The implementation of value‐based medicine reflects a transformation from volume incentivized care to a quality‐of‐care directed reimbursement model. Value‐based medicine aims to concurrently improve health care quality and control growing health care expenditures by aligning evidence‐based and patient‐centered interventions with sustainable resource use. We apply a value‐based medicine framework to abdominal aortic aneurysm care delivery, highlighting opportunities to improve patient outcomes, optimize resource allocation, and reduce health care expenditures across the continuum of disease management. A comprehensive literature review was conducted, evaluating recent clinical guidelines, economic analyses, and real‐world practice data on abdominal aortic aneurysm management, including screening, surveillance, timing of intervention, modality selection (endovascular aneurysm repair versus open surgical repair), and follow‐up strategies. Contemporary real‐world published practice patterns reveal wide variation in screening uptake, surveillance intensity, repair criteria thresholds, procedure and device selection, and post‐endovascular aneurysm repair imaging, producing inconsistent outcomes and inefficient spending. Endovascular aneurysm repair predominates in elective abdominal aortic aneurysm repair because of lower perioperative morbidity and shorter length of stay; however, downstream costs from surveillance, endoleak management, and reinterventions may erode its initial economic advantage over open surgical repair. Key value drivers include risk‐aligned screening, standardized surveillance anchored to anatomy and device risk, judicious use of advanced imaging, optimized perioperative pathways, and careful device selection. Savings opportunities include predictive analytics to individualize surveillance, deescalation of routine computed tomography after documented sac shrinkage, smoking cessation, medical optimization, and structured shared decision‐making aligned with life expectancy and patient preferences. Integrating value‐based medicine principles into abdominal aortic aneurysm care through regional centers of excellence, bundled reimbursement models, transparent cost structures, and surveillance strategies may offer a pragmatic roadmap to achieve safer, economically sustainable, and patient‐centered management, ultimately advancing both clinical outcomes and cost efficiency.

Objective Frailty is increasingly recognized as a key driver of postoperative risk in vascular surgery, yet the comparative accuracy of major frailty indices in patients undergoing aortic surgery remains unclear. We compared the predictive accuracy of the Modified Frailty Index, Risk Analysis Index, Vascular Quality Initiative Frailty Index, and Vascular Quality Initiative Procedure-Based Index in predicting adverse postoperative outcomes in patients undergoing open and endovascular aortic aneurysm repair. Methods In this retrospective single-center cohort study, 131 patients who underwent open or endovascular aortic aneurysm repair between January 1 and December 31, 2023, were included. Frailty scores were calculated retrospectively based on data available at the time of preoperative evaluation. Primary outcomes were 30-day and 60-day hospital readmissions, in-hospital mortality, and 1-year mortality. Secondary outcomes included 30-day stroke, acute kidney injury, myocardial infarction, and reintervention. Statistical associations were evaluated using logistic regression models. Results The cohort's mean age was 70.6 ± 9 years, 31% were female, and pathology included abdominal aortic aneurysm (70%), thoracic aortic aneurysm (11%), thoracoabdominal aortic aneurysm (13%), and aortic dissection (6%). Interventions included endovascular aneurysm repair (34%), thoracic endovascular aortic repair (19%), fenestrated endovascular aortic repair (16%), and open repair (31%). Thirty-day readmission was the only outcome significantly associated with frailty across multiple indices. In the combined, open and endovascular, cohort, the Modified Frailty Index (odds ratio, 2.15; 95% confidence interval, 1.28-3.78; P = .01; area under the curve, 0.71), Risk Analysis Index (odds ratio, 1.09; 95% confidence interval, 1.01-1.18; P = .02; area under the curve, 0.72), and Vascular Quality Initiative Frailty Index (odds ratio, 1.74; 95% confidence interval, 1.25-2.52; P = .002; area under the curve, 0.73) demonstrated significant associations with 30-day readmission. Conclusions In patients undergoing aortic aneurysm repair, frailty indices demonstrated limited predictive value across most postoperative outcomes. Thirty-day readmission was the only outcome consistently associated with frailty scores, with no significant performance differences among the four indices tested. The vascular-specific indices did not outperform generic measures in this cohort, highlighting the need for aortic-specific risk stratification tools.

Innovation in the treatment of ascending aorta and arch pathology with novel catheter-based and hybrid procedures has driven the need for a strategy to guide their safe application. The ARCH-ARC (Aortic Arch Academic Research Consortium) was established to pragmatically develop consistent clinical end points and to standardize definitions for use in studies of these new technologies. The ARCH-ARC team, consisting of independent international specialists in cardiac surgery, vascular surgery, vascular medicine, cardiology, neurology, radiology, and clinical trials, along with US Food and Drug Administration, industry, and contract research organization representatives, held virtual meetings from 2021 to 2025. Consensus was used to identify appropriate clinical end points and to standardize definitions of end points for endovascular, hybrid, and open surgical procedures in clinical trials in the ascending aorta and arch. Drawing on previous ARC work in cardiac, neurological, renal, and bleeding end points, the ARCH-ARC focused on definitions and end points related to aortic arch-specific anatomy, pathology, and procedures and clinical, device, and imaging. The adoption of the ARCH-ARC consensus definitions and end points will provide a template for consistent adjudication and event reporting and facilitate comparisons of clinical research studies involving devices for ascending aorta and arch pathology.

OBJECTIVE:Aneurysm behavior after fenestrated and branched endovascular aortic repair (F/B-EVAR) is a marker of treatment success and has been linked with long-term survival. This study aimed to characterize longitudinal changes in residual aneurysm sac behavior after F/B-EVAR and relate these changes to aortic outcomes. METHODS:We retrospectively analyzed F/B-EVARs performed in 10 sponsor-investigator investigational device exemption trials (2005-2024). Serial imaging after repair was evaluated for changes in residual aneurysm sac behavior. Changes in sac behavior over time were investigated with a multistate time-to-event survival model, and the time-dependent effect of sac behavior on outcomes was analyzed with a competing risks model for aortic events and nonaortic death. RESULTS:A total of 1932 patients met the study criteria; 1223 patients (63%) were treated for thoracoabdominal aneurysm with a median preoperative maximum aortic diameter of 61 mm (interquartile range [IQR], 57-67 mm). The median follow-up was 3.5 years (IQR, 2.3-4.6 years) with 3 surveillance imaging studies (IQR, 2-5 studies) available per patient. Endoleak occurred in 1043 patients (54%) and 343 (18%) underwent reintervention. At 1 year, the predicted probabilities of sac states were: 32% for regression (95% confidence interval [CI], 25-40), 42% stability (95% CI, 35-49), expansion 6% expansion (95% CI, 4-7), and 7% death (95% CI, 6-9); the probability of the aneurysm state not yet observed was 14% (95% CI, 10-20). The presence and absence of endoleak at any time in follow-up were associated with the risks of transition to a state of sac expansion (hazard ratio [HR], 1.3; 95% CI, 1.1-1.6; log-rank P = .003) or regression (HR, 2.1; 95% CI, 1.6-2.9; log-rank P < .0001), respectively. Aortic events, including rupture, dissection, and death, occurred in 78 patients (4%). Sac expansion demonstrated at any time after F/B-EVAR was associated with the cause-specific hazards of an aortic event (HR, 3.2; 95% CI, 1.6-6.4; log-rank P = .009), as well as nonaortic death (HR, 1.3; 95% CI, 1-1.6; log-rank P = .02). The hazard of an aortic event did not differ between states of stability and regression, but the presence of an endoleak significantly modified the hazard of aortic event with sac stability (HR, 2.2; 95% CI, 1.1-4.6; log-rank P = .04). CONCLUSIONS:Residual aneurysm sac behavior after F/B-EVAR is dynamic and influenced by the presence of an endoleak. Sac expansion, even when occurring later in follow-up, was associated with increased hazards of both aortic events and nonaortic death. These findings underscore the importance of diligent surveillance and timely intervention for endoleaks after F/B-EVAR.

Background:Clinically significant carotid stenosis remains a major cause of ischemic stroke (IS), yet prediction of disease progression is limited. Polygenic risk scores (PRSs) for coronary artery disease (CAD) and peripheral artery disease (PAD) have demonstrated associations with atherosclerosis burden and major cardiovascular disease (CVD) events, but whether these insights extend to carotid stenosis is unclear. We evaluated the association and discriminative performance of validated PRSs for CAD, PAD, IS, and carotid intima-media thickness (cIMT) with carotid stenosis among participants of the Mass General Brigham Biobank (MGBB). Methods:Carotid stenosis was identified in genotyped MGBB participants using validated ICD- and CPT-based phenotyping algorithms. Logistic regression adjusted for age, sex, and 10 ancestry principal components assessed PRS associations. Incremental discrimination was evaluated using changes in Harrell's C-statistic. Results:Compared with 52,636 controls, 670 participants with carotid stenosis were more frequently male (61.5% vs 44.1%), older (70.8 SD 9.0 vs 53.4 SD 17.2 years), and more likely to be European (95.7% vs 84.1%). The IS (OR 1.31, 95% CI 1.21-1.41), CAD (OR 1.62, 95% CI 1.50-1.75), and PAD (OR 1.66, 95% CI 1.54-1.80) PRSs were each associated with carotid stenosis (all p<0.0001), while the cIMT PRS was not (OR 1.04, 95% CI 0.97-1.13; p=0.28). The PAD PRS demonstrated the greatest improvement in discrimination beyond age, sex, and ancestry (ΔC-statistic 0.017; C-statistic 0.845, 95% CI 0.833-0.856). A fully adjusted model incorporating established CVD risk factors achieved a C-statistic of 0.852 (95% CI 0.841-0.862), with modest further improvement after PAD PRS inclusion (ΔC-statistic 0.008). Individuals in the top 5% of the PAD PRS distribution and top 4% of CAD PRS demonstrated 3-fold greater odds of carotid stenosis. Conclusions:A PAD and CAD PRS may help identify individuals at high likelihood for carotid stenosis, though broad discriminative performance remains limited. These findings support further investigation of CVD PRSs as adjunctive risk stratification tools.

OBJECTIVE:The use of cerebrospinal fluid drains (CSFDs) for the prevention or mitigation of spinal cord ischemia (SCI) is a subject of debate for patients undergoing branch/fenestrated endovascular aortic repair. We sought to evaluate the practices surrounding CSFD use concurrently with rates of SCI occurrence, recovery, and CSFD complications in the US Aortic Research Consortium. METHODS:We conducted a retrospective analysis of the US Aortic Research Consortium registry consisting of patients undergoing branch/fenestrated endovascular aortic repair under individual physician-sponsored investigational device exemptions from January 2011 to April 2024. A composite variable consisting of SCI, major CSFD complication, or intracerebral hemorrhage was designated as the primary outcome. Patterns of CSFD use, rates of SCI and recovery, and CSFD complications were analyzed by year. Subanalyses were stratified by Crawford extent (CE) classification based on the length of aortic coverage, with high-risk patients defined as CE I to III. To further characterize the relationship between SCI and CSFD use, patient cohorts were compared by prophylactic CSFD (pCSFD) (n = 949), therapeutic CSFD (tCSFD) (n = 27), and no CSFD (n = 1609). Multivariable logistic regression was performed to determine variables associated with the composite outcome. Survival analysis was conducted using the Kaplan-Meier method. RESULTS:Among 2585 patients, 196 (7.6%) experienced the composite outcome, gradually declining from a maximum of 25.0% (5 patients) in 2011 to 2.9% (11 patients) in 2023. Concurrently, the use of pCSFDs declined from a maximum of 100% in 2011 to 11.0% in 2023 without any substantial increase in tCSFDs. Among high-risk patients (n = 1026), 132 (12.9%) experienced the primary composite outcome, declining from a maximum of 38.5% (5 patients) in 2013 to 3.1% (4 patients) in 2023. PCSFDs in high-risk patients, although nearly universal (92.9%-100%) until 2016, have also been on a continuous decline, reaching a minimum of 23.1% in 2024, without increase in tCSFD use (0%-5.9%). The degree of SCI resolution was not significantly different in the pCSFD (94 patients, 45.7% complete resolution), tCSFD (23 patients, 43.5% complete resolution), or no CSFD (21 patients, 42.9% complete resolution) cohorts (P = .11). Major CSFD complications did not differ between the pCSFD and tCSFD cohorts (13.4% vs 12.0%; P = .85). Multivariable logistic regression revealed CE II (odds ratio [OR], 2.35; 95% confidence interval [CI], 1.48-3.75; P < .001) and III (OR, 2.11; 95% CI, 1.31-3.40; P = .002), staging (OR, 1.66; 95% CI, 1.17-2.35; P = .004), and estimated blood loss of >350 mL (OR, 1.52; 95% CI, 1.11-2.09; P = .009) to be associated significantly with the composite outcome. CONCLUSIONS:Composite outcome rates have continued to improve despite declining pCSFD use. SCI recovery was not impacted favorably regardless of pCSFD, tCSFD, or no CSFD use. In the setting of comprehensive SCI prevention protocols, pCSFD use may not be warranted, even in most high-risk patients.

OBJECTIVE:Prognostication after acute type B aortic dissection (aTBAD) may be limited when relying upon static computed tomographic angiography (CTA) images to evaluate a dynamic process. We performed an exploratory study to characterize variations in luminal contrast attenuation on CTA, as a surrogate for blood flow in dissection, and to determine whether the resulting parameters held prognostic value. METHODS:Retrospective, single-institution data for patients with aTBAD were gathered from 1999 to 2020. Patients with prior dissection repairs were excluded. Dissection morphology was classified by the joint Society for Vascular Surgery/Society of Thoracic Surgeons scheme and location/number of fenestrations. Hounsfield unit ratios (HURs) comparing lumina, phases, and aortic zone were calculated. Aortic growth, false lumen thrombosis, and need for intervention were evaluated with logistic regression. RESULTS:After exclusions, 74 patients were identified. Most fenestrations were in zones 4/5 (56.5%) and associated with more equilibrated HUR (0.93) compared with dissections without fenestration (0.65; P = .04). Intervention occurred in 68.9%. Increased arterial phase false-to-true HUR was strongly associated with eventual need for intervention (odds ratio, 25.3; 95% confidence interval, 4.15-188.4; P = .001), whereas the increased delayed-to-arterial phase false lumen HUR was associated with fewer interventions (odds ratio, 0.49; 95% confidence interval, 0.25-0.89; P = .02). CONCLUSIONS:In patients with aTBAD, calculated permutations of HUR across lumina and between CTA phases may give insight into blood flow dynamics, which in turn likely impact the need for intervention. Future prospective studies of time-resolved CTA are likely to hold significant prognostic value and alter management.

A 50-year-old woman required an emergent operative exploration after an unsuccessful attempt at bedside removal of a ruptured intra-aortic balloon pump (IABP). Initial fluoroscopy demonstrated that the IABP tip moved dynamically with blood flow, but retraction and advancement caused significant bowing of the proximal external iliac artery. After unsuccessful endovascular snaring and resheathing, an exploratory laparotomy was required to remove the entrapped IABP via a longitudinal external iliac arteriotomy. Proximal to the patch angioplasty, an occlusive dissection flap was identified, requiring stent placement. Back table examination showed an exposed metallic knob, concerning for a manufacturing or iatrogenic defect, that likely caused this complication. The patient’s health care proxy consented to the publication of this patient’s operative course.

OBJECTIVE:Aneurysm sac behavior after fenestrated or branched endovascular repair (FB-EVAR) of thoracoabdominal aortic aneurysms (TAAAs) remains a key knowledge gap. The purpose of this study was to identify independent predictors of sac behavior after FB-EVAR and assess the relationship between sac behavior and long-term survival. METHODS:Patients undergoing FB-EVAR between 2005 and 2023, in 10 physician-sponsored investigational device exemption studies in the United States, were analyzed. Patients who underwent elective FB-EVAR for juxtarenal, suprarenal, or extent 1 to 5 TAAAs and had 30-day and 1-year computed tomography follow-up imaging were included. Patients with chronic aortic dissections were excluded. Sac regression or expansion (≥5 mm) was defined using the Society for Vascular Surgery guidelines. Independent predictors of sac growth were identified using multivariable logistic regression analysis and survival rates were compared using Kaplan-Meier curves. RESULTS:Of 3057 patients who underwent FB-EVAR, 1497 were eligible for analysis. Median follow-up was 2.9 years (interquartile range, 1.3-4.0 years). At 1 year, 103 (6.9%) patients experienced sac expansion, 694 (46.4%) experienced sac regression, and 700 (46.7%) had a stable sac. Variables independently associated with sac expansion were age (odds ratio [OR] 1.04; 95% confidence interval [CI], 1.01-1.07; P = .0057), prior aortic surgery (OR, 2.22; 95% CI, 1.32-3.40; P = .0026), prior EVAR (OR, 1.84; 95% CI, 1.07-3.14; P = .0264), larger aneurysm diameter (OR, 1.03; 95% CI, 1.01-1.04; P = .0014), type II endoleak observed on 30-day follow-up computed tomography (OR, 2.15; 95% CI, 1.36-3.41; P = .0011), and any secondary intervention during the first year (OR, 2.19; 95% CI, 1.35-3.55; P = .0016). Overall survival at 1 year was significantly lower in the expansion group compared with the stable and regression groups (85.6% vs 90.9% vs 93.1%, respectively). This effect persisted on 5-year evaluation (48.1% vs 63.0% vs 67.7%, respectively). Both expansion and stability at 1 year were both associated with increased long-term mortality in unadjusted cox model (expansion, hazard ratio, 2.083; 95% CI, 1.47-2.95; P < .0001; stability, hazard ratio, 1.26; 95% CI, 1.02-1.56; P = .0298) vs regression. CONCLUSIONS:Both aneurysm sac expansion and stability (lack of regression) one year after FB-EVAR are associated with decreased long-term survival compared with sac regression. These outcomes underscore the need for vigilant monitoring of patients without sac regression and to better understand if interventions to address factors associated with unfavorable aneurysm sac behavior can improve long-term survival.

OBJECTIVE:Cervical debranching was traditionally performed for occlusive disease of the proximal cervical branches of the aortic arch. However, as endovascular technology has evolved, cervical debranching is more commonly performed to optimize proximal landing zones for thoracic endovascular aortic repair (TEVAR). Cervical debranching and TEVAR can be performed in either a staged or synchronous fashion with little-to-no data regarding the optimal treatment strategy. Therefore, the purpose of this study was to evaluate outcomes of patients undergoing cervical debranching and TEVAR in a staged vs synchronous fashion. METHODS:This was a retrospective single-center review of patients undergoing cervical debranching to optimize proximal landing zones for TEVAR from 2010 to 2023. Patients were excluded if they had a salvage cervical debranching following an aortic intervention or had an open aortic repair following cervical debranching. Patients were stratified on whether the cervical debranching and TEVAR were staged or synchronous. Cervical debranching was defined as a bypass or transposition of the vessels of the aortic arch (including vertebral artery). The primary outcome was major adverse events (MAEs), which was a composite variable consisting any of the following: 30-day mortality, myocardial infarction, respiratory failure, cerebrovascular accident, hematoma/bleeding, complications, nerve injury, chyle leaks, and acute kidney injury. RESULTS:A total of 148 patients met study criteria, with 162 cervical debranching procedures performed. There were 112 staged (75.7%) and 36 synchronous (24.3%) patients. There were three patients (2.7%) in the staged cohort that were intended to be staged but did not undergo TEVAR due to complications of their cervical debranching procedure. Synchronous patients were more likely to have non-elective repairs (44.4% vs 18.8%; P = .004) and zone 0 TEVAR deployments (5.5% vs 0%; P = .042) than staged repairs. The overall rate of MAEs for the cohort was 35.8% (n = 53). There were no differences in MAEs between staged and synchronous patients (34.8% vs 38.9%; P = .692). Although not statistically significant, there were lower rates of myocardial infarctions (2.7% vs 8.3%; P = .155), respiratory complications (16.1% vs 30.6%; P = .089), cerebrovascular accidents (11.6% vs 22.2%; P = .167), and bleeding complications (10.7% vs 22.2%; P = .095) in the staged group. The rate of nerve injury for the total cohort was 5.4%, with no differences between the staged and synchronous cohorts (4.5% vs 8.3%; P = .403). The overall technical success rate for cervical debranching procedures was 99.4% (n = 161) with no differences between staged and synchronous procedures (99.1% vs 100%; P = .998). There were no differences in primary, primary-assisted, and secondary patency of the cervical debranching procedures over 5 years between staged and synchronous procedures. CONCLUSIONS:Staged and synchronous cervical debranching and TEVAR had statistically similar perioperative outcomes despite synchronous procedures being performed more often in the non-elective setting. However, there were clinically relevant trends toward better outcomes with staging. Cervical debranching can be performed with a high technical success rate with excellent mid-term patency. Currently, both staged and synchronous strategies appear to be safe and should be tailored towards patients' clinical presentations.

Objective: To assess patient radiation exposure as reflected by cumulative air kerma (CAK) and dose area product (DAP) during fenestrated-branched endovascular aortic repair (FB-EVAR). Summary Background Data: Patient radiation exposure during FB-EVAR has been reported inconsistently. Methods: Data from 2,111 patients enrolled in 10 physician-sponsored investigational device exemption studies (2012-2022) were analyzed from the United States Aortic Research Consortium database. Procedures were performed using seven fixed imaging systems (A to G). Patients were classified into three groups by imaging era: 2012-2015 (Group 1), 2016-2018 (Group 2), and 2019-2022 (Group 3). Primary endpoints were CAK and DAP risk factors, assessed using linear mixed-effect models. Secondary endpoints were diagnostic reference levels (DRL) for FB-EVAR. Results: Of the 2,111 patients (71% males; mean 74±9 years years-old) treated by FB-EVAR; 263 (12%) were in Group 1, 541 (26%) in Group 2, and 1,307 (62%) in Group 3. Use of ≥4 vessel stent-graft designs increased from 69% (Group 1) to 79% (Group 3) ( P <0.001). Median CAK decreased from 3,644 mGy (Group 1) to 1,753 mGy (Group 3), and DAP from 441 Gy.cm² to 208 Gy.cm² ( P <0.001). Higher BMI, iliac branch device (IBD) use, and longer fluoroscopy time (FT) were associated with increased CAK and DAP, while experienced operators and systems D, F, and G were protective ( P <0.05). DRLs for Group 3 were 2,800 mGy (CAK) and 340 Gy.cm² (DAP). Conclusions: Radiation exposure during FB-EVAR significantly decreased over time. Higher BMI, IBD use, and FT were linked to increased exposure, while experienced operator and System D, F or G were protective. Trial registration : URL: https://www.clinicaltrials.gov; Unique identifiers: NCT02043691 NCT00583817 NCT00483249 NCT01937949 NCT02050113 NCT02323581 NCT01874197 NCT01654133 NCT02266719.

OBJECTIVE:Intramural hematoma (IMH) carries significant risk of morbidity and mortality, and although thoracic endovascular aortic repair (TEVAR) is increasingly used as a treatment, the optimal timing for its intervention remains uncertain. This study aimed to compare outcomes between patients undergoing urgent TEVAR (within 24 hours of admission) and those undergoing elective TEVAR (beyond 24 hours from admission). METHODS:Patients who underwent TEVAR between aortic zones 2 and 5 for IMH from 2013 to 2023 were included, excluding those with rupture. Propensity scores were generated using covariates such as age, sex, race, obesity, anemia, transfer status, hypertension, diabetes, prior myocardial infarction, congestive heart failure, smoking history, chronic obstructive pulmonary disease, cerebrovascular disease, dialysis status, medication use, and previous aortic surgery, to adjust for assignment to urgent/emergent or elective TEVAR. Perioperative outcomes were assessed using inverse probability-weighted logistic regression. Association of urgent or elective TEVAR with 5-year mortality was assessed using Cox regression stratified by IMH symptom status. RESULTS:Among 345 patients, 165 (48%) underwent elective repair. The urgent group had a higher rate of transfers from outside institutions (64% vs 43%; P = .01), were less likely to use beta-blockers before presentation (69% vs 84%; P = .003), and were more frequently symptomatic at presentation (98% vs 72%; P < .001). There were no significant differences in IMH disease extent or graft landing zones between groups. Perioperative mortality (6.3% vs 0.6%; adjusted odds ratio [aOR] 19; 95% confidence interval [CI], 3.01-764; P = .02) and reintervention during index admission (8.3% vs 2.4%; aOR, 4.92; 95% CI, 1.67-19.5; P = .01) was significantly greater in the urgent group. Five-year survival was lower in the urgent group, but this difference was not statistically significant. In symptomatic patients, the urgent cohort had significantly higher perioperative mortality (7.3% vs 0.8%; aOR, 10; 95% CI, 2.11-152; P = .02), acute kidney injury (9.0% vs 2.5%; aOR, 3.28; 95% CI, 1.12-12.1; P = .04), and reintervention (8.5% vs 2.5%; aOR, 5.26; 95% CI, 1.61-25.6; P = .01) rates. Conversely, the elective group had a longer total length of stay (32% vs 21%; aOR, 0.48; 95% CI, 0.28-0.82; P = .01). Five-year survival in the symptomatic cohort was lower in the urgent group, but this difference was not statistically significant. CONCLUSIONS:Patients undergoing urgent TEVAR for IMH experience worse perioperative outcomes compared with those undergoing elective repairs, despite comparable baseline risk profiles. Although emergent repair may be necessary in certain cases, these data advocate for a patient management strategy that prioritizes stabilization before intervention.

Vascular calcification represents a convergent pathological feature of diverse cardiovascular diseases, yet the upstream molecular programs orchestrating this process remain poorly defined. Here, we uncover fibronectin type III domain-containing 1 (FNDC1) as a previously unrecognized regulator of vascular calcification across both microvascular and macrovascular beds. Integrative transcriptomic profiling of human calciphylaxis lesions and atherosclerotic coronaries identified FNDC1 as one of the most significantly upregulated genes. In primary human vascular smooth muscle cells, FNDC1 drove osteogenic phenotype switch and vascular calcification through activation of PI3K/AKT signaling and metabolic reprogramming. Mechanistically, FNDC1 directly binds to nicotinamide phosphoribosyltransferase (NAMPT) resulting in elevated intracellular NAD⁺ levels, thus coupling vascular signaling to control of NAD⁺ biosynthesis. In murine models, genetic deletion of Fndc1 or pharmacologic inhibition of NAMPT suppressed arterial calcification and prolonged survival. Clinically, circulating FNDC1 levels were elevated in patients with both calciphylaxis and coronary artery disease and independently predicted cardiovascular risk in 42,687 UK Biobank participants. Together, these findings establish FNDC1 as a central mediator of vascular pathology and highlight the FNDC1- NAMPT-NAD + axis as a promising target for therapeutic intervention.