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Abstract 16911: Burden of Micro(nano)plastics and Complicated Plaque Phenotype in Human Carotid Atherosclerotic Plaques
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Researchers examined plaque tissue removed from 22 human carotid arteries, measuring tiny plastic particles of different sizes. Plaques with complications like rupture or hemorrhage had higher levels of nanoplastics (smaller particles), but not microplastics, compared to plaques without these features. Polyvinyl chloride was the most common plastic type found.
Background: Micro(nano)plastics (MNPs) have been identified in human carotid atheromas, but whether the microplastic (MP) and nanoplastic (NP) fractions differ in relation to complicated plaque morphology is unclear. Hypothesis: Higher NP burden is associated with complicated carotid artery plaque (cCAP), a histologic proxy of American Heart Association (AHA) type VI plaque. Methods: Carotid endarterectomy plaques with paired MNP and histologic profiling (n=22) were analyzed. After size fractionation into NP and MP fractions, 11 targeted polymers were quantified by pyrolysis–gas chromatography/mass spectrometry and normalized to tissue mass. Serial sections underwent hematoxylin and eosin (H&E), Masson trichrome, and Oil Red O staining. cCAP was defined as rupture/surface ulceration, intraplaque hemorrhage, or luminal/mural thrombus; plaques without these features were classified as non-cCAP. Histologic classification was performed blinded to MNP measurements. Necrotic core area, Oil Red O lipid area, Masson collagen area, and a vulnerability index proxy [(necrotic core%+lipid%)/collagen%] were quantified. Between group differences were tested with Mann-Whitney U tests; histology-MNP relationships were assessed using Spearman correlation. Results: cCAP was present in 7 plaques and absent in 15. Mean total MNP content was 104.87 μg/g tissue. Six of 11 targeted polymers were detected: polyvinyl chloride (PVC) was predominant (59.29%; 22/22 plaques), followed by polyethylene (PE, 16.64%; 19/22), polyamide-66 (15.41%; 15/22), polystyrene (PS, 6.53%; 21/22), polypropylene (1.41%; 7/22), and poly(methyl methacrylate) (0.73%; 1/22). NP burden was higher in cCAP than non-cCAP plaques (75.68 [46.24-117.26] vs 36.90 [16.17-58.21] μg/g; p=0.026), whereas total MNP burden (p=0.200) and MP burden (p=0.971) did not differ. In univariable exact logistic regression, higher NP burden was associated with greater odds of cCAP (OR per 5 μg/g tissue, 1.17; 95% CI, 1.02-1.40). Polymer-specific analyses showed a nonsignificant trend toward higher PVC burden in cCAP (p=0.091), while PS (p=0.500) and PE (p>0.999) were not different. NP burden was not significantly correlated with necrotic core area (ρ=0.123, p=0.587), Oil Red O lipid area (ρ=-0.284, p=0.200), Masson collagen area (ρ=-0.072, p=0.751), or vulnerability index proxy (ρ=0.340, p=0.122). Conclusions: In this pilot human carotid plaque study, NP burden, but not MP burden, was associated with a cCAP/AHA type VI phenotype. The lack of parallel associations with global lipid, necrotic core, or collagen measurements suggests that NP enrichment may relate more closely to plaque complication features than to bulk plaque composition. Larger studies are warranted to validate the size-specific relationship between nanoplastic accumulation and adverse carotid plaque biology.
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