Plaque phenotypes across remodeling patterns in vertebrobasilar atherosclerosis: a high-resolution magnetic resonance vessel wall imaging study

Figures

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  Figure 1. Remodeling patterns. Categories of remodeling: negative (inward) remodeling is characterized by constriction of the outer wall (delineated by the green circle with a reduction in lumen size); expansion of the outer wall during plaque development with relative preservation of the lumen constitutes positive (outward) remodeling. Variables of interest include LA (area shown in black), WA (area shaded in gray), and VA (area circumscribed by the green outer wall). LA, lumen area; VA, vessel area; WA, wall area.

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  Figure 2. A 63-year-old male with a 2-day history of dizziness accompanied by right-sided limb weakness. DWI and ADC maps demonstrated restricted diffusion within the left brainstem (A,B), indicating an acute ischemic lesion. MRA revealed severe stenosis of the basilar artery (C). Vessel wall plaque characterization (3D-T1-SPACE): precontrast imaging perpendicular to the long axis of the basilar artery demonstrated an irregular plaque predominantly located in the ventral and left lateral vessel walls (D). Postcontrast imaging showed significant plaque enhancement (E,F). Vessel and lumen areas: VA and LA were measured at the site of MLN and at the proximal reference site (G,H). The RI was calculated as follows: RI = (VA at MLN/VA at reference) =0.1654 cm2/0.2164 cm2 =0.76. The RI was <0.95, indicating negative remodeling. WA and plaque burden: WA =VA – LA. WA at MLN =0.1654 cm2 – 0.01468 cm2=0.1507 cm2. WA at reference =0.2164 cm2 – 0.06376 cm2 =0.1526 cm2. Plaque burden at MLN = (WA at MLN/VA at MLN) =0.1507 cm2/0.1654 cm2 =0.91 (91%). Luminal stenosis: percentage luminal area stenosis at MLN = [1 – (LA at MLN/LA at reference)] × 100% = [1 – (0.01468 cm2/0.06376 cm2)] × 100% =77.0%. The…

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  Figure 3. Vascular remodeling-dependent distribution of hemodynamic parameters. Violin plots with embedded boxplots demonstrating the distribution of (A) luminal stenosis severity rate and the (B) plaque burden rate across vascular remodeling phenotypes, including PR (n=133), IR (n=35), and NR (n=40). *, P<0.05; ***, P<0.001; NS, not significant. IR, intermediate remodeling; NR, negative remodeling; PR, positive remodeling.

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  Figure 4. Multivariate predictors of stroke risk stratified by remodeling phenotype. Forest plot displaying the aORs from multivariate logistic regression models for the nonpositive remodeling group (n=75) and the positive remodeling group (n=133). *, per 10% increase odds ratio change. aORs, adjusted odds ratios; CI, confidence interval.

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  Figure 5. Discriminative performance of stroke predictors stratified by remodeling phenotype. (A,B) The ROC curves of the discriminative performance of individual plaque features and their combined models in predicting stroke occurrence in two distinct vascular remodeling subgroups: (A) non-positive remodeling and (B) positive remodeling. In both panels, the combined model outperformed any single feature, as evidenced by its higher AUC. (A) The combined model consisting of plaque enhancement and plaque location had an AUC of 0.802, while (B) the combined model consisting of plaque enhancement, surface morphology and distribution patterns had an AUC of 0.812, indicating slightly better predictive power in the positive remodeling group. Notably, plaque enhancement emerged as the strongest individual predictor across both groups [(A) AUC =0.701; (B) AUC =0.714], suggesting its consistent clinical relevance regardless of remodeling status. In contrast, features such as surface morphology and distribution patterns showed a greater contribution in the positive remodeling group when combined (B), suggesting that these features may be more informative when vascular remodeling is present. AUC, area…

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  Figure 6. Comparison of luminal stenosis degree, plaque burden, and vascular remodeling index between the stroke and nonstroke group. The violin plot compares three key vascular parameters between the stroke and nonstroke groups. The stroke group (red) showed significantly higher stenosis percentage (P<0.001) and plaque burden (P<0.001) compared to the nonstroke group (blue). No significant difference was observed in the remodeling index. Box plots within violins indicate the median, interquartile range, and data spread. ***, P<0.001; NS, not significant.

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  Figure 7. Relationship between plaque burden and stenosis across the remodeling phenotypes. Linear regression for stenosis degree as a function of plaque burden measurements. A stenosis of 0% corresponded to a plaque burden of 59.4% for all intracranial atherosclerotic lesions in the posterior circulation. A stenosis of 0% corresponded to plaque burdens of 43.3%, 59.0%, and 60.1% for the negative, intermediate, and positive remodeling patterns, respectively.