Background:Ascending thoracic aortic dissection (ATAD) is characterized by extensive macrophage (MΦ) accumulation and profound inflammation; however, the mechanisms sustaining pro-inflammatory MΦ activation remain incompletely defined. Emerging evidence indicates that epigenetically generated immune memory drives innate immune cells toward persistent inflammatory states. In this study, we investigated whether epigenetic reprogramming governs MΦ phenotypic fate and contributes to ATAD pathogenesis. Methods:We performed single-cell RNA sequencing of human ascending aortic tissues from controls, patients with ascending thoracic aortic aneurysm (ATAA), and patients with acute ascending thoracic aortic dissection (ATAD). We also performed integrated single-cell RNA sequencing, single-cell ATAC sequencing, and spatial transcriptomics in an angiotensin II (Ang II)-infused mouse model. The role of the STING-IRF3 signaling axis in MΦ epigenetic programming was examined using MΦ- Sting -/- and MΦ- Irf3 -/- mice. Results:In human and mouse aortic tissues, we identified multiple functional MΦ populations including pro-inflammatory, phagocytic/anti-inflammatory, proliferative, and reparative/healing MΦs. Aortic MΦs in both sporadic ATAD patients and Ang II-induced ATAD mice exhibited a pronounced pro-inflammatory bias with enhanced differentiation toward pro-inflammatory MΦs and impaired differentiation toward phagocytic/anti-inflammatory states. Pro-inflammatory MΦs were particularly abundant in dissection sites, whereas phagocytic MΦs were enriched in discrete adventitial niches. Origin analyses revealed a substantial increase in CCR2 ⁺ recruited MΦs within the aortic wall, which preferentially differentiated into pro-inflammatory MΦs. In contrast, LYVE1 ⁺ resident MΦs- predominantly biased toward phagocytic phenotypes-were markedly depleted in ATAD. Single-cell ATAC sequencing identified coordinated chromatin remodeling with increased accessibility at pro-inflammatory gene loci and decreased accessibility at phagocytic gene loci. Among candidate transcriptional regulators identified, IRF family TFs, including IRF3 emerged as unique factors capable of simultaneously promoting pro-inflammatory gene programs while suppressing phagocytic gene expression. Mechanistically, STING-IRF3 signaling orchestrates this biased transcriptional state, likely through coordinated BRG1-dependent chromatin opening at pro-inflammatory gene loci and chromatin closing at phagocytic/anti-inflammatory gene loci. MΦ specific Sting -/- and Irf3 -/- mice exhibited attenuated inflammatory reprogramming and reduced aortic destruction and dissection. Conclusions:These findings identify STING-IRF3-mediated epigenetic programming of MΦs as a fundamental mechanism driving aortic inflammation and ATAD development. Targeting MΦ epigenetic programming may represent a promising therapeutic strategy to prevent aortic dissection. Graphic Abstract:

Objective Postoperative stroke after thoracoabdominal aortic aneurysm (TAAA) repair is an uncommon but devastating complication that has been understudied. This analysis aimed to identify patients at highest risk for ischemic or hemorrhagic stroke after TAAA repair. Methods We analyzed data from 3765 patients who underwent open TAAA repair from 1986 to 2024 at a single high-volume aortic surgery practice. We used multivariable logistic regression modeling to evaluate preoperative and operative predictors of all and persistent ischemic and hemorrhagic stroke. The effect of new-onset atrial fibrillation was evaluated. Results Postoperative stroke persisted to death or hospital discharge in 93 patients (2.5%) and was transient in 29 (0.8%). Those with persistent stroke had a higher mortality rate (61.3%, n=57/93) than those without any stroke (7.3%, n=267/3643). Most persistent strokes were ischemic (76.3%) rather than hemorrhagic (26.9%). Significant predictors of persistent ischemic stroke included older age (odds ratio [OR]=1.04, P=.007) and chronic kidney disease (OR=1.98; P=.01), whereas Crawford extent III (OR=0.38; P=.01) and IV repairs (OR=0.35; P=.008) were protective. Significant predictors of persistent hemorrhagic stroke included heritable thoracic aortic disease (OR=2.34; P=.04) and prophylactic cerebrospinal fluid drainage (OR=7.99; P=.006). Prolonged aortic clamp time (OR=1.03, P=.03) was associated with greater odds of death after a stroke. Conclusions This analysis of a large, single-practice series identified variables associated with stroke and stroke-related mortality after TAAA repair. While stroke remains infrequent, its lethality highlights the importance of risk modeling. Mitigating the risk of hemorrhagic stroke in patients with heritable thoracic aortic disease should be prioritized.

Objective: Cardiac surgery-associated acute kidney injury (CSA-AKI) is a common complication after surgery, yet few risk models are used in practice. We evaluated whether a cardiac diuretic responsiveness index (CDRI) can accurately predict CSA-AKI. Methods: Time-series hemodynamic, intake/output volumes, medication, and laboratory data were extracted from electronic health records for 2016 patients who underwent cardiac surgery (2017-2022) and linked to the institutional Society of Thoracic Surgeons Baylor St Luke's Medical Center database. Patients with serum creatinine >4 mg/dL, dialysis before surgery, or those without diuretics administered were excluded. CDRI was defined as urine output in the first hour after initial diuretic administration adjusted for patient weight and diuretic dose (cc/kg/hr/mg furosemide). CSA-AKI was defined by Kidney Disease Improving Global Outcomes creatinine criteria. Segmental regression identified the optimal CDRI threshold. Results: Median time to first dose was 26.4 hours. CSA-AKI occurred in 16.2% (n = 326) of patients who were primarily stage 1 (82.8%, n = 270). Patients who developed CSA-AKI had significantly lower CDRI values (0.0611 vs 0.111 cc/kg/hr/mg furosemide; P < .0001). A CDRI threshold of 0.075 predicted CSA-AKI with a C-statistic 0.86), outperforming traditional oliguria criteria (<0.5 mL/kg/h, C-stat 0.8). Conclusions: CDRI outperforms oliguria in predicting CSA-AKI, enabling real-time stratification, and may inform timely intervention to prevent AKI progression.

Objective:Obesity is a chronic disease linked to high mortality and morbidity after cardiac procedures, but its relationship to outcomes after total aortic arch replacement (TAR) remains unclear. We examined TAR data to determine whether obesity is associated with greater perioperative risk. Methods:Among 787 TARs performed from 1990 to 2023, we excluded patients who lacked body mass index (BMI) data, had nonelective or nonstandard repairs, or were underweight (BMI <18.5 kg/m2). The remaining 521 patients did not have obesity (18.5 ≤BMI <30; n = 389) or did (BMI ≥30; n = 132). Patients with obesity were class 1 (30 ≤ BMI < 35), class 2 (35 ≤ BMI < 40), or class 3 (BMI ≥40). We compared preoperative and perioperative variables for BMI ≥30 (obesity) versus BMI <30. Adverse events were operative mortality, persistent stroke, spinal cord deficit, and renal failure. We performed multivariable logistic regression and Kaplan-Meier survival analysis. Results:Patients with obesity had greater rates of obstructive sleep apnea, transient spinal cord deficit, and acute renal dysfunction than patients with normal weight. During repair, the use of antegrade cerebral perfusion often exceeded 30 minutes in patients with obesity. Operative mortality and adverse events did not differ among BMI or obesity groups. Greater BMI was not predictive of operative mortality, whereas chronic kidney disease (odds ratio, 2.28; P = .01), pulmonary disease (1.87, P < .001), longer aortic clamp time (1.01, P = .03), and antegrade cerebral perfusion time >30 minutes (2.17, P = .047) were. Survival did not differ significantly by obesity status. Conclusions:Obesity was not associated with operative mortality or adverse events in patients who underwent TAR. Therefore, patients should not be deemed ineligible for TAR on the basis of obesity alone.

PURPOSE:Variants of uncertain significance (VUS) represent are clinical challenging. We hypothesize that bioinformatic tools can identify VUS that are "high risk." METHODS:Primary analyses were performed in the Penn Medicine Biobank, which is composed of 43,731 participants, 11,925 of whom carried at least 1 missense VUS in the 11 genes associated with heritable thoracic aortic disease. VUS rare exome variant ensemble learner, AlphaMissense, and minor allele frequency high-risk thresholds were derived using cutpointR. These cutpoints were used to test the association of high-risk VUS with prevalent thoracic aortic disease. RESULTS:In the Penn Medicine Biobank, being heterozygous for a VUS was associated with a modest increased risk of thoracic aortic aneurysm (TAA: OR = 1.14, 95% confidence interval [CI] 1.01 to 1.29, P = .034) but no increased risk of aortic dissection (OR = 1.04, 95% CI 0.55 to 2.00, P = .896). Using cutpointR, we derived are exome variant ensemble learner (>0.649), AlphaMissense (>0.2543), and minor allele frequency (<8.16 × 10-6) cutpoints that identified 435 high-risk VUS that were robustly associated with prevalent dissection (OR = 7.85, 95% CI 4.73 to 13.03, P < .001), although the association with TAA was attenuated (OR = 2.35, 95% CI 1.62 to 3.42, P < .001). Similar results were observed in 2 independent validation cohorts. CONCLUSION:High-risk VUS were strongly associated with aortic dissection, suggesting that high-risk thresholds may be applied clinically.

OBJECTIVE:As endovascular aortic repair (EAR) has become more frequent over the past 3 decades, so has the need for endograft explantation followed by open aortic reconstruction (OAR). We retrospectively examined our experience and outcomes with these procedures. METHODS:Between 1996 and 2025, 181 patients (median age 65 years [interquartile range, 53-72 years]; 70.2% male) underwent endograft explantation (33.7% partial and 66.3% complete) with OAR at our center. Previous EAR were primarily thoracic (48.1%) and abdominal (41.4%). We analyzed trends in practice, preoperative characteristics, operative details, early outcomes, and factors associated with operative mortality (death within 30 days of repair or before final hospital discharge). Survival was estimated with Kaplan-Meier and competing risk analyses. RESULTS:Median time from index EAR to explant was 2.7 years [interquartile range, 0.6-5.8 years] overall and was shorter (1.4 years [interquartile range, 0.2-3.4 years]) in patients with hereditary aortopathies. Endograft explantation increased from <1% of OAR cases (11/2150) in 1996-2005 to 6% (78/1214) in 2006-2015 to 20% (92/469) in 2016-2025. Thirty-eight patients (21.0%) were ≤50 years old, 34 (18.8%) had Marfan or Loeys-Dietz syndrome, and 74 (40.9%) had aortic dissection. Operative complexity was high: 20.4% (n = 37) had infection, 18.8% (n = 34) had a redo incision, and 61.3% (n = 111) underwent thoracoabdominal aortic repair. Operative mortality was 13.8% (n = 25). Survival was 53% at 5 years. CONCLUSIONS:Endograft explantation with OAR is technically demanding and high-risk, especially when the endograft is infected. These findings highlight the importance of long-term surveillance and careful patient selection for EAR, especially when patients are young or have aortic dissection.

OBJECTIVE:We compared longitudinal echocardiographic data between patients with Marfan syndrome who underwent aortic valve-sparing (AVS) and aortic valve-replacing (AVR) aortic root replacement procedures. METHODS:Of 316 patients enrolled at 19 sites in 5 countries, 239 (75%) were treated with AVS and 77 (25%) with AVR. Transthoracic echocardiograms were collected at postoperative years 1, 3, 5, 7, 10, 12, 14, 16, 18, and 20. Mixed-effects models were used to evaluate echocardiographic changes over time. Inverse probability-weighted Cox regression models were used to compare the risk of persistent postoperative aortic regurgitation (AR) grade ≥2+ and AV reintervention between AVS and AVR. RESULTS:Echocardiographic studies showed greater AR grades in the AVS group during early-to-midterm follow-up (P < .001). The AVS group also had somewhat larger annular size (P < .001) and left ventricular end-systolic (P < .001) and end-diastolic (P = .003) diameters. AV mean gradient, AV systolic velocity, left ventricular ejection fraction, and sinus of Valsalva diameter did not have significantly different trajectories over time between the AVS and AVR groups. Although the AVS and AVR groups did not differ in overall survival (P = .2) or AV reintervention rates (P = .2), persistent AR grade ≥2+ was associated with AV reintervention (P = .01). CONCLUSIONS:Although patients with Marfan syndrome who underwent AVS had greater annular dilatation and greater AR grades than patients who underwent AVR, the likelihood of AV reintervention and death was similar between the groups.

BACKGROUND:Acute renal failure remains a significant complication after open thoracoabdominal aortic aneurysm (TAAA) repair and is associated with high mortality. Rigorous risk estimation for this complication is vital for these patients. METHODS:Data were analyzed from 2809 patients who underwent elective, open TAAA repair between 1986 and 2024 at a single practice. Persistent renal failure was defined as the need for dialysis at time of operative discharge (including any hospital transfer) or death. The effectiveness of 4 predictive models-multivariable logistic regression, random forest, support vector machine, and gradient boosting machine-was compared by using the test C statistic (C) from an 80:20, 1000-iteration cross-validation scheme. The regression model was converted into a nomogram for patient counseling. RESULTS:Persistent renal failure necessitating dialysis developed in 158 (5.6%) patients, of whom 90 (57.0%) experienced operative death. Of the 4 models, the regression model was the most predictive (C = 0.75 [0.72-0.77]). The highest performing machine learning model, the gradient boosting machine, had similar efficacy (C = 0.73 [0.70-0.76]). The final regression model included 8 factors: Crawford extent II repair (odds ratio [OR], 1.86; P = .001), chronic aortic dissection (OR, 1.72; P = .01), symptomatic aneurysm (OR, 1.47; P = .03), maximum distal aortic diameter ≥6 cm (OR, 1.44; P = .06), age (OR, 1.04; P < .001), preoperative estimated glomerular filtration rate (OR, 0.97; P < .001), male sex (OR, 0.65; P = .01), and Crawford extent I repair (OR, 0.43; P = .004). CONCLUSIONS:The regression model, built using preoperative factors, effectively predicted persistent renal failure necessitating dialysis in patients undergoing elective, open TAAA repair. We converted this model into a nomogram to aid in preoperative counseling.

OBJECTIVE:We tested the hypothesis that ciprofloxacin exposure increases the incidence of aortic dissection and arterial rupture in vascular Ehlers-Danlos (vEDS) mice. BACKGROUND:While data support that fluoroquinolones exacerbate lethal sequela in some types of aortic pathology, the potential danger of these drugs has not been studied in the context of vEDS. METHODS:Eight-week-old male and female vEDS mice ( Col3a1[G209S/WT] ) and wild-type littermates ( Col3a1[WT/WT] ) were randomly assigned to receive either ciprofloxacin (n=25) or vehicle control (n=24) through daily gavage for 2 weeks and were monitored for 4 weeks. We compared groups based on survival, aortic dissection and rupture incidence, and aortic tissue levels of collagen, lysyl oxidase (LOX), matrix metalloproteinases (MMP), macrophages, and apoptosis. RESULTS:All vEDS mice that received vehicle and all littermate controls survived the 4-week study period. In contrast, 44% of vEDS mice that received ciprofloxacin died ( P <0.001) due to aortic or arterial rupture manifesting as hemopericardium or hemothorax, most within 7 days of exposure. Findings were similar in male and female vEDS mice. Compared with aortic tissue from vehicle-treated vEDS mice, tissue from ciprofloxacin-treated vEDS mice exhibited decreased collagen content, decreased LOX, increased MMP2 and 9 levels, increased macrophage infiltration, and increased apoptosis (all P <0.001). CONCLUSIONS:In a mouse model of vEDS, ciprofloxacin exposure resulted in aortic inflammation, collagen disruption, cell death, reduced LOX, and increased risk of fatal dissection and rupture of the aorta and branch arteries. These novel translational findings strongly support recommendations to avoid fluoroquinolones in patients with vEDS.

OBJECTIVE:We compared 10-year outcomes of aortic valve-replacing (AVR) and aortic valve-sparing (AVS) root replacement in patients with Marfan syndrome (MFS). METHODS:Patients who met strict Ghent diagnostic criteria for MFS and who underwent either AVR or AVS between March 1, 2005, and December 31, 2010, were enrolled in a 3-year prospective observational study. The follow-up, which was clinical and echocardiographic, was later extended to 20 years. Time-to-event analyses were performed with and without inverse probability weighting to adjust for baseline differences; comparison between groups assessed major adverse valve-related (MAVRE) and other events. RESULTS:Of 316 patients enrolled, 77 underwent AVR and 239 underwent AVS; 214 gave reconsent for 20-year follow-up. For survivors, median durations for clinical and echocardiographic follow-up were 12.1 years (interquartile range, 4.6-15.1 y) and 10.1 years (interquartile range, 3.0-14.1 y), respectively. Ten-year adjusted survival rates for the AVR and AVS groups were similar (77.9% ± 4.4% vs 88.4% ± 2.6%; P = .2), as were adjusted rates of MAVRE (36.1% ± 4.2% vs 35.0% ± 3.3%; P = .5). Inverse probability weighting-adjusted competing-risk modeling associated AVS with greater cumulative incidences of structural valve deterioration or nonstructural valve dysfunction (24.9% vs 4.4%; P = .01) and aortic regurgitation ≥2+ (26.5% vs none; P < .001); similar analysis associated AVR with a greater cumulative incidence of bleeding (23.2% vs 2.7%; P < .001). CONCLUSIONS:Ten years postoperatively, the accumulation of structural valve deterioration in patients who underwent AVS and bleeding events in patients who underwent AVR balance out in terms of MAVRE. We plan to follow this cohort for 20 years after aortic root replacement, which may reveal late differences in reintervention rates.

OBJECTIVE:Certain comorbid atherosclerotic diseases have known associations with worse outcomes in thoracoabdominal aortic aneurysm (TAAA) repair; however, the association is less clear with peripheral arterial disease (PAD). This study investigates the relationship between PAD and TAAA repair outcomes. METHODS:This retrospective, single-practice study analyzed data from 3772 patients who underwent TAAA repair between 1990 and 2023, including 891 patients (23.6%) with PAD and 2881 (76.4%) without PAD. Outcomes included adverse events, which comprised operative death (before final hospital discharge or ≤30 days postoperatively) and key events persisting at discharge: stroke, spinal cord deficit (SCD; paraplegia or paraparesis), or renal failure necessitating dialysis. RESULTS:Patients with PAD were older than patients without PAD (median, 69 years [interquartile range (IQR), 64-75 years] versus 66 years [IQR, 56-73 years]; P < .001). Patients with PAD had a lower rate of aortic dissection (21.1% vs 41.2%; P < .001). Patients with PAD more often underwent extent IV repair (30.4% vs 16.8%; P < .001), whereas patients without PAD more often had extent I repair (29.4% vs 16.9%; P < .001). Operative mortality did not differ between patients with PAD and those without PAD (9.2% vs 8.4%; P = .5). However, PAD patients had more SCD (12.3% vs 9.1%; P = .004) and persistent stroke (3.6% vs 2.0%; P = .009); these differences were pronounced in extent II repair (18.6% vs 12.8% [P = .02] and 6.7% vs 3.0% [P = .005], respectively). CONCLUSIONS:Our data suggest that PAD is associated with higher rates of SCD and persistent stroke after TAAA repair. This difference may necessitate the development of protective techniques for patients with PAD who undergo TAAA repair.

BACKGROUND:This study's purpose was to assess whether larger volumes of reinfused unwashed shed autologous blood (SAB) were associated with adverse events within 30 days for patients undergoing open thoracoabdominal aortic aneurysm (TAAA) repair. During TAAA repair, our institution uses a system wherein SAB is filtered, but not washed or centrifuged, and then returned to the patient via a rapid-infusion device. By reinfusing SAB, the system preserves the patient's autologous whole blood and may reduce the number of allogenic transfusions required during TAAA repair, but the end-organ effects of reinfusing unwashed SAB have not been extensively evaluated. METHODS:Using a prospectively maintained database, we retrospectively analyzed data from 972 consecutive patients who underwent open TAAA repair at our institution from 2007 to 2021 and who received SAB. Multivariable logistic regressions were performed to assess whether SAB reinfusion volume was associated with a composite outcome of adverse events, as well as operative mortality, a composite of cardiac complications, a composite of pulmonary complications, or persistent paraplegia, stroke, or postoperative renal failure. RESULTS:Among the cohort of 972 patients, the median volume of reinfused SAB was 4159 mL (quartile1-quartile3 [Q1-Q3]: 2524-6790 mL). Greater reinfusion volumes of unwashed SAB were not associated with greater odds of composite adverse events (odds ratio [OR], 1.02 per 1000 mL increase, 97.5% confidence interval [CI], 0.94-1.09, P = .624), nor with any individual outcome-operative mortality (OR, 1.02 per 1000 mL increase, 97.5% CI, 0.93-1.12, P = .617), a composite of cardiac complications (OR, 0.98 per 1000 mL increase, 97.5% CI, 0.93-1.04, P = .447), a composite of pulmonary complications (OR, 1.00 per 1000 mL increase, 97.5% CI, 0.94-1.06, P = .963), renal failure necessitating hemodialysis (OR, 1.01 per 1000 mL increase, 97.5% CI, 0.92-1.11, P = .821), persistent paraplegia (OR, 0.97 per 1000 mL increase, 97.5% CI, 0.84-1.13, P = .676), persistent stroke (OR, 0.85 per 1000 mL increase, 97.5% CI, 0.70-1.04, P = .070), or reoperation to control bleeding (OR, 0.99, 97.5% CI, 0.87-1.13, P = .900)-when adjusted for confounders. CONCLUSIONS:For patients undergoing open TAAA repair, larger reinfusion volumes of unwashed SAB were not associated with greater odds of major early postoperative complications.

BACKGROUND:Spinal cord injury is a risk for patients undergoing thoracoabdominal aortic aneurysm (TAAA) repair, the most substantial deficit being persistent paraplegia (PP). Adequately estimating patients' risk of PP is vital for patient counseling and postoperative risk stratification. METHODS:Patients who underwent open, elective TAAA repair (1986-2024; N = 2827) at a single practice were categorized into 4 groups: those with PP (n = 68) at discharge or death, those with persistent paraparesis (n = 55) at discharge or death, those with transient paraplegia or paraparesis (n = 132), and those without any spinal cord deficit (SCD, n = 2572); 4 cohorts were created comprising combinations of these groups. Several models were evaluated, including logistic regression and machine-learning approaches, to better understand predictors of PP and other SCDs in key cohorts. RESULTS:Regarding prediction of PP, the gradient boosting machine was best (C = 0.79 [0.75-0.81]); however, the multivariable logistic regression model was similar (0.78 [0.74-0.81]) and was converted into a nomogram to highlight the predictive value of diabetes (odds ratio, 2.48; P = .009), previous percutaneous coronary intervention (OR, 3.04; P < .001), chronic kidney disease (OR, 2.48; P < .001), tobacco use (OR, 13.25; P = .01), symptomatic aortic disease (OR, 1.96; P = .01), and Crawford extent of TAAA repair (II: OR, 4.00; P < .001). Predictors of PP and SCD in key cohorts were similar. CONCLUSIONS:For patients undergoing elective, open TAAA repair, the risk of PP can be estimated from preoperative characteristics and explained by an intuitive nomogram to aid personalized preoperative counseling, with greater-risk patients prioritized perioperatively for rigorous blood pressure monitoring, increased cerebrospinal fluid drainage, or a lower threshold for transfusion.

Objective:Obesity can complicate surgical repair, but its relationship to outcomes after open thoracoabdominal aortic aneurysm (TAAA) repair remains uncertain. Therefore, we examined whether obesity is associated with greater operative risk after elective TAAA repair. Methods:We retrospectively evaluated data from 2517 open, elective, single-practice TAAA repairs (from 1986 to 2023) and compared patients without obesity or underweight (body mass index [BMI] 18.6-29.9; n = 1977) with patients with obesity (BMI ≥30; n = 540 [21.5%]). Multivariable logistic regression modeling identified predictors of operative mortality in patients with obesity. We created propensity-matched cohorts (n = 540 pairs) and compared their early and late outcomes, including late survival, by Kaplan-Meier analysis and log-rank testing. Results:Compared with patients without obesity, patients with obesity were younger (median age, 64 years [Q1-Q3: 56-71] vs 68 [59-73] years; P < .001) and had greater rates of aortic dissection (45.7% vs 34.5%; P < .001) and diabetes (13.1% vs 6.9%; P < .001). Extent I repairs were more frequent in patients with obesity (30.6% vs 24.9%; P = .008). Operative mortality did not differ between groups (5.6% vs 6.6%; P = .9); however, persistent stroke was more frequent in patients with obesity (3.7% vs 2.0%, P = .02). Overall, BMI was not associated with operative mortality; within the patients with obesity, multivariable modeling found aortic dissection was independently associated with operative mortality. Propensity matching revealed no substantial differences in examined outcomes. Conclusions:Patients with obesity undergoing TAAA repair differed from their counterparts without obesity regarding several factors. However, adjusted early outcomes after TAAA replacement did not differ by the presence or severity of obesity. We conclude that obesity alone should not deter surgeons from offering elective TAAA repair.

Objective: Failure to rescue (FTR) is a metric of postoperative care, measuring a center’s ability to prevent operative death after a surgical complication. We evaluated trends in and contributors to FTR after proximal aortic surgery at a high-volume institution. Methods: Of 4180 patients in our single practice who underwent open proximal aortic repair from 1990 to 2024, 1304 (31.2%) had at least 1 of 4 FTR-related complications identified by the Society of Thoracic Surgeons (STS). Operative death was defined as death within 30 days of surgery or before hospital discharge or transfer. We analyzed FTR rate by specific complication, including the number and combination of complications. We then evaluated the association of elective versus emergency repair and aortic dissection with FTR rate. Finally, a multivariable model was built to predict FTR in these patients. Results: Of 1304 patients with an STS complication, 303 (23.2%) had operative death and thus an FTR. The FTR rate was 13% for patients with 1 complication and increased to 48%, 68%, and 100% with each additional complication. The 2 STS complications most associated with FTR were stroke (odds ratio, 5.92; P < .001) and renal failure necessitating dialysis (odds ratio, 8.24; P < .001). Neither emergency repair nor acute aortic dissection were significant FTR predictors after adjustment for covariates. A 6-variable predictive model to predict FTR achieved a test C-statistic of 0.79 (0.77-0.81). Conclusions: The FTR rate significantly increased with each additional complication. We built a model that can effectively predict FTR. Better understanding of FTR rates can identify areas for improvement in postoperative care.