
00097322
Volume
95
Issue
7
Year of publication
1997
Pages
1791 - 1798
Database
ISI
SICI code
0009-7322(1997)95:7<1791:COIART>2.0.ZU;2-P
Abstract
Background Adaptive remodeling occurs to compensate for the accumulati on of atherosclerotic plaque. Lumen reduction depends on the relative rates of plaque deposition and adaptive remodeling responses. Intravas cular ultrasound permits detailed, high-quality, cross-sectional imagi ng of the coronary arteries in vivo. Methods and Results Preinterventi on intravascular ultrasound was used to study 603 focal, new, nonostia l significant coronary artery stenoses in patients with chronic stable angina. Measurements of the target lesion of the external elastic mem brane (EEM), lumen: and plaque plus media (P&M; P&M = EEM - Lumen) cro ss-sectional areas (CSAs) were com pared with a proximal reference seg ment (most normal-looking cross section within 10 mm proximal to the l esion but distal to any side branch). Inadequate remodeling was define d as lesion/ reference EEM CSA that exceeded the upper limits of norma l arterial tapering (lesion/reference EEM CSA ratio less than or equal to 0.75 or a 21% reduction in EEM CSA per 10-mm length). Overall, the lesion/reference EEM CSA ratio was 1.00+/-0.22; 15% of lesions had in adequate remodeling, and 37% of the 603 lesions had less plaque than e xpected. This represented a lesion-specific response. The only predict or of inadequate remodeling was the are of superficial lesion calcium. Conclusions Inadequate remodeling is present in al least 15% of chron ic, focal, new coronary arterial stenoses in patients with stable angi na. The magnitude of arterial remodeling appears to be a lesion-specif ic response.