BACKGROUND AND PURPOSE: Serial in vivo imaging of atherosclerosis is important for understanding plaque progression and is potentially useful in predicting cardiovascular events and monitoring treatment efficacy. This prospective study aims to quantify temporal changes in carotid atherosclerotic plaque volume and plaque composition using MDCTA. MATERIALS AND METHODS: In 109 patients with TIA or ischemic stroke, serial MDCTA of the carotid arteries was performed after 5.3 ± 0.7 years. The carotid bifurcation was semiautomatically registered for paired baseline follow-up datasets. Outer vessel wall and lumen boundaries were defined using semiautomated segmentation tools. Plaque component volumes were measured using HU thresholds. Annual changes in plaque volume and plaque component proportions were calculated. RESULTS: One-hundred-ninety-three carotid arteries were analyzed. Plaque volume decreased in 31% and increased in 69% of vessels (range -5.6-10.1%/year). Overall, plaque volume increased 1.2% per year (95% CI, 0.8-1.6, P ≤ .001). Plaque composition changed significantly from BL (fibrous 66.4%, lipid 28.8%, calcifications 4.8%): fibrous tissue decreased by 1.5%, lipid decreased by 1.8%, and calcification increased by 3.3% (P < .001). Intraobserver reproducibility of all volume and proportion measurements was good (ICC 0.78-1.00) and interobserver reproducibility was moderate (ICC 0.76-0.99). CONCLUSIONS: Changes in carotid plaque burden and plaque composition can be quantified by using serial MDCTA. Plaque burden development is a heterogeneous and slow process.
BACKGROUND AND PURPOSE: Serial in vivo imaging of atherosclerosis is important for understanding plaque progression and is potentially useful in predicting cardiovascular events and monitoring treatment efficacy. This prospective study aims to quantify temporal changes in carotid atherosclerotic plaque volume and plaque composition using MDCTA. MATERIALS AND METHODS: In 109 patients with TIA or ischemic stroke, serial MDCTA of the carotid arteries was performed after 5.3 ± 0.7 years. The carotid bifurcation was semiautomatically registered for paired baseline follow-up datasets. Outer vessel wall and lumen boundaries were defined using semiautomated segmentation tools. Plaque component volumes were measured using HU thresholds. Annual changes in plaque volume and plaque component proportions were calculated. RESULTS: One-hundred-ninety-three carotid arteries were analyzed. Plaque volume decreased in 31% and increased in 69% of vessels (range -5.6-10.1%/year). Overall, plaque volume increased 1.2% per year (95% CI, 0.8-1.6, P ≤ .001). Plaque composition changed significantly from BL (fibrous 66.4%, lipid 28.8%, calcifications 4.8%): fibrous tissue decreased by 1.5%, lipid decreased by 1.8%, and calcification increased by 3.3% (P < .001). Intraobserver reproducibility of all volume and proportion measurements was good (ICC 0.78-1.00) and interobserver reproducibility was moderate (ICC 0.76-0.99). CONCLUSIONS: Changes in carotid plaque burden and plaque composition can be quantified by using serial MDCTA. Plaque burden development is a heterogeneous and slow process.
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