Abstract 16675: Intraplaque Hemorrhage-induced Atherosclerotic Plaque Progression as the Bridge Between Intact and Ulcerated Plaques: An Imaging-based Natural History Study
Introduction: Previous studies have associated intraplaque hemorrhage (IPH) with future ischemic events, of which the mechanisms are less understood.
Hypothesis: Understanding morphological features and progression behaviors of plaques with and without IPH would allow us to define the role of IPH in the natural history of atherosclerosis.
Methods: In an ongoing study, asymptomatic subjects with 16-79% stenosis on ultrasound underwent 3-dimensional carotid MRI. Those with carotid plaque(s) on MRI were recruited and a follow-up scan was performed 1-year later using the same protocol. Individual plaques (maximum thickness>1.5 mm) within scan coverage were identified in bilateral carotids, of which morphological data were collected at baseline and plaque progression was determined by comparing both scans while blinded to the time sequence.
Results: Twenty-nine subjects have completed the study. A total of 64 de novo plaques were identified, of which 15 (23.4%) demonstrated IPH. Plaques with IPH are more likely to have an ulcerated surface than those without IPH (60.0% vs. 8.2%, odds ratio: 16.9 [3.9, 72.3]). Furthermore, there was a stepwise progression in baseline morphological measures from IPH-/ulcer- plaques to IPH+/ulcer- plaques and to ulcer+ plaques (Table), suggesting that IPH+/ulcer- plaques may be at the intermediate stage between IPH-/ulcer- and ulcer+ plaques. During the 1-year period, IPH+/ulcer- plaques had significantly greater increases in mean wall thickness and percent luminal stenosis compared to IPH-/ulcer- plaques, indicating further progression towards ulcer+ plaques. In contrast, ulcer+ plaques, as the most stenotic group, showed little plaque burden change on average.
Conclusions: Collectively, our data support the conjecture that IPH promotes plaque progression and appears to be an intermediate step toward surface ulceration. IPH could be a critical step in phenotype transition from asymptomatic to symptomatic plaques.
Author Disclosures: J. Sun: None. J. Liu: None. N. Balu: None. D.S. Hippe: None. D. Xu: None. G. Canton: None. T.S. Hatsukami: None. C. Yuan: Consultant/Advisory Board; Modest; Philips Healthcare. Research Grant; Significant; Philips Healthcare.
- © 2015 by American Heart Association, Inc.