Long-Term Carotid Plaque Progression and the Role of Intraplaque Hemorrhage: A Deep Learning-Based Analysis of Longitudinal Vessel Wall Imaging.

BACKGROUND

Carotid atherosclerosis is a major contributor in the etiology of ischemic stroke. Although intraplaque hemorrhage (IPH) is known to increase stroke risk and plaque burden, its long-term effects on plaque dynamics remain unclear. This study aimed to evaluate the long-term impact of IPH on carotid plaque burden progression using deep learning-based segmentation on multi-contrast magnetic resonance vessel wall imaging (VWI).

METHODS

Twenty-eight asymptomatic subjects with carotid atherosclerosis underwent an average of 4.7 ± 0.6 VWI scans over 5.8 ± 1.1 years. Deep learning pipelines were developed and validated to segment the carotid vessel walls and IPH. Bilateral plaque progression was analyzed using generalized estimating equations, and linear mixed-effects models evaluated long-term associations between IPH occurrence, IPH volume, and plaque burden (%WV) progression.

RESULTS

IPH was detected in 23/50 of arteries. Of arteries without IPH at baseline, 11/39 developed new IPH that persisted, while 5/11 arteries with baseline IPH exhibited it throughout the study. Bilateral plaque growth was significantly correlated (r = 0.54, p < 0.001), but this symmetry was weakened with IPH presence. The progression rate for arteries without IPH was -0.001 %/year (p = 0.90). However, IPH presence or development at any point was associated with a 2.3% absolute increase in %WV on average (p < 0.001). The volume of IPH was also positively associated with increased %WV (p = 0.005).

CONCLUSIONS

Deep learning-based segmentation pipelines were utilized to identify IPH, quantify IPH volume, and measure their effects on carotid plaque burden during long-term follow-up. Findings demonstrated that IPH may persist for extended periods. While arteries without IPH demonstrated minimal progression under contemporary treatment, presence of IPH and greater IPH volume significantly accelerated long-term plaque growth.