- Poster presentation
- Open Access
Can 3D-CMR solve the apparent disassociation between carotid artery plaque and outcomes?
© Biederman et al; licensee BioMed Central Ltd. 2010
- Published: 21 January 2010
- Plaque Morphology
- Plaque Component
- Carotid Artery Disease
- Lipid Pool
- Carotid Disease
Aggressive pharmacologic strategies dramatically lower incidence of MI and CVA. Yet, when examined at the arterial lumen, only nominal changes are seen. CMR, able to detect by 2D (single slice) underlying plaque characteristics, currently has not identified such features by 3D. A 3D volumetric approach may better define plaque 'vulnerability' while disentangling this conundrum.
We hypothesize that in statin-naive pts with high grade carotid artery disease, 3D CMR integrates plaque components with lipid fractions superior to 2D while solving the 'disassociation' between outcome and % stenosis.
Via CMR (1.5 T GE, WI), 860-two mm contiguous in vivo slices of advanced carotid disease (>50%; mean 63 ± 22) representing 38 complete bilateral human plaques (age 65 ± 13 yrs) were analyzed for 2D and 3D extent of vascular wall: lipid pool, fibrous cap, matrix and minima/maxima of each. All were related to fasting lipids relative to %stenosis via QPlaque (Medis, The Netherlands). Plaque morphology was determined by T1 and T2/PD.
35/38 in vivo plaques were successfully imaged. Mean resolution: 1 × 1 × 2 mm. The mg/dL range of LDL was 63-186, HDL: 25-70 and TG: 81-213. Lipid pool represented 19 ± 8% and fibrous plaque 9 ± 24% of total vessel wall. LDL, not total cholesterol (CholT), was related to mean fibrous cap (mm) (r = 0.6 p = < 0.05) while triglycerides were related to max fibrous cap but inversely to the lipid pool (r = 0.6, -0.5, p < 0.05 for both). The LDL:HDL and CholT:HDL ratios were related to fibrous cap (r = 0.6, p < 0.05 for both). The CholT: LDL was related to min fibrous cap (mm) (r = 0.7 p < 0.05). Via 3D volumetrics only HDL was related to lipid volume while CholT, LDL, LDL: HDL and CholT:HDL ratios were all related to fibrous cap volume (r > 0.5-0.7, p < 0.005 for all). Importantly, relating % stenosis to any vessel wall component or its ratio revealed no relationship.
CMR can depict plaque composition demonstrating important relationships with common lipid fractions and even stronger relations via 3D volumetrics not visible by 2D approaches. Critically, in statin-naive pts, 3D CMR defined plaque morphology is highly related to 'clinical risk' not % luminal stenosis, potentially serving as an easily identifiable marker and thus solving the quandary.
This article is published under license to BioMed Central Ltd.