Our study juxtaposed demographic, geometric, imaging, and laboratory datasets between normal individuals and those exhibiting right -side moderate carotid plaque. The findings elucidated significant disparities across various parameters among subjects with right carotid plaque.
Subjects with right moderate carotid plaques exemplified a correlation with advanced age when contrasted with the normal cohort. The ageing phenomenon contributes to escalated vessel rigidity and stiffness14, deriving from endothelial dysfunction triggered by oxidative stress and localized inflammatory processes15,16. Moreover, the medial wall of large arteries, comprising smooth muscle cells, collagen, and elastic fibers, undergoes through age-related structural and functional changes, predisposing to plaque accrual. The degeneration-induced stiffening of elastic fibers further augments endothelial dysfunction in older demographics17. Complementary investigations have illuminated a decline in the density and continuity of circumferential and longitudinal elastin in carotid arteries, potentially facilitating passive dilatation and increased arterial wall rigidity 18,19.
Regarding CAB/CCA diameter and sectional area, the plaque-affected group presented with diminished bifurcation and an enlarged CCA relative to the normal group. While it may appear that bifurcation parameters and carotid stenosis measurements could converge, diverse methodologies were employed to ascertain the optimal fit diameter and sectional area of the carotid artery, minimizing similar measurement acquisition. The association of smaller CAB and larger CCA with carotid stenosis intimates that the unique anatomical configuration of the carotid artery may predispose the area to flow disturbances, thereby facilitating plaque development. Jiang et al.’s study reinforced this by correlating reduced luminal expansion at carotid bifurcations with vulnerable carotid plaques20. Other research suggests that reduced bifurcation expansion correlates with flow disturbance and elevated wall shear stress21,22, predisposing arteries to plaque formation. Nevertheless, the primary pathogenic mechanisms diverge from classic atherosclerosis pathology, necessitating advanced investigations, possibly through computational fluid dynamics or 4D flow MRI, to elucidate the nexus between bifurcation geometry and plaque development.
Our analysis also highlighted a significant association between the right CCA diameter and sectional area at the 2cm-point from the bifurcation and the presence of ipsilateral moderate plaque. The increased CCA diameter observed in the plaque group could stem from bifurcation stenosis, where heightened intraluminal pressure distal to carotid stenosis may precipitate distal CCA enlargement, as demonstrated in a preceding study23.
Furthermore, GFR levels in patients with moderate carotid plaques were markedly lower compared to normal subjects (69.46 ± 23.52 versus 84.90 ± 22.55 mL/min, *p* ). Despite chronic kidney disease not being recognized in the Framingham score as a cardiovascular risk 24factor24, reduced GFR has been substantiated to correlate with an elevated risk of cardiovascular events. The research by Tonelli et al. advocates for the inclusion of chronic kidney disease in the criteria delineating patients at heightened risk for coronary 25events25. Another study within a Chinese cohort with normal to mildly decreased kidney function identified a significant relationship between GFR and the 10-year risk of atherosclerotic cardiovascular disease26. In chronic kidney disease scenarios, an expedited atherosclerotic process is noted, marked by early atherosclerotic plaque formation and arterial wall thickening due to calcification 27.
Following both univariate and multivariate logistic regression analyses, several variables were identified as independently correlated with the presence of right carotid moderate plaque, including aortic arch calcification, carotid bulb calcification, carotid bifurcation sectional area, and GFR. These findings align with other studies indicating a strong correlation between systemic arterial calcification (aortic valve, carotid, and peripheral artery) 28and low GFR28. Additional research noted a link between carotid artery distensibility coefficient or arterial wall stiffness, as assessed via B-mode ultrasound, and thoracic aorta 29calcification29. As elaborated upon, chronic kidney disease accelerates the atherosclerotic process through myriad mechanisms, encompassing oxidative stress, endothelial dysfunction, inflammation, toxic 30effluents, and albuminuria30. These pathophysiological pathways contribute to systemic arterial calcification, culminating in atherosclerosis across critical arterial systems, including coronary, carotid, intracranial, and peripheral 31arteries31. Given the multifaceted mechanism of plaque development, integrating geometric, imaging, and laboratory data into a predictive model for carotid plaque enhances the practical applicability and viability of our findings.
Nonetheless, our study is subject to several limitations. Firstly, the retrospective and cross-sectional design may introduce selection bias. Conducted at a tertiary hospital, our patient cohort typically manifests greater comorbidities and heightened vascular risk compared to the general population. To mitigate this limitation, an extensive sample size exceeding 1900 cases was employed in the initial data screening, aiming to diminish bias. Secondly, our cross-sectional study design inadequately captures the long-term impact of cardiovascular risk factors on carotid plaque development, thereby emphasizing the need for a prospective, longitudinal study to unravel detailed mechanisms. Thirdly, the Glagov phenomenon might introduce bias due to the exclusive reliance on CTA for lumen 32measurement32. While CTA facilitates relatively straightforward assessment of the carotid lumen, distinguishing arterial wall and plaque proves challenging due to similar density with surrounding tissue. Consequently, a future study amalgamating CTA with vessel wall imaging, either through ultrasound or MRI, appears imperative.
In summation, right moderate carotid plaque exhibits independent associations with carotid bifurcation and CCA sectional area, alongside aortic arch and carotid bulb calcification and diminished GFR in high cardiovascular risk patients. These intrinsic variables warrant consideration in evaluating carotid atherosclerosis development.