Thoracic aortic dissection (TAD), a lethal cardiovascular emergency, lacks effective pharmacological interventions. Endothelial dysfunction and hydrogen sulfide (H2S) deficiency drive TAD progression, but existing H2S donors exhibit uncontrolled release and cytotoxicity. Herein, we developed a GSH-responsive H2S-releasing polymer, named PSG12, using a gas-click polymerization strategy under mild conditions. PSG12 achieved tunable H2S release (4.27-fold higher at 2mm than 0.5mm GSH) and sustained plasma levels (more than 650nm for 12h post-injection). In TNF-α-challenged endothelial cells, PSG12 reduced the level of ROS (77% reduction), suppressed senescence (92.4% reduction), inhibited apoptosis (63% reduction), reduced inflammation (29.35% decrease in IL-1β protein expression), and preserved extracellular matrix (47.83% decrease in MMP-2 protein expression). In BAPN-induced TAD mice, PSG12 reduced aortic rupture (from 53.3% to 20.0%), improved survival (from 46.7% to 80.0%). On the one hand, PSG12 restored the homeostasis of endothelial cells in multiple dimensions; on the other hand, PSG12 maintained the concentration of plasma H2S. This precision gas therapy platform enables multi-pathway synergistic modulation for TAD.

IntroductionMycotic thoracic aneurysms in children are rare and carry high mortality, particularly when complicated by erosion into adjacent pulmonary structures. Early recognition and surgical intervention are essential to prevent catastrophic outcomes.Case ReportA 14-year-old presented with respiratory symptoms. Imaging revealed a large mycotic aneurysm of the aorta with compression of multiple mediastinal structures. During induction of anaesthesia, aneurysm rupture caused haemoptysis and hypovolemic arrest. Emergent femoral cannulation enabled initiation of cardiopulmonary bypass and novel use of endotracheal suction with autologous cell salvage facilitated surgical exposure and successful aneurysm repair.DiscussionThoracic mycotic aneurysms present diagnostic complexity and potential catastrophic outcomes. In this patient, rapid multidisciplinary coordination, dual-arterial cannulation and intraoperative blood-salvage techniques proved critical to restoring circulation and achieving surgical control.ConclusionThoracic mycotic aneurysms in children require extreme vigilance and adaptable surgical strategies. This case demonstrates that survival is possible with innovative management in the face of life-threatening complications.

To evaluate and compare outcomes of single- and double-fenestrated physician-modified endovascular grafts (PMEGs) for aortic arch pathologies treated in an emergent setting. All patients consecutively treated for an emergent aortic arch pathology were included in this retrospective single-center cohort study between July 2014 and March 2023. In each case, the distal smaller fenestration for the left subclavian artery (LSA) was the only 1 stented. For a double-fenestrated endograft, a proximal larger fenestration that incorporated both the brachiocephalic trunk and the left common carotid artery was added. A total of 86 patients with complicated aortic arch lesions were treated, with 74% being men and a mean age of 68 years. Of these, 63% underwent single LSA fenestration, while 37% had double-fenestrated thoracic endovascular aortic repair. The main indications for repair included acute complicated type B aortic dissection (TBAD) (54%), traumatic transection of the aorta (TTA) (19%), and other conditions such as penetrating aortic ulcer (PAU), degenerative aneurysm (DA), pseudoaneurysm (PSA), and aortic thrombus. The technical success rate was 91%, with modification times of 10 minutes for single fenestration and 23 minutes for double fenestration. Thirty-day mortality was 19%, with no significant difference between the 2 fenestration types. Neurologic events occurred in 3 patients (3%), and 3 (3%) patients had perioperative retrograde dissection. Endoleaks occurred in 5% (type 1) and 2% (type 3), with no type 2 endoleaks. Eight patients (9%) required reintervention, and all supra-aortic trunks remained patent. During a follow-up of 27.6 months, no patients experienced aortic rupture (AR), neurological events, or required conversion to open surgery. Single and double PMEGs are suitable and reproducible treatment for emergent serious aortic arch lesions, with comparable outcomes whatever the aortic landing zone and number of fenestrations.Clinical ImpactFenestrated physician-modified endovascular grafts for emergent aortic arch repair appear to be a promising treatment, offering reproducibility, rapid deployment, and limited manipulation of supra-aortic trunks. The standardized technique eliminates the need for complex sizing and benefits from consistent aortic arch anatomy in most patients. It provides clinicians with a practical and efficient option in emergency settings, achieving high technical success with acceptable complication rates.

Abdominal aortic aneurysm (AAA) rupture remains a significant cause of morbidity and mortality, but predictors of continued growth and rupture risk remain limited. The aim of this study was to investigate the relationship between abdominal aortic calcification and AAA growth via a secondary cohort analysis of the Non-Invasive Treatment of Abdominal Aortic Aneurysm Clinical Trial (N-TA3CT), a prospective multicenter randomized study. Arterial calcification Agatston scores and maximum transverse diameter were measured in non-contrast computed tomography (CT) scans in patients enrolled in N-TA3CT. Uni- and multi-variable linear regression were used to assess the association of anatomic calcium burden and comorbid conditions with rate of aneurysm growth. Of the 261 randomized patients in the trial, 136 patients met inclusion criteria for analysis. On univariable analysis, baseline calcium score at all assessed anatomic locations- the superior mesenteric artery (spearman correlation coefficient (SCC) -0.20, p = 0.0176), renal artery (-0.22, p = 0.0120, infrarenal aorta (-0.26, p = 0.0020), common iliac artery (-0.19, p = 0.024), external iliac artery (-0.26, p = 0.003), and sum of all measured sites (-0.28, p = 0.001)- was significantly associated with lower AAA diameter growth rates. Of individually measured sites, baseline infrarenal aortic calcification had the strongest negative association with aneurysm growth. Interestingly, infrarenal calcium score was not significantly associated with baseline aneurysm diameter (R2 0.0001, spearman correlation p = 0.94), or diabetes status (p = 0.59). In a multivariable regression model, factors significantly associated with faster diameter growth included baseline volume and current tobacco use. Factors associated with reduced growth rate included diabetes and baseline infrarenal aorta calcium score thereby establishing aneurysmal calcification as a marker for slower aneurysm growth.

Intro: Risk for dissection and rupture of aorta is determined, in part, by geometry. Diameter is the most commonly assessed risk factor, but other aspects of geometry also influence risk. In retrospective studies, greater aortic length, arch width, tortuosity, and aortic volume have been associated with adverse aortic events. One large-scale prospective analysis has linked 3D aortic geometry to future risk of arrhythmia and heart failure(Beeche et al., 2024). However, to our knowledge, 3D geometric measurements beyond length and diameter remain to be linked to adverse aortic events in a prospective cohort. Aims: We sought to measure the geometric properties of the aorta and link them to future risk for aortic dissection. Methods: We developed 3D semantic segmentation (voxel labeling) deep learning models and applied these to available magnetic resonance imaging from UK Biobank (application #41664), followed by performing centerline extraction. We defined a novel thoracic aortic measurement in which all centerline points were projected onto the same axial plane, with the distance between the two farthest points defined as the “projected aortic arch width.” Disease association was computed using Cox models. Results: 3D aortic measurements were computed in 63,114 UK Biobank participants. For a composite of aortic interventions, aortic dissection, or death attributed to aortic disease (53 events), both ascending aortic diameter (hazard ratio [HR] 2.10 per standard deviation [SD], 95% confidence interval [CI] 1.92-2.29) and projected aortic arch width (HR 2.81 per SD, 95% CI 2.26-3.49) were associated when tested separately after adjustment for age and sex. When tested in a joint model, they remained independently associated: HR 1.93 (95% CI 1.73-2.14) for diameter and HR 2.07 (95% CI 1.62-2.65) for arch width. Conclusions: A measurement extracted from 3D aortic geometry, the projected aortic arch width, is an independent risk factor for adverse aortic events.

Background: The total burden of lethal acute aortic dissection (AD) and subsequent aortic rupture causing sudden cardiac death (SCD) is unknown as previous SCD studies presume cardiac/arrhythmic causes without autopsy; these are now considered presumed SCD (pSCD) by international consensus. Moreover, current epidemiology reflects only diagnosed survivors, missing occult cases undetected before death. We evaluated data from the POST SCD Study to determine the true burden of AD among all community sudden deaths. Methods: POST SCD is an ongoing prospective study using autopsy and clinical records to adjudicate cardiac (e.g., acute MI, cardiomyopathy) vs. non-cardiac (e.g., overdose, stroke) causes among 1210 incident pSCDs meeting WHO criteria aged 18-90 years in San Francisco County from 2/1/2011 to 10/23/2024. We defined AD as an aortic intimal tear allowing blood to split the wall layers to form a false lumen. Type A involves the ascending aorta (may extend to descending); Type B is limited to the descending aorta. We compared AD deaths to pSCDs due to other causes. Results: Of 1210 pSCDs, 692 (57%) were due to cardiac and 518 (43%) non-cardiac causes; 66 (5.5% of all pSCDs, 13% of non-cardiac) were due to AD (mean 63 years, 73% male): 55 (83%) Type A and 11 (17%) Type B. Other leading causes included acute and chronic coronary artery disease (CAD; 55% of cardiac), and occult overdose and neurologic, 38% and 14% of non-cardiac causes, respectively. Most AD sudden deaths (62/66 [94%]) progressed to aortic rupture and hemorrhage, 39 (63%) of which had proximal (root and ascending) intimal tears without signs of prior dissection. HTN (62%, p=0.003) and chronic CAD (73%, p<0.001) were more prevalent in AD cases, but only 10% of CAD was diagnosed premortem, while dyslipidemia (11%, p=0.01) and obesity (23%, p=0.04) were less prevalent. More AD cases (33/66 [50%]) had severe aortic atherosclerosis (>50% intimal coverage) than non-AD pSCDs (317/947 [33%], p=0.006). Conclusion: In this 14-year countywide postmortem study of pSCDs, AD comprised 5.5% of total sudden mortality and was the third leading non-cardiac cause. The majority of cases advanced to rupture with a 5:1 Type A/B ratio, higher than the published 2:1 estimate in survivors. Higher prevalence of HTN in AD vs. non-AD pSCDs underscores its importance in AD pathogenesis and suggests the need for greater screening and management, especially in patients with major atherosclerosis, to prevent AD sudden deaths.

Background: Bicuspid aortic valve (BAV) is the most common congenital defect affecting 1-2% of general population. It often presents with progressive AV stenosis/regurgitation and ascending aortopathy (AA) which often require surgical intervention. Objective: We sought to report characteristics and long-term outcomes of a contemporary cohort of patients with BAV and concomitant AA. Methods: We included 3782 patients with a documented BAV and an unrepaired AA (≥4 cm) who underwent a clinical evaluation between 1/2010 and 12/2023 at our large tertiary referral center. Patients presenting with acute aortic dissection/rupture as an initial presentation were excluded. Clinical (including aortic surgery/dissection/rupture during follow-up) and imaging data were collected. Primary outcome was all-cause mortality. Results: Characteristics of the patients are shown in Figure 1. At 1±2.2 years from initial evaluation, 2363 (62%) patients underwent surgery (AV repair/replacement [882 {37%}], isolated ascending aortic replacement [402 {17%}] and combined AV+ascending aortic surgery [1079 {46%}]), with 6 (0.25%) in-hospital deaths. Of 2096 AV surgeries, there were 241 (12%) mechanical prostheses, 1326 (63%) bioprosthesis, 16 (1%) homografts, 44 (2%) autografts and 473 (23%) AV repairs. During a mean follow-up of 3.9±3.9 years (range 0-15 years), there were 171 deaths (4.5%), 65 (1.7%) aortic dissections and 4 (0.1%) aortic ruptures. At 1571±1405 days following an evaluation, aortic dissection/rupture occurred in 25/1419 (1.8%) unoperated and 44/2363 (1.9%) operated patients (p=ns). Of these 44 operated patients with dissection, 28 occurred in the distal aorta in those with AA replacement. On survival analysis, longer-term deaths were higher in the unoperated vs. operated patients (71/1419 [5.0%) vs. 100/2363 (4.2%), p-value 0.03, Figure 2). Longer-term deaths were similar in patients undergoing AV repair/replacement (39/843 [4.6%]) vs. isolated AA replacement (20/402 [5.0%]) vs. combined AV+AA surgery (41/1079 [3.8%]), p-value 0.69, Figure 3). Conclusions: In a large contemporary cohort of patients with BAV and AA managed at a high-volume tertiary care center, majority eventually undergo surgery, with a very high longer-term survival and freedom from aortic dissection/rupture. There were no differences in the longer-term survival of patients getting isolated AV or aortic surgery vs. combination AV/aortic surgery.

Introduction: Heritable thoracic aortic disease (HTAD) encompasses a spectrum of genetic syndromes and mutations that increase the risk of aortic aneurysm, dissection, and rupture. International guidelines recommend genetic evaluation in patients with thoracic aortic disease diagnosed before age 60, those with a family history of thoracic aortic dissection, and individuals with aneurysms in other vascular beds. Despite recommendations, real-world uptake of genetic testing remains unclear. Research Question: This study examined national trends in genetic testing among patients at elevated risk for HTAD using a large multicenter health network, evaluating adherence to testing recommendations and disparities across demographic subgroups. Methods: A retrospective cohort study was conducted using TriNetX, a federated database of de-identified EHRs from academic and community health systems across the U.S. Three guideline-based risk cohorts were identified using ICD-10 codes: thoracic aortic aneurysm or dissection diagnosed before age 60, family history of TAD, and non-thoracic arterial aneurysms. Genetic testing was defined using codes for screening or confirmed genetic diagnoses. Demographic variables included age, sex, race, and ethnicity. Results: Among 57,935 patients diagnosed with thoracic aortic disease before age 60, genetic testing prevalence was 2.09%, higher in females (3.56%) than males (1.50%), and most common in children aged 0–9 (4.6%). By race/ethnicity, testing was highest in American Indian/Alaska Native (4.98%). In 2,811,862 patients with a family history of TAD, testing prevalence was 2.38%, higher in females (3.12%) than males (1.37%) and most common in those aged 10–19 (~4.6%). Among 347,000 patients with non-thoracic aneurysms, testing prevalence was 1.42%, higher in females (1.80%) than males (1.08%), and most frequent in ages 10–19 (~2.8%). By race, rates were highest in White patients (1.60%), followed by Black or African American (1.23%) patients. Conclusion: Genetic testing for heritable aortic disease is markedly underutilized, with fewer than 2.5% of at-risk patients screened, even when clinically indicated. Testing rates were consistently low across age, sex, and racial/ethnic groups, though modestly higher in younger patients and females. The higher testing rate in women may reflect data that shows a more severe disease progression in women, despite higher overall prevalence in men. These findings reveal a gap between guidelines and practice.

Background: Aortic aneurysm and dissection (AAD) are life-threatening diseases characterized by progressive degradation of the aortic wall. The loss of contractile phenotype in vascular smooth muscle cells (SMCs) promotes AAD development. Phosphodiesterase 1A (PDE1A), predominantly expressed in contractile vascular SMCs, regulates vascular contractility; however, its role in AAD remains unclear. Methods: PDE1A and contractile gene expression was analyzed by published sequencing datasets, qPCR and immunostaining in human and mouse AAD tissues. The role of PDE1A in AAD was investigated using global PDE1A knockout (KO) mice and vascular SMC-specific PDE1A KO mice. Both high-fat diet with Angiotensin II infusion (HFD/Ang II) induced sporadic AAD, and elastase/BAPN-induced abdominal aortic aneurysm (AAA) model were used. Results: PDE1A expression in vascular SMCs was decreased in both human and mouse AAD. In the HFD/Ang II model, global PDE1A KO significantly lowered the incidence of aortic aneurysm, dissection, and rupture in both genders, which was confirmed in the elastase/BAPN model. PDE1A expression in the aortic media of AAD mice positively correlated with contractile marker gene expression (e.g., Myh11, Sm22, and Cnn1 ), a finding confirmed in human samples. Interestingly, PDE1A global KO mice under basal conditions showed reduced contractile gene expression in media, a result replicated in rat aortic SMCs with PDE1A knockdown, indicating PDE1A is a critical regulator of vascular SMC contractile gene expression. To define the role of vascular SMC-expressed PDE1A in AAD, we generated vascular SMC-specific PDE1A KO mice (PDE1A-KO VSMC ) using Itga8-CreER mice. PDE1A-KO VSMC mice also showed decreased expression of contractile markers in media. In contrast to the global PDE1A KO, PDE1A-KO VSMC mice aggravated aortic dilation and elastin degradation in the elastase/BAPN model. Since PDE1A expression was also detected in the adventitia and was upregulated in early stages of AAD, the potential role of adventitial fibroblast-expressed PDE1A in AAD pathogenesis is currently under investigation. Conclusion: Global deletion of PDE1A protects against AAD; whereas vascular SMC-specific deletion of PDE1A exacerbates AAD, possibly due to impaired vascular SMC contractile function. These findings highlight the essential role of PDE1A in vascular contractility and suggest a distinct role for PDE1A in adventitia fibroblasts in AAD.

Background: Aortic stenosis remains a significant cause of morbidity and mortality worldwide. Transcatheter aortic valve replacement (TAVR) has become a transformative therapy for patients with severe aortic stenosis who are not suitable candidates for traditional surgical valve replacement in developed countries. However, access to TAVR therapy is highly variable, particularly in developing countries where resources and infrastructure may be limited. Objective: This study aims to elucidate the existing disparities in access to TAVR therapy in developing nations and propose sustainable strategies. We report over a decade of experience and outcomes from performing TAVR during humanitarian missions in a resource-limited setting of a developing country. Methods: This is a case series conducted on patients who underwent TAVR in Santo Domingo, Dominican Republic, between June 2010 and May 2024. Eligibility criteria included symptomatic severe aortic stenosis deemed high-risk or inoperable for surgical valve replacement in patients of limited economic resources. Baseline clinical characteristics and main outcomes, such as intra- and post-procedural complications, as well as the 30-day mortality rate, were obtained. Results: A total of 18 patients were included, with a mean age of 76 years (SD ± 5), predominantly female (56%). High rates of hypertension (88.9%), diabetes mellitus (44.4%), and heart failure (16.7%) were observed. Balloon-expandable valves were implanted in 56% of cases, while the remaining 44% received self-expandable valves. Two patients had complications during the procedure, including left ventricular perforation leading to cardiac tamponade and aortic annular rupture in another patient. Both patients expired intra-op or within 24 hours post-op. One patient developed complete heart block requiring permanent pacemaker placement. Self-resolving groin hematoma was seen on one occasion. None of the patients required re-intervention. There were no significant paravalvular leaks post valve implantation. The mortality rate at 30-day follow-up was 11%. Conclusion: Disparities in access to TAVR persist in developing countries, disproportionately affecting individuals of lower socioeconomic status. Strategies targeting the equitable distribution of healthcare resources and financial assistance programs are warranted. This humanitarian experience demonstrates the viability of performing TAVR as part of humanitarian medical missions to developing countries.

Introduction: The decision to perform ascending thoracic aortic aneurysm (aTAA) repair is primarily guided by diameter thresholds, but the optimal timing remains debated among guidelines due to limited natural history data. We aimed to analyze ATAA outcomes in a large cohort of veterans. Research Question: Among veterans with ATAA under clinical surveillance, how does baseline aneurysm diameter relate to the risk of adverse aortic events and mortality, and how might this inform decisions regarding prophylactic surgical repair? Methods: We conducted a retrospective cohort study of ATAA patients with diameter ≥4.0cm who underwent surveillance between 1998 and 2024 at a Veterans Affairs medical center. Baseline clinical data, imaging, interventions, and outcomes were collected from electronic health records. Outcomes included surgical repair, all-cause mortality, and aortic events—aortic dissection or rupture. A competing risks regression model evaluated the association of diameter with all-cause mortality, adjusting for age, smoking, and aortic valve phenotype. Results: We included 764 veterans (98.0% male) with median (IQR) age of 75.0 (9.3) years and ATAA diameter of 4.40 (0.50) cm. Median follow-up was 5.4 (6.1) years. Surgical repair occurred in 86/764 patients (11.3%). Aortic dissection occurred in two patients (0.3%), both within the 4.0–4.5cm group, with an incidence of 0.05 events per 100 person-years (95% CI, 0.00–0.11). All-cause mortality rates were 2.86 (2.20–3.56), 3.22 (2.36–4.15), 5.82 (3.81–8.06), and 24.60 (12.30–38.94) deaths per 100 person-years for ATAA diameters 4.0–4.4, 4.5–4.9, 5.0–5.4, and ≥5.5 cm, respectively (p<0.001). In multivariable analysis, all-cause mortality was independently associated with increasing ATAA diameter (HR, 1.40 per 0.5 cm increase; 95% CI, 1.17–1.68; p<0.001) and increasing age (HR, 1.07 per year; 1.05–1.09; p<0.001). Conclusions: ATAA all-cause mortality is associated with baseline diameter, with a sharp seven-fold incidence increase in aneurysms ≥5.5cm. Our findings support the current 5.5-cm threshold for prophylactic ATAA repair and emphasize the need for selective intervention in smaller aneurysms.

Background and Objective: Kommerell's diverticulum is a special type of proximal subclavian artery aneurysm that is associated with the aberrant subclavian artery. Although most patients are asymptomatic, there is a high risk of aortic rupture and aortic dissection. This study aimed to investigate the clinical characteristics, treatment strategies, and long-term prognosis of this specific type of proximal subclavian artery aneurysm (Kommerell's diverticulum) through a single-center retrospective study, providing valuable support for clinical decision-making. Methods: Patient data were collected from the medical records system from February 2011 to April 2022 for patients who had computer tomography scan reports indicating Kommerell's diverticulum and underwent intervention at our institution. A total of 76 adult patients aged 18 years and above with Kommerell's diverticulum were included in this study, of which 48 had concomitant aortic dissection and 28 without. Results: The overall early postoperative mortality rate for the included cases in this study was 9.2% (7/76 cases), with a 30-day mortality rate of 12.5% (6/48 cases) for the group with concomitant aortic dissection and 3.6% (1/28 cases) for the non-aortic dissection group. The median follow-up time for all included patients in this study was 4.0 years. Preoperative coronary artery atherosclerotic heart disease was identified as a risk factor associated with surgical mortality (OR=3.15, P=0.0163). Central nervous system complications occurred in 10 patients (13.2%), and respiratory system complications occurred in 4 patients (5.3%), with both cases in the group with concomitant aortic dissection resulting in postoperative death within 30 days due to compression of the right main bronchus by the aneurysm, leading to lung infection and respiratory failure. The 3-year, 5-year, and 7-year survival rates for the group with concomitant aortic dissection were 82.5%, 79.7%, and 75.1%, respectively, while the survival rates for the non-aortic dissection group were all 88.9%. Conclusion: The treatment approach for patients with this specific type of proximal subclavian artery aneurysm (Kommerell's diverticulum) should be based on comprehensive evaluation including age, symptoms, and imaging findings. Attention should be paid to the relationship and compression of the aortic dissection with the right main bronchus in patients with Kommerell's diverticulum and a right-sided aortic arch.

Background: Marfan syndrome (MFS) is a heritable autosomal dominant multisystem disorder of connective tissues caused by variants in FBN1 gene, which encodes fibrillin-1, a major component of microfibrils in extracellular matrix. Most premature deaths are related to thoracic aortic aneurysm that grows and progresses to catastrophic aortic rupture or dissection without prior symptoms. Previous reports showed that intraperitoneal injections with transforming growth factor (TGF)-β neutralizing antibodies mitigated aortic aneurysm formation in MFS ( Fbn1 C1041G/+ ) mice. However clinical application in MFS patients has not yet been achieved. Recent research on vaccination has extended its scope from infectious diseases to chronic diseases, including hypertension and dyslipidemia. The aim of this study is to design a TGF-β vaccine for prevention of aortic aneurysm in MFS mice. Methods: We created TGF-β vaccines (vaccine A and B) by mixing a peptide that recognizes the two amino acid sequences (p.304-313 and p.313-322), common to human and mouse TGF-β1 as antigens with a carrier protein and an adjuvant. We injected subcutaneously two candidate vaccines to C57BL/6J background Fbn1 +/+ mice and antibody titers were measured using ELISA. The vaccine with higher titers was selected from two candidate vaccines, and TGF-β vaccine and control vaccine were injected subcutaneously twice at two-week intervals, followed by a third injection one week later, for a total of three injections in 4-week-old male Fbn1 +/+ and Fbn1 C1041G/+ mice. Results: Significant increase in antibody titers was observed in the serum of TGF-β vaccines-injected Fbn1 +/+ mice for both vaccine A and B. However, ELISA using recombinant TGF-β1 as antigen showed a significant increase in antibody titer only in vaccine A. In 16-week-old TGF-β vaccine A-injected Fbn1 C1041G/+ mice, the enlargement of aortic diameter was significantly suppressed, as compared with control vaccine-injected Fbn1 C1041G/+ mice. Histologically, aortic wall thickening with degeneration of elastic fibers and proteoglycan deposition and downstream signaling of the TGF-β pathway were attenuated in ascending aorta of TGF-β vaccine A-injected Fbn1 C1041G/+ mice. No inflammatory cell infiltration was observed in any of the organs, including the heart, kidneys, and liver in the TGF-β vaccine A-injected group. Conclusion: Our findings support that the TGF-β vaccine could be a novel therapeutic agent for suppressing aortic aneurysm progression in MFS.

Introduction: Iatrogenic aortocoronary dissection (IACD) is a life-threatening complication of coronary angiogram. Clinical Case: A 66-year-old female with, history of paroxysmal atrial fibrillation on apixaban and DVT, presented to the emergency department due to epigastric discomfort. Ischemic evaluation was negative. Two weeks later patient had a follow up visit and reported ongoing symptoms. Coronary CT angiography was completed and showed 70-75% stenoses of Left Main and Left Anterior Descending arteries. The patient underwent coronary angiogram, confirming the diagnosis. During guide catheter introduction for IFR measurement, the artery was dissected and the dissection flap extended retrograde to the aortic root and ascending aorta. Prompt placement of a drug eluting stent in the left main was performed. Post-dilation, the dissection flap had closed. Patient was started on IV cangrelor, high dose beta blocker and transferred to the cardiac ICU. CTA chest demonstrated dissection flap in ascending and descending aorta. Cardiothoracic surgery was consulted and opted to observe with follow up imaging as patient was hemodynamically stable. Follow up CT chest showed a stable dissection flap, IV cangrelor was switched to aspirin and clopidogrel, and home apixaban was resumed. Hospital course was uneventful except for an episode of atrial fibrillation with rapid ventricular response, treated accordingly with beta blocker and amiodarone. CT chest in one month demonstrated an increase in aortic intramural thickness from 3.3mm to 9mm. Aspirin and apixaban were discontinued and retrievable IVC filter was placed. CT chest one month later demonstrated complete resolution of ascending intra-mural hematoma. Patient’s apixaban was resumed. CT chest in two weeks showed no new hematoma. IVC filter was removed and patient remained asymptomatic during the follow up course. Given patient had family history of aortic aneurysm and dissection, genetic testing was pursued and was negative. Discussion: This patient had a rare, extensive IACD with extension to descending aorta which was managed medically. This patient required treatment with anti-coagulation, however due to expansion of hematoma, the risk of aortic rupture compared to stroke/clotting risk was deemed to be higher. She also was treated aggressively with high dose beta-blocker, as tolerated, to keep her heart rate below 60. Along with holding aspirin, these strategies resulted in hematoma resolution.

Introduction: Acute ischemic stroke is a known complication of aortic dissection (AD), either by extension, thromboembolism, or cerebral hypoperfusion. The incidence ranges from 6–32% among patients with AD. Case Presentation: A 42-year-old male with a history of hypertension and chronic Stanford type A/DeBakey I AD post aortic arch and valve repair (11 years prior), with thoracoabdominal dissection and aneurysmal changes, presented with difficulty in speech and unsteady gait. Blood pressure (BP) was 183/102 mmHg. ECG showed normal sinus rhythm. The last well-known was 45 minutes before the presentation; the National Institutes of Health stroke scale (NIHSS) was 6. The non-contrast CT head was unremarkable; CT angio showed left M2 MCA occlusion in the Sylvian fissure, Stanford type A AD with flaps crossing the origins of the brachiocephalic, left common carotid, and left subclavian. CT head perfusion revealed 65 cc of ischemic penumbra in the left MCA territory and a core infarct of 7 cc. MRI of the brain revealed an acute infarct in the left frontal and parietal lobes; CT chest/abdomen/pelvis showed an aneurysmal thoracoabdominal aorta (descending: 6x5.9 cm; suprarenal: 4.1x4 cm; infrarenal: 5.4x6.1 cm) with mural thrombus in the false lumen. On day 0, his mental status declined, NIHSS increased to 16 and he required intubation. He was taken for emergent percutaneous intracranial mechanical thrombectomy (MT) through left carotid artery access by vascular surgery, followed by interventional neurology rescue and achieved thrombolysis in cerebral ischemia score (TICI) 2C. He was extubated on day 1, and NIHSS improved to 3 over the next 3 days. Discussion: In our patient, chronic AD with mural thrombus, chronic tobacco use, hypertension, and dyslipidemia increased the risk of stroke. Intravenous thrombolysis among patients with AD can lead to serious complications, including aortic rupture and cardiac tamponade. MT may improve neurologic outcomes. AIS secondary to large vessel occlusion in our patient led to worsening neurological function, which was significantly improved after MT with near-complete reperfusion. In our patient, carotid access was chosen as femoral access poses a high risk in AD. MT is a standard intervention secondary to large vessel occlusion, but data regarding the efficacy of MT among patients with AD is sparse. He was discharged on apixaban; antihypertensives were optimized, and cardiology follow-up was arranged for elective aortic repair.

To evaluate the feasibility and safety of total arch replacement with a frozen elephant trunk in patients with Stanford type B aortic dissection and an entry ≤ 10mm distal to the left subclavian artery. We retrospectively reviewed 40 consecutive patients who underwent either total arch replacement with a frozen elephant trunk (n = 30) or thoracic endovascular aortic repair (n = 10). The primary outcome was late all-cause mortality. Secondary outcomes included major complications, planned additional endovascular repair after total arch replacement with a frozen elephant trunk, false lumen thrombosis, and aortic remodeling. In the thoracic endovascular aortic repair group, procedure-related complications occurred, including retrograde type A dissection and one death from aortic rupture. In the total arch replacement with a frozen elephant trunk group, all deaths were unrelated to the index procedure. Planned additional endovascular repair was more frequently performed after total arch replacement with a frozen elephant trunk. Total arch replacement with a frozen elephant trunk is safe for anatomically challenging type B aortic dissection with an entry near the left subclavian artery and represents a viable treatment option in this setting.

Elastase-2 deletion prevents vascular remodeling and abdominal aortic aneurysm development in a mice model induced by angiotensin II.

Acute Type A aortic dissection (ATAAD) is characterized by acute onset and rapid progression, with aortic rupture due to dissection extension being the primary lethal mechanism. Timely identification of high-risk patients is critical for prioritizing surgical intervention to reduce rupture incidence. This study aimed to develop and validate an interpretable machine learning model to predict aortic rupture in ATAAD patients, thereby improving risk classification and supporting clinical decisions. Medical records of ATAAD patients from Xiamen Cardiovascular Hospital (January 2019–October 2024) were retrospectively analyzed. Predictors were screened via statistical significance (p0.05) using seven machine learning algorithms, with the Salp Swarm Optimization Algorithm (SSA) optimizing hyperparameters for Random Forest and XGBoost models. To address class imbalance (47 rupture cases, 6.1%), SMOTE was implemented for data augmentation. Model performance was evaluated by accuracy, F1-score, precision, ROC-AUC, sensitivity, and specificity, supplemented by interpretability analyses through feature importance ranking and SHAP. Among 774 included ATAAD patients, the SSA-optimized Random Forest model achieved optimal performance (test dataset: 97.41% accuracy, 0.980 ROC-AUC, 81.82% F1-score). Key predictors included estimated glomerular filtration rate (eGFR), hypotension at admission, and white blood cell count. This work provides a quantitative tool for emergency care prioritization, with SSA enhancing model precision for high-risk patient identification, though multicenter studies are needed to validate generalizability.

A 47-year-old man with a history of drug addiction sustained an aortic rupture with a clinical status of shock and sepsis. An open repair was not possible because of his unstable hemodynamics, the suspicion of an infected aorta and a very hostile abdomen. However, the endovascular approach would have been very challenging due to a very narrow infrarenal aorta. A Gore iliac branch endoprosthesis was successfully deployed as a bifurcated aortic stent graft and the aortic rupture was completely excluded. The patient was discharged after 20 days with long-term antibiotic and antifungal therapy. No signs of migration or limb occlusion at 6 months computed tomography scan were detected. This off-label use of an iliac branch device (IBD) with a precannulated gate appears to be a good solution in emergency repair of a very narrow ruptured aorta.Clinical ImpactWe report the case of an iliac branch endoprosthesis used as a bifurcated aortic stent graft in a very narrow ruptured infrarenal aorta. The report describes a new approach that can be useful in emergencies to deal with aortic ruptures when a narrowed lumen forbids the use of a standard endograft.

Abdominal aortic aneurysm (AAA) is a dilatation of the distal aorta to a diameter of 50% or more of its normal size of about 2 cm. Risk of aortic rupture can be nearly eliminated with either open surgery or endovascular repair. Procedural risks limit the value of these interventions unless the diameter of the aneurysm has reached a critical threshold (established as 5.5 cm in men or 5.0 cm in women). Thus, patients are monitored until this threshold is reached. Approximately 80% of small AAA will grow and exceed the threshold, providing a therapeutic window for altering this natural history and reducing the risk of rupture. Previous work in our lab has utilized adipose-derived mesenchymal stem cells (ASCs) to treat AAA in vivo, preserving elastic fibers and slowing aneurysm expansion. This work sought to create a delivery system for therapeutic extracellular vesicles (ASC-EVs) secreted by ASCs. Our delivery system incorporated the biocompatibility of regenerated silk fibroin (RSF), the magnetic moveability of iron oxide nanoparticles (IONPs), and the regenerative nature of ASC-EVs to create silk-iron packaged extracellular vesicles (SIPEs). Using this system, we tested the ability to magnetically localize the SIPEs and release their encapsulated ASC-EVs to exert their regenerative effects in vitro. We were successful in magnetically localizing the SIPEs in vitro and silk-iron microparticles (SIMPs) in vivo and in detecting their releasates via flow cytometry and cellular uptake assays. However, while their releasates were detected, their biological effects were diminished compared to unencapsulated controls. Thus, additional optimization related to loading efficiency is needed.