Relationship Between Pericarotid Fat Density and Pathology-Based Carotid Plaque Risk Characteristics

Objectives: In this study, the authors aimed to evaluate the relationship between pericarotid fat density (PFD) and pathologic carotid plaque risk characteristics. Methods: The authors retrospectively evaluated 58 patients (mean age: 66.66 ± 7.26 y, 44 males) who were subjected to both carotid endarterectomy and carotid artery computed tomography angiography (CTA) at the authors’ institution. The computed tomography values of the adipose tissue around the most severe stenosis carotid artery were measured, and the removed plaques were sent to the Department of Pathology for American Heart Association (AHA) classification. The Wilcoxon signed-rank test was used to detect the difference in PFD values between the operative and nonoperative sides. According to carotid plaque risk characteristics, the associations between PFD and 4 different risk characteristic subgroups were analyzed. The Student t test and χ 2 test were used to compare differences between different risk subgroups. Receiver operating characteristic curve analysis was used to evaluate the predictive efficacy of PFD for carotid plaque risk characteristics. Results: The operative side had higher mean Hounsfield units (HU) values compared with the nonoperative side ( P < 0.001). The AHA VI and the intraplaque hemorrhage (IPH) subgroups had higher mean HU values compared with the non-AHA VI and the non-IPH subgroups ( P < 0.05). Male patients presented with IPH more than female patients ( P = 0.047). The results of receiver operating characteristic curve analysis showed that the mean HU value (operative side; area under the curve: 0.729, Sensitivity (SE): 59.26%, Specificity (SP): 80.65%, P = 0.003) had a certain predictive value for diagnosing high-risk VI plaques. Pericarotid fat density ≥ −68.167 HU is expected to serve as a potential cutoff value to identify AHA VI and non-AHA VI subgroups. Conclusion: PFD was significantly associated with vulnerable plaques, high-risk AHA VI plaques, and IPH, which could be an indirect clinical marker for vulnerable plaques.