ABSTRACT
Aim
The fundamental objective of endovascular aortic repair (EVAR) is the effective exclusion and subsequent shrinkage of the aneurysm sac. Nevertheless, a clinical challenge persists in a subset of patients who exhibit progressive sac enlargement despite the total absence of detectable endoleaks, a phenomenon known as endotension or type V endoleak. This study investigates the morphological, biomechanical, and systemic determinants of persistent sac expansion following EVAR.
Materials and Methods
A longitudinal analysis was performed on 41 consecutive patients with a minimum 18-month follow-up. We evaluated anatomical metrics via thin-slice computed tomography angiography, biochemical markers including high-sensitivity C-reactive protein (hs-CRP), and systemic comorbidities. Multivariable logistic regression was employed to identify independent predictors of adverse sac dynamics.
Results
Sac expansion (≥5 mm) was observed in 14.6% of the cohort during the follow-up period. Multivariable analysis demonstrated that a preoperative sac diameter exceeding 60 mm [odds ratio (OR): 3.24] and an increased mural thrombus burden (OR: 2.86) were the strongest independent biomechanical predictors of persistent enlargement. Patients with adverse sac behavior frequently exhibited elevated hs-CRP levels and a higher prevalence of systemic conditions such as obesity, chronic obstructive pulmonary disease, and hypothyroidism
Conclusion
Post-EVAR sac expansion is a multifactorial systemic phenotype influenced by landing zone quality, mural thrombus biomechanics, and host inflammatory status. These findings suggest that in endotension cases, the transmission of pulsatile energy through the mural thrombus may maintain sac pressurization even without a visible flow channel. Recognizing persistent expansion as a distinct phenotype necessitates a shift in post-EVAR surveillance from a binary endoleak-focused approach toward a more comprehensive assessment of longitudinal sac dynamics and biomechanical risk factors.
INTRODUCTION
Endovascular aortic repair (EVAR) has fundamentally transformed the therapeutic landscape for abdominal aortic aneurysms and selected dissections, offering a minimally invasive alternative with superior perioperative morbidity and recovery profiles compared to open surgical repair1-3. The traditional paradigm of EVAR success relies on the effective exclusion of the aneurysmal sac from systemic pressure, typically manifesting as sac shrinkage or stabilization over time3.
Despite technical advancements, long-term durability is frequently jeopardized by persistent sac expansion3, 4. While endoleaks-categorized into well-defined subtypes based on their source are considered the primary drivers of expansion, clinical practice has revealed a paradoxical subgroup of patients4. These individuals demonstrate progressive sac enlargement despite the total absence of detectable endoleaks on high-resolution serial imaging, a phenomenon known as “endotension” or type V endoleak5, 6. This phenomenon suggests that sac pressurization may persist through occult mechanisms, including graft porosity, transmission of pulsatile energy through the mural thrombus, or micro-collateral flow5, 6.
Furthermore, emerging evidence indicates that the host’s systemic environment encompassing chronic inflammation, collagen metabolism disorders (e.g., fibrillin gene defects), and metabolic dysregulation may critically influence the failure of sac regression6, 7. This study aims to move beyond binary endoleak classifications to explore the integrative morphological, biochemical, and biomechanical determinants of persistent sac expansion in a well-defined longitudinal cohort.
MATERIALS AND METHODS
Study Design and Population
This retrospective observational study was conducted at the Department of Cardiovascular Surgery, a tertiary referral center. We screened 41 consecutive patients who underwent primary endovascular stent-graft implantation for aortic aneurysm between January 2009 and February 2013. The study protocol received Maltepe University Faculty of Medicine Clinical Research Ethics Committee (approval number: AN023, date: 27.11.2013) and all participants provided written informed consent.
Patients were eligible for inclusion if they were treated with endovascular stent-graft implantation for primary aortic pathology and possessed comprehensive preoperative, perioperative, and postoperative clinical data. A strict minimum follow-up duration of 18 months with standardized imaging assessments was mandatory, alongside voluntary consent for medical record analysis. Conversely, the study excluded patients presenting with congenital aortic malformations, penetrating aortic ulcers, or those requiring emergency EVAR under hemodynamically unstable conditions that precluded standardized preoperative imaging. Furthermore, patients were excluded if they possessed severe concomitant valvular stenosis or regurgitation that could significantly alter systemic aortic hemodynamics, or if they had incomplete follow-up records.
Imaging Protocol and Definitions
Preoperative and postoperative assessments were performed using contrast-enhanced computed tomography angiography (CTA) with thin-slice acquisitions (≤1.5 mm). In the postoperative period, serial imaging was conducted according to a standardized surveillance protocol, with contrast-enhanced CTA performed at 3, 6, 12, and 18 months, provided that clinical conditions permitted intravenous contrast administration. In addition, Doppler ultrasonography was routinely used for interim evaluation at 9 months. In patients in whom intravenous contrast administration was contraindicated, follow-up assessments were performed using Doppler ultrasonography and/or non-contrast-enhanced computed tomography to ensure continuity of sac diameter measurements. Aneurysm sac diameter was defined as the maximal transverse diameter measured perpendicular to the centerline of flow. Persistent sac expansion was strictly defined as a ≥5 mm increase in the maximal sac diameter relative to the first postoperative baseline measurement. Endotension was classified as persistent sac expansion in the absence of any detectable type I-IV endoleak on serial arterial- and delayed-phase CTA.
Clinical and Biochemical Assessment
In addition to standard anatomical metrics (neck angulation, thrombus distribution), we evaluated systemic comorbidities including obesity (body mass index), spirometry results, presence of systemic hypertension, complete blood count and thyroid function tests. Inflammatory status was quantified using high-sensitivity C-reactive protein (hs-CRP) and the neutrophil-to-lymphocyte ratio.
Statistical Analysis
Statistical analyses were performed using specialized software (SPSS version 25.0). Continuous variables were assessed for normality using the Shapiro-Wilk test and expressed as mean ± standard deviation or median with interquartile range. Categorical variables were reported as frequencies.
To identify predictors of sac expansion, we employed a rigorous two-stage modeling approach. Initially, univariable analysis (Student’s t-test, Mann-Whitney U, or chi-square/Fisher’s exact test as appropriate) was used to screen potential risk factors. Variables demonstrating clinical relevance or statistical significance (p<0.10) were then entered into a multivariable logistic regression model using a backward stepwise elimination method. This was done to determine independent associations and calculate odds ratios (ORs) with 95% confidence intervals. To account for the dynamic nature of sac changes, longitudinal data were further analyzed using generalized estimating equations to evaluate the impact of time-dependent variables on sac diameter. A p-value<0.05 was considered statistically significant.
RESULTS
Patient Characteristics
Between January 2009 and February 2013, a total of 41 patients who underwent EVAR for aortic aneurysm or aortic dissection met the inclusion criteria and were included in the final analysis. All patients completed a minimum follow-up duration of 18 months, with serial imaging available for longitudinal assessment of aneurysm sac behavior.
The study cohort consisted predominantly of male patients and represented a typical EVAR population with advanced age and a high prevalence of cardiovascular risk factors. Baseline demographic characteristics and comorbid conditions were comparable across the cohort and are summarized in Table 1.
Sac Dynamics and Procedural Outcomes
Technically successful stent-graft deployment was achieved in all 41 cases, with no immediate type I or III endoleaks detected on completion angiography. However, the 18-month longitudinal follow-up revealed that aneurysm sac behavior is a complex, multifactorial process that cannot be adequately explained by endoleak classification alone. Persistent sac expansion, defined as an increase of >5 mm, was recorded in 6 patients (14.6%), highlighting that expansion can occur despite apparently complete aneurysm exclusion. This observation underscores the inherent limitations of a purely binary success–failure paradigm, as the absence of traditional endoleaks did not guarantee sac stability or shrinkage in our cohort. Anatomical and procedural characteristics of the study population are summarized in Table 2.
Endoleak Patterns and the Endotension Phenotype
A distinct subgroup of patients (n=2, 4.9%) developed progressive sac enlargement in the total absence of any detectable endoleak on serial CTA, consistent with the phenomenon of endotension (type V endoleak). In our study, endotension emerged as a clinically meaningful postoperative phenotype with potential implications for long-term outcomes, rather than a rare incidental finding. Conversely, persistent collateral flow (Arc of Riolan) was identified as a driver in two other expansion cases, specifically linked to patent lumbar arteries where retrograde filling was confirmed in delayed-phase imaging.
Our findings demonstrate a significant dissociation between endoleak status and sac stability; while some patients with documented low-flow endoleaks showed stable or regressing diameters, others without any detectable leak exhibited continued expansion. This reinforces the concept that endoleak presence alone is an insufficient surrogate marker for aneurysm stability, requiring clinicians to interpret imaging findings within the broader context of longitudinal sac dynamics and systemic forces.
Shared Features and Independent Predictors
A comparative analysis revealed that adverse sac behavior was associated with specific systemic and anatomical factors. Patients with expanding sacs shared common features such as elevated hs-CRP levels (mean 3.8 mg/L), uncorrected hypothyroidism, chronic anemia, and persistent diastolic hypertension. Furthermore, clinical features suggestive of subclinical connective tissue vulnerability, potentially related to fibrillin associated matrix fragility, were more frequently observed in the expansion group; however, no molecular confirmation was available, and this observation should be interpreted as hypothesis-generating.
In multivariable analysis (Figure 1), a larger preoperative sac diameter (>60 mm; OR: 3.24, p = 0.031) and a high mural thrombus burden (OR: 2.86, p = 0.042) emerged as the strongest independent predictors of persistent post-EVAR sac expansion, whereas procedural factors and the brand of the graft were not significantly associated with adverse sac behavior. Independent predictors identified in multivariable logistic regression analysis are summarized in Table 3. These results reinforce the concept that post-EVAR sac dynamics are predominantly driven by pre-existing anatomical and biological factors rather than isolated procedural or imaging-defined findings.
Illustrative Case Scenarios of Adverse Sac Behavior Guiding Post-EVAR Clinical Decision-making
Case 1: Type II Endoleak with Progressive Sac Enlargement Leading to Open Conversion
A 67-year-old female patient with diabetes mellitus and collagen tissue disease underwent EVAR for an infrarenal abdominal aortic aneurysm with a preoperative sac diameter of 69.7x107.1mm (Figure 2A).
After the EVAR procedure follow-up imaging demonstrated limited sac regression, measuring 69.6x106.4 mm at 6 months and 69.5x107.0 mm at 12 months. At the 18-month CTA, the sac diameter increased to 69.6x110.9 mm, corresponding to a cumulative 3-mm expansion (Figure 2B). The Doppler ultrasonography demonstrated persistent pulsatile flow within the sac, and contrast-enhanced CTA confirmed a type II endoleak originating from lumbar arteries (Figure 2C).
Given the documented sac enlargement exceeding guideline-recommended thresholds and ongoing sac pressurization, an endovascular attempt at lumbar artery embolization using occluder devices was performed but proved unsuccessful due to extensive and complex collateral flow. As sac pressurization persisted despite endovascular intervention, open surgical conversion was undertaken, resulting in definitive resolution.
Case 2: Early Type II Endoleak with Moderate Sac Expansion Managed with Intensified Surveillance
A 69-year-old male patient underwent EVAR for an infrarenal abdominal aortic aneurysm with a preoperative sac diameter of 60 mm. At the 6-month follow-up, contrast-enhanced CTA demonstrated a type II endoleak, with the aneurysm sac measuring 63 mm, corresponding to a 3-mm increase in diameter (Figure 3A). Detailed imaging analysis identified retrograde sac perfusion through lumbar arteries supplied via collateral flow from the arc of Riolan, indicating a mesenteric–lumbar collateral pathway as the source of the endoleak (Figure 3B, C).
Given the moderate degree of sac enlargement, the early timing after EVAR, and the absence of rapid expansion or high-risk features, a strategy of repeated imaging surveillance was adopted rather than immediate reintervention, with a low threshold for secondary intervention should further sac expansion be observed.
The moderate degree of sac enlargement, early post-EVAR timing, and identification of a collateral-driven type II endoleak without high-risk features supported a management strategy of intensified imaging surveillance rather than immediate reintervention, with a low threshold for secondary intervention should further sac expansion occur.
Case 3: Endotension Phenotype with Minimal Sac Growth Managed Conservatively
A 71-year-old male patient with hypertension and chronic obstructive pulmonary disease underwent EVAR for an infrarenal abdominal aortic aneurysm with a baseline sac diameter of 58mm. Serial CTA demonstrated 58 mm at 6 months, 59 mm at 12 months, and 60 mm at 18 months, reflecting a total sac enlargement of 2 mm over 18 months (Figure 4A, B). No demonstrable endoleak was identified on repeated imaging, and no graft-related complications were observed. Given the low expansion rate, absence of endoleak (Figure 4C), and stability over time, the patient was classified as having an endotension phenotype and managed with close radiological surveillance rather than reintervention, in accordance with guideline-based recommendations.
Case 4: Minimal Sac Enlargement with Type II Endoleak Managed Conservatively
A 73-year-old female patient with hypertension and obesity underwent EVAR for an aneurysm
with a baseline sac diameter of 62 mm. Follow-up imaging demonstrated 62 mm at 6 months and 63 mm at 12 months, corresponding to a 1-mm increase over one year. CTA revealed a type II endoleak originating from lumbar arteries. Given the minimal degree of sac enlargement, potential measurement variability, and absence of rapid progression, the patient was managed with conservative, very close follow-up, without immediate reintervention (Figure 5A, B).
Case 5: Accelerated Late Sac Expansion Following Aorto-uni-iliac EVAR and Distal Type I Endoleak Prompting Open Conversion
A 75-year-old male patient underwent EVAR for an infrarenal abdominal aortic aneurysm with a preoperative maximum sac diameter of 96.4 mm. Due to anatomical considerations, the procedure was performed using an aorto-uni-iliac stent-graft configuration, combined with a femoro–femoral crossover bypass to maintain bilateral lower limb perfusion. Early postoperative imaging confirmed appropriate graft positioning and satisfactory exclusion of the aneurysm sac. During follow-up, the aneurysm sac initially appeared stable; however, at the 6-month evaluation, interval sac enlargement was detected, raising concern for persistent sac pressurization.
Given imaging findings (Figure 6A, B) suggestive of retrograde pelvic inflow, and the assumption that the left internal iliac artery was chronically occluded, an endovascular occlusion of the left internal iliac artery using an occluder device was performed (Figure 6C). Serial contrast-enhanced CTA suggested a high-pressure endoleak originating from the distal sealing zone near the right common iliac artery, consistent with a distal type I endoleak (Figure 6D). As the aneurysm sac diameter exceeded 101 mm (Figure 6B), and given the progressive nature of expansion despite secondary endovascular intervention, a decision was made to proceed with open surgical conversion.
Despite this intervention, subsequent imaging demonstrated continued and progressive sac enlargement. Intraoperatively, the aneurysm sac was found to be pressurized. An attempt at mechanical banding of the distal iliac neck failed to achieve a meaningful reduction in intra-sac pressure. Upon opening the sac, a relatively fresh thrombus was encountered (Figure 7), within which the trajectory of active endoleak flow could be traced circumferentially around the right common iliac artery, confirming the distal sealing zone as the source of persistent sac filling. Consequently, the endograft material was completely explanted (Figure 7), and definitive repair was achieved by performing an aortobifemoral bypass, resulting in successful exclusion and decompression of the aneurysm sac.
DISCUSSION
The present study demonstrates that aneurysm sac behavior following EVAR is governed by an intricate interplay of anatomical, mechanical, and systemic factors7. Type II endoleaks represent the most frequently encountered endoleak subtype after EVAR, with an overall reported incidence ranging between 20% and 40% among EVAR-treated patients and accounting for nearly half of all identified endoleaks8. These endoleaks commonly originate from retrograde collateral flow through branches such as the inferior mesenteric artery, lumbar arteries, median sacral artery, or accessory renal arteries8. Importantly, type II endoleaks may remain clinically silent or radiographically occult during early follow-up and are not infrequently detected only after aneurysm sac enlargement becomes evident8. Consequently, in cases of continued or progressive sac expansion despite technically successful stent-graft implantation, type II endoleak is often the first and most plausible diagnosis considered in clinical practice. Consistent with these observations, type II endoleaks were not uncommon in our study cohort and constituted a substantial proportion of patients exhibiting adverse sac behavior, underscoring their continued clinical relevance in post-EVAR surveillance. One of the most important insights of the present study is the identification of a distinct subgroup of patients who developed progressive aneurysm sac enlargement in the absence of any detectable endoleak. The presence of this phenotype underscores the critical importance of prolonged follow-up and careful longitudinal assessment, as extended surveillance allows for a more accurate characterization of the factors contributing to endotension9. In this context, the true incidence of endotension reported in the literature may be underestimated, potentially reflecting artificially low rates driven by relatively short follow-up durations rather than a genuine rarity of the condition10. Accordingly, cohorts with extended imaging surveillance, such as the present study population, are particularly valuable for elucidating the determinants and natural history of endotension-related adverse sac behavior. Rather than representing a rare event, endotension in our cohort emerged as a meaningful postoperative phenotype. Several mechanisms may explain this persistent pressurization, including the transmission of pulsatile forces through the stent-graft material, microleakage below the resolution of conventional imaging, and the biomechanical effects of mural thrombus9-11. Our results support the concept that anatomical factors, particularly those related to landing zone quality and thrombus morphology, play a central role in determining these dynamics.
The role of persistent lumbar artery inflow in type II endoleaks deserves particular attention. While type II leaks are often considered benign, our findings in two cases suggest that lumbar arteries can act as high-pressure conduits reinforced by systemic paraspinal circulation. This persistent inflow prevents the expected fibrotic transformation of the sac11. Furthermore, the association between elevated hs-CRP and sac growth suggests that a systemic inflammatory state may keep the mural thrombus in a “fluid” state, facilitating the transmission of systemic pressure even in the absence of a visible flow channel12, 13.
The failure of banding during open conversion in our series provides a critical clinical lesson. It suggests that in the setting of advanced sac expansion or endotension, the biomechanical failure is often circumferential or material-related12. Simple mechanical constriction of the neck may be insufficient to counteract the transmitted forces, making total graft excision a more definitive, albeit invasive, necessity13. This reinforces the need to view sac expansion, regardless of endoleak status, as a warning signal warranting intensified surveillance and individualized decision making13, 14. Beyond anatomical determinants, persistent sac expansion after EVAR may also reflect a systemic vascular phenotype characterized by chronic inflammation, impaired arterial compliance, and altered extracellular matrix remodeling. Patients with adverse sac dynamics in our cohort more frequently exhibited elevated hs-CRP levels, obesity, chronic obstructive pulmonary disease, hypothyroidism, and diastolic hypertension. Although these variables did not consistently remain independent predictors in multivariable analysis, their clustering suggests that systemic inflammatory burden and vascular wall vulnerability may contribute to sustained intra-sac pressurization14. Obesity and chronic obstructive pulmonary disease, in particular, are well recognized to promote low-grade systemic inflammation, endothelial dysfunction, and increased arterial stiffness, mechanisms that may plausibly facilitate transmission of pulsatile forces to the excluded aneurysm sac15-17. Taken together, these observations support the concept that failure of sac regression should not be interpreted solely as a graft-related phenomenon but rather as the interaction between local biomechanical conditions and host-related biological susceptibility18-20. In this context, persistent sac expansion should not be interpreted solely as a local graft-related phenomenon but rather as the downstream manifestation of an unfavorable anatomical–biological milieu. This integrated perspective may help explain why sac regression fails to occur in certain patients despite technically successful EVAR and underscores the importance of incorporating systemic patient characteristics into postprocedural risk stratification and surveillance strategies.
Finally, the integration of metabolic and genetic factors reveals that sac behavior is a systemic phenotype. Hypothyroidism and anemia likely impair the metabolic pathways required for vascular wall remodeling, while diastolic hypertension provides a constant stressor that prevents sac contraction18. In patients with underlying connective tissue weakness, such as fibrillin defects, these forces are amplified19. Recognizing persistent sac expansion as a distinct post-EVAR phenotype may enable more refined risk stratification and contribute to improved selection of patients requiring secondary intervention by supporting surveillance strategies that integrate longitudinal sac behavior with anatomical risk markers and systemic inflammatory status, rather than relying exclusively on conventional endoleak classification1, 20-22. In this context, persistent aneurysm sac expansion should be interpreted as a clinically meaningful indicator of adverse postprocedural dynamics reflecting the combined influence of anatomical configuration, biomechanical forces, and host-related biological susceptibility. Accordingly, longitudinal sac monitoring may represent a more robust marker of procedural durability than endoleak status alone. This perspective is consistent with evidence from large randomized trials such as EVAR-1 (1), DREAM (21), and OVER (22), which established the central role of aneurysm sac dynamics as a surrogate marker of long-term outcomes after EVAR. Incorporation of sac behavior into postprocedural surveillance frameworks may therefore facilitate more individualized follow-up strategies and support timely decision-making regarding secondary intervention in selected patients.
Study Limitations
This study has several limitations that should be acknowledged. First, its retrospective design inherently limits causal inference and may be subject to selection bias. Second, the study was conducted at a single center with a relatively limited sample size, which may restrict the generalizability of the findings to broader populations or different EVAR platforms.
Additionally, direct measurement of intra-sac pressure was not performed, and conclusions regarding biomechanical mechanisms are therefore inferential rather than mechanistically proven. Advanced imaging modalities capable of detecting microleakage or dynamic pressure transmission were not routinely available during the study period.
Nevertheless, the study benefits from a well-defined cohort, standardized imaging follow-up, and complete longitudinal data without loss to follow-up. The homogeneity of procedural technique and surveillance protocols may, in fact, strengthen internal validity by reducing confounding variability.
CONCLUSION
Persistent aneurysm sac expansion after EVAR represents a complex and clinically relevant phenomenon that extends beyond conventional endoleak classification. Our findings demonstrate that sac behavior is influenced by a constellation of anatomical and procedural factors and should be interpreted as an independent marker of post-EVAR success or failure.
Routine follow-up strategies should place greater emphasis on longitudinal sac dynamics rather than reliance on endoleak status alone. Recognizing endotension and related sac expansion phenotypes may improve patient selection for secondary interventions and contribute to more personalized post-EVAR management strategies.
Future studies incorporating advanced imaging, biomechanical modeling, and direct pressure measurements are warranted to further elucidate the mechanisms underlying persistent sac expansion and to optimize long-term outcomes following EVAR.
