Abstract
Atherosclerosis often leads to myocardial infarction and stroke. We examined the influence of baseline plaque characteristics on subsequent vascular remodeling in response to changes in plaque size. Using optical coherence tomography (OCT) and intravascular ultrasound (IVUS), we examined 213 plaques from 138 patients with acute coronary syndrome at baseline and repeated IVUS at the 12-month follow-up. The change in external elastic membrane (EEM) area for each 1 mm2 change in plaque area (i.e., the slope of the regression line) was calculated as a measure of vascular remodeling capacity. In plaques with static positive remodeling, the slope was smaller than in plaques without static positive remodeling. In addition, the slope of the regression line for lesions with a large plaque burden was much smaller than that for lesions with a small plaque burden. Multivariate linear regression analysis showed that diabetes, calcification and static positive remodeling were inversely and independently associated with the level of change in EEM area/change in plaque area. Lesions with a large plaque burden, calcifications or static positive remodeling had less remodeling capacity, and calcification and static positive remodeling were independent predictors of reduced subsequent remodeling. Therefore, calcifications and static positive remodeling could be used as morphological biomarkers to predict decreased subsequent arterial remodeling.
Highlights
Atherosclerosis is the main underlying cause of myocardial infarction and stroke and accounts for greater than one-half of all deaths worldwide
Arterial remodeling in response to plaque accumulation has been widely recognized as a mechanism for lumen preservation during coronary atherosclerosis development [1,2,3,4]
To the best of our knowledge, this is the first in vivo human study to systematically investigate the relationship between baseline plaque characteristics and serial vascular remodeling
Summary
Atherosclerosis is the main underlying cause of myocardial infarction and stroke and accounts for greater than one-half of all deaths worldwide. Arterial remodeling in response to plaque accumulation has been widely recognized as a mechanism for lumen preservation during coronary atherosclerosis development [1,2,3,4]. Intravascular ultrasound (IVUS) is an established imaging technology that can be used to evaluate vascular structure geometry and study coronary arterial remodeling in vivo [5,6,7,8]. In the static method of assessment, remodeling of individual lesions is determined by comparing the external elastic membrane (EEM) area of the lesion site to the mean EEM area of the proximal and distal reference sites [5, 9]. Direct evidence of vascular remodeling requires the serial method of assessment in which the www.impactjournals.com/oncotarget
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