Aortic dissection (AD) is a life-threatening vascular disorder whose incidence has risen steadily in recent years (1, 2). Although the pathogenesis of AD is still not fully clarified, it is known to correlate closely with hypertension, hyperlipidaemia and inherited connective-tissue disorders such as Marfan syndrome (3, 4). Clinically, AD most often presents with sudden-onset chest or back pain described as a tearing sensation (5).Today, computed-tomography angiography (CTA) of the thorax and abdomen remains the diagnostic gold standard for AD because it clearly delineates intimal tears and the true-and false-lumen channels. According to the extent of intimal-tear involvement, AD is classified into Stanford Type A aortic dissection (TAAD), Stanford Type B aortic dissection (TBAD) and “non-A non-B” variants (6, 7). This anatomical distinction directs therapy: open surgical replacement is generally required for TAAD, whereas thoracic endovascular aortic repair (TEVAR) has become the first-line treatment for TBAD (8–10).

Despite the advantages of TEVAR, a frequent and clinically important complication is the persistence of a residual false lumen around the implanted stent graft. Such a persistent channel promotes late aortic aneurysm formation, raises rupture risk and can ultimately prove fatal (11–13). Elucidating the mechanisms that drive residual false-lumen formation after TEVAR, and intervening early, are therefore critical to improving long-term prognosis and quality of life for these patients.

Emerging evidence highlights the pathophysiological importance of perivascular adipose tissue (PVAT) in a spectrum of vascular diseases, including coronary artery disease and aortic aneurysms (14–16). Situated immediately adjacent to the vessel wall, PVAT mirrors local inflammatory and atheromatous activity and thus offers a promising, non-invasive window into vascular health. In abdominal aortic aneurysm progression, for instance, PVAT that lies closest to the wall displays larger density shifts than more distant adipose tissue (17, 18). Nonetheless, the influence of PVAT characteristics on vascular remodelling and clinical outcomes after TEVAR remains largely unexplored.

Accordingly, the present study investigates whether PVAT attenuation indices are associated with the development of a residual false lumen following TEVAR for TBAD. By clarifying this relationship, we aim to provide an early-warning biomarker that can guide surveillance intensity and inform timely adjunctive interventions in high-risk patients.

In this study, we explore the role of PVAT in the development of residual false lumen formation following TEVAR in patients with TBAD. Our findings indicate that the attenuation of PVAT, particularly the difference in density between regions near and far from the aortic wall (HU_Δ) and the ratio of these values (HU_ratio), are significant predictors of residual false lumen formation post-TEVAR. These results suggest that PVAT could serve as a valuable non-invasive biomarker for predicting postoperative vascular outcomes and identifying high-risk patients. The association between PVAT and residual false lumen formation underscores the potential of PVAT as a key indicator of the vascular environment following TEVAR and highlights the need for further investigation into its underlying pathophysiological mechanisms.

The basic principle of TEVAR is to deploy a covered stent within the true lumen of the aortic dissection, which expands the true lumen and reduces the false lumen by promoting thrombosis (23). This reduces the risk of aortic rupture by sealing the proximal rupture site. With advances in TEVAR technology, postoperative complications such as endoleaks, stroke, and organ ischemia have been significantly reduced (24, 25). However, challenges remain, particularly the issue of residual false lumen formation at the distal end of the stent. This complication arises because the stent generally seals only the proximal rupture, leaving the distal decompression port uncovered. As a result, residual channels remain between the true and false lumens. While most of these residual false lumens undergo thrombosis over time, some may progress to form aneurysms, which carry the risk of rupture and potentially fatal outcomes (26, 27). Identifying high-risk patients with residual false lumen in the early postoperative period and providing timely intervention could significantly improve treatment outcomes and long-term prognosis.

Previous studies have primarily focused on factors such as the geometric structure of the aorta, inflammatory markers, platelet activation markers, coagulation factors like D-dimer, coated stent material and hemodynamics (28, 29). These factors are all closely related to the structural remodeling of the aortic dissection and are implicated in its occurrence, progression, treatment, and prognosis. Recently, there has been increasing recognition of the critical role of perivascular adipose tissue in the development of vascular diseases such as coronary artery disease and aortic aneurysm (17, 18). PVAT, a specialized type of adipose tissue, surrounds most blood vessels, excluding the cerebral vasculature (30). This metabolically active tissue consists of both white and brown adipose tissue (31). White adipose tissue serves as an energy reservoir and secretes various hormones, cytokines, and enzymes that influence inflammation, metabolism, and vascular homeostasis. Brown adipose tissue is thought to contribute to thermogenesis (32, 33). Studies have shown that the thoracic aorta is primarily composed of brown adipose tissue, while the abdominal aorta is mainly composed of white adipose tissue (34, 35). Under normal physiological conditions, PVAT is involved in the regulation of vascular tone. However, under pathological conditions, PVAT can exacerbate oxidative stress, leading to adverse vascular remodeling. Although studies have established the role of PVAT in the development and prognosis of abdominal aortic aneurysms following endovascular repair, its role in false lumen remodeling after TEVAR remains underexplored (36). This study aims to address this gap by investigating the correlation between PVAT and residual false lumen formation post-TEVAR.

We retrospectively analyzed a cohort of 132 patients with TBAD who underwent TEVAR at our institution. We collected baseline data, biochemical indicators, and imaging data. The patients were classified into two groups: those with residual false lumen and those with closed false lumen, based on the status of the aortic dissection around the stent at discharge. There were no significant differences in baseline characteristics such as age, gender, BMI, comorbidities, or blood lipid levels between the two groups, ensuring comparability. Comparison of early postoperative blood tests revealed that white blood cell count (WBC), activated partial thromboplastin time (APTT), and D-dimer levels were significantly higher in the residual false lumen group compared to the closed false lumen group. This finding is consistent with the work of Kimura et al., which emphasized the impact of inflammatory factors on the long-term outcome of the false lumen following TEVAR (37). This study further corroborates that early postoperative coagulation parameters, such as D-dimer and APTT, significantly influence residual false lumen formation and should be closely monitored during the early postoperative period.

Although our multivariate analysis identified HU_Δ and HU_ratio as independent predictors, several unmeasured or incompletely adjusted variables may confound the observed associations. First, BMI influences both the quantity and metabolic phenotype of PVAT; obesity-induced whitening of brown PVAT can lead to lower CT attenuation values regardless of dissection status (31, 32). Second, the widespread perioperative use of statins and other lipid-lowering or anti-inflammatory agents in TBAD patients may reduce PVAT density through pleiotropic effects, potentially attenuating HU_Δ and HU_ratio and blunting their predictive accuracy. Third, systemic inflammatory states—ranging from postoperative systemic inflammatory response syndrome to chronic low-grade inflammation associated with metabolic syndrome—could simultaneously increase PVAT attenuation and impair false-lumen thrombosis, thereby acting as a mediating pathway. Propensity-matched or longitudinal designs that explicitly control for these variables will be essential for isolating the true causal contribution of PVAT characteristics to false-lumen persistence.

Our quantitative analysis demonstrated that patients with residual false lumen had significantly higher HU_Δ values and lower HU_ratio values compared to those with closed false lumen (P < 0.001 for both). Moreover, logistic regression confirmed that early postoperative HU_Δ and HUratio are independent risk factors for residual false lumen formation around the stent in the short term after TEVAR. ROC curve analysis indicated that the optimal threshold for HU_Δ was 7.170, with a sensitivity of 0.895 and a specificity of 0.762, while the optimal threshold for HUratio was 0.790, with a sensitivity of 0.947 and a specificity of 0.667.

Translating these findings into practice, HU_Δ and HU_ratio can be incorporated into a tiered surveillance algorithm. Patients exceeding the high-risk cut-offs (> 7.170 for HU_Δ or ≤ 0.790 for HU_ratio) could undergo an intensified imaging schedule—CTA or MRA at 1–3 months, followed by 6-monthly scans during the first year—while those below the thresholds continue with standard follow-up. Likewise, knowledge of an adverse PVAT profile pre-operatively or on immediate postoperative CTA may encourage more aggressive intra-operative strategies, such as extended-coverage stent grafting, adjunctive distal bare-metal stenting, or prophylactic left subclavian revascularization (23, 28). From a medical-management standpoint, early initiation or up-titration of statins, β-blockers, ACE inhibitors, and anti-inflammatory agents might help modulate PVAT activity and foster false-lumen thrombosis (38–40). Finally, serial assessment of PVAT attenuation during routine scans provides a dynamic biomarker that could trigger timely re-intervention—endovascular fenestration, coil embolization, or open conversion—before aneurysmal degeneration ensues.

Previous research has shown that HU_Δ and HU_ratio values reflect the degree of vascular wall inflammation by quantifying the attenuation of adipose tissue around the aortic wall (41). Our study further elucidates that greater attenuation may correlate with more severe inflammation in the vascular wall, contributing to adverse remodeling of the false lumen following TEVAR. In addition, HU_Δ and HU_ratio values may also be related to local coagulation changes within the vessel, suggesting a complex interplay between inflammation and coagulation that warrants further investigation. These findings provide valuable insights into the pathophysiological mechanisms underlying residual false lumen formation and underscore the potential of PVAT as a non-invasive biomarker for predicting postoperative outcomes in TEVAR-treated patients.

Looking ahead, targeting PVAT represents a promising supplementary treatment approach following TEVAR (42). Given its significant role in vascular inflammation and remodeling, modulating PVAT could help reduce the risk of residual false lumen formation post-surgery. Therapeutic strategies aimed at reducing oxidative stress, modulating the release of inflammatory cytokines, or enhancing PVAT's regenerative potential could be integrated into TEVAR treatment regimens. By targeting PVAT, clinicians may be able to further improve postoperative vascular health and reduce long-term complications such as aneurysm formation or rupture. However, further research is needed to explore the safety, feasibility, and efficacy of PVAT-targeted therapies as adjunctive treatments in TEVAR. The integration of such strategies could provide a significant improvement in the long-term outcomes for patients undergoing TEVAR.

One limitation of this study is its retrospective design, which may introduce selection bias and limit the generalizability of the findings. The sample size, while adequate, is relatively small, and larger, multicenter studies are needed to validate the results. Additionally, while we focused on the early postoperative period, the long-term effects of PVAT attenuation on false lumen remodeling were not assessed. Another limitation is the reliance on imaging techniques for measuring PVAT density, which, despite advances in technology, may still be subject to variability in interpretation and resolution. Finally, although the TotalSegmenter model provides a novel approach for extracting PVAT density values, it has not been extensively validated in a broader clinical context, and further refinement and testing of this tool are required to ensure its widespread applicability.

In conclusion, this study highlights the significant role of perivascular adipose tissue (PVAT) attenuation, particularly HU_Δ and HU_ratio, as key predictors of residual false lumen formation following TEVAR in patients with Stanford Type B aortic dissection. PVAT attenuation may serve as a valuable non-invasive biomarker for identifying high-risk patients and predicting postoperative outcomes. These findings underscore the potential of PVAT in guiding clinical decision-making and highlight the need for further research into PVAT's underlying mechanisms and its potential role in adjunctive therapies for improving long-term TEVAR outcomes.