Research Progress on Aortic Root Aneurysms.

Aortic root aneurysms are one of the most common aortic root diseases, involving the aortic valve, aortic sinus, bilateral coronary arteries, and part of the ascending aorta. It is a life-threatening aortic disease with a high mortality rate of approximately 90%, due to aortic aneurysm rupture. Aortic valve insufficiency is one of the most common complications of aortic root aneurysms that can lead to acute left heart failure. The etiology of aortic root aneurysms is not yet completely clear and is mainly related to genetic diseases, such as Marfan syndrome and atherosclerosis. It can also occur secondary to aortic valve stenosis or a bivalve deformity. Surgery is the primary treatment for aortic root aneurysms, and aortic root replacement is a classic surgical method. However, the incidences of perioperative complications and mortality are relatively high, particularly in high-risk patients. In recent years, the anatomical structure of the aortic root has been gradually refined, and an in-depth understanding of root aneurysms has led to individualized treatment methods. Conservative drug therapy (ß-receptor blockers, angiotensin-converting enzyme inhibitors, or angiotensin receptor blockers), Bentall and modified Bentall surgeries (Button technology, Cabrol surgery, and modified Cabrol surgery), valve-sparing aortic root replacement (David and Yacoub), personalized external aortic root support, and endovascular intervention therapy have significantly improved the perioperative and long-term survival rates of patients with aortic root aneurysms. However, different treatment methods have their own advantages and disadvantages. This review aimed to summarize the current research progress and treatment of aortic root aneurysms.

Thoracic Aortic Aneurysmal Disease: Comprehensive Recommendations for the Primary Care Physician.

Thoracic aortic aneurysm (TAA) is a commonly encountered disease that is defined as aortic dilation with an increase in diameter of at least 50% greater than the expected age- and sex-adjusted size. Thoracic aortic aneurysms are described by their size, location, morphology, and cause. Primary care clinicians and other noncardiologists are often the first point of contact for patients with TAA. This review is intended to provide them with basic information on the differential diagnosis, diagnostic evaluation, and medical and surgical management of TAAs. Management decisions depend on having as precise a diagnosis as possible. Fortunately, this can often be achieved with a stepwise diagnostic approach that incorporates imaging and targeted genetic testing. Our review includes recommendations. In this review, we discuss these issues at a basic level and include recommendations for patients considering pregnancy.

Animal Models, Pathogenesis, and Potential Treatment of Thoracic Aortic Aneurysm.

Thoracic aortic aneurysm (TAA) has a prevalence of 0.16-0.34% and an incidence of 7.6 per 100,000 person-years, accounting for 1-2% of all deaths in Western countries. Currently, no effective pharmacological therapies have been identified to slow TAA development and prevent TAA rupture. Large TAAs are treated with open surgical repair and less invasive thoracic endovascular aortic repair, both of which have high perioperative mortality risk. Therefore, there is an urgent medical need to identify the cellular and molecular mechanisms underlying TAA development and rupture to develop new therapies. In this review, we summarize animal TAA models including recent developments in porcine and zebrafish models: porcine models can assess new therapeutic devices or intervention strategies in a large mammal and zebrafish models can employ large-scale small-molecule suppressor screening in microwells. The second part of the review covers current views of TAA pathogenesis, derived from recent studies using these animal models, with a focus on the roles of the transforming growth factor-beta (TGFß) pathway and the vascular smooth muscle cell (VSMC)-elastin-contractile unit. The last part discusses TAA treatment options as they emerge from recent preclinical studies.

The current and future role of imaging of thoracic aortic disease: a North American society for cardiovascular imaging commentary on the 2022 AHA/ACC guidelines for the diagnosis and management of aortic disease.

The 2022 AHA/ACC Guidelines for the Diagnosis and Management of Aortic Disease introduced important updates for managing thoracic aorta aortic disease (TAD). In particular, the Guidelines underscore multimodality imaging's role in diagnosis, risk assessment, and monitoring of patients with TAD. This commentary aims to distill key imaging aspects from the Guidelines to provide a concise reference for the cardiovascular imaging community. Primary areas of focus include: (1) The importance of imagers in the multidisciplinary TAD care team, (2) Appropriate imaging techniques along with their strengths and weaknesses, (3) Aortic measurement methods and how aortic size and growth should contribute to TAD risk assessment, (4) Imaging evaluation of acute aortic syndrome. We have also highlighted several areas of ongoing uncertainty and confusion, specifically related to aortic measurement techniques and descriptive terminology. Finally, a perspective on the future of TAD imaging is discussed with a focus on advanced imaging tools and techniques as well as the potential role of artificial intelligence.

Molecular Mechanisms in Genetic Aortopathy-Signaling Pathways and Potential Interventions.

Thoracic aortic disease affects people of all ages and the majority of those aged <60 years have an underlying genetic cause. There is presently no effective medical therapy for thoracic aneurysm and surgery remains the principal intervention. Unlike abdominal aortic aneurysm, for which the inflammatory/atherosclerotic pathogenesis is well established, the mechanism of thoracic aneurysm is less understood. This paper examines the key cell signaling systems responsible for the growth and development of the aorta, homeostasis of endothelial and vascular smooth muscle cells and interactions between pathways. The evidence supporting a role for individual signaling pathways in pathogenesis of thoracic aortic aneurysm is examined and potential novel therapeutic approaches are reviewed. Several key signaling pathways, notably TGF-ß, WNT, NOTCH, PI3K/AKT and ANGII contribute to growth, proliferation, cell phenotype and survival for both vascular smooth muscle and endothelial cells. There is crosstalk between pathways, and between vascular smooth muscle and endothelial cells, with both synergistic and antagonistic interactions. A common feature of the activation of each is response to injury or abnormal cell stress. Considerable experimental evidence supports a contribution of each of these pathways to aneurysm formation. Although human information is less, there is sufficient data to implicate each pathway in the pathogenesis of human thoracic aneurysm. As some pathways i.e., WNT and NOTCH, play key roles in tissue growth and organogenesis in early life, it is possible that dysregulation of these pathways results in an abnormal aortic architecture even in infancy, thereby setting the stage for aneurysm development in later life. Given the fine tuning of these signaling systems, functional polymorphisms in key signaling elements may set up a future risk of thoracic aneurysm. Multiple novel therapeutic agents have been developed, targeting cell signaling pathways, predominantly in cancer medicine. Future investigations addressing cell specific targeting, reduced toxicity and also less intense treatment effects may hold promise for effective new medical treatments of thoracic aortic aneurysm.

Acute aortic dissection: evidence, uncertainties, and future therapies.

Remarkable progress has become especially apparent in aortic medicine in the last few decades, leading to essential changes in how thoracic aortic dissection is understood and treated. This state-of-the-art review article addresses the mechanisms of acute aortic dissection, explaining the role of its primary entry location, proximal, and distal dissection extension in their clinical presentation and impact on the decision-making process towards the best treatment approach. The latest evidence on novel treatment methods for acute aortic syndromes is presented, and the diverse dissection classification systems that remain uncertain are discussed, which reveals the need for shared terminology and more clarity. Finally, future aspects are discussed in treating acute aortic dissection, such as the endovascular treatment of aortic dissection Type A and biomarkers for acute aortic syndromes.

A fluorescent nano vector for early diagnosis and enhanced Interleukin-33 therapy of thoracic aortic dissection.

Thoracic aortic dissection (TAD) is the most devastating complication of vascular disease. The accuracy of the clinical diagnosis and treatment of TAD at the early stage is still limited. Herein, we report a nano-delivery strategy for early diagnosis and the first case of interleukin-33 (IL-33) based therapy for the effective intervention of TAD. A targeted fluorescent nano vector (FNV) is designed to co-assemble with IL-33, which protects IL-33 and prolongs its half-life. With specific targeting ability to the thoracic aorta, FNV can diagnose TAD at its early stage through fluorescent imaging. FNV@IL-33 nanocomplex presents better therapeutic effects on mice TAD progression compared with that of IL-33 alone by reducing smooth muscle apoptosis. Administration of FNV@IL-33 two weeks before onset, the development of TAD is greatly intervened. Our study provides a novel approach for early diagnosis and effective IL-33 therapy of TAD, which opens attractive opportunities for clinical prevention of cardiovascular diseases.

A review on the deeper understanding of inflammation and infection of the thoracic aorta.

OBJECTIVE: To review the current literature regarding infection and inflammation of the thoracic aorta and to summarise its aetiologies, pathogenesis and clinical presentation. Additionally, the authors sought to compare diagnostic methods and to analyse the different management options. METHOD: A comprehensive electronic search using PubMed, MEDLINE, Scopus and Google Scholar was conducted to find relevant journal articles with key search terms including: 'aortitis', 'thoracic aortic infection' and 'surgical management of infected thoracic aortic aneurysms'. Prominent publications from 1995 till present (2021) were analysed to achieve a deeper understanding of thoracic aorta infection and inflammation, and the information was then collated to form this review. RESULTS: The literature review revealed that infectious causes are more prominent than non-infectious causes, with Gram positive bacteria such as Staphylococcus, Enterococcus and Streptococcus accounting for approximately 60% of the infections. The authors also noted that Staphylococcus Aureus was associated with poorer outcomes. Key diagnostic tools include MRI and multi-slice CT imaging, which are useful imaging modalities in defining the extent of the disease thus allowing for planning surgical intervention. Surgical intervention itself is extremely multifaceted and the rarity of the condition means no large-scale comparative research between all the management options exists. Until more large-scale comparative data becomes available to guide treatment, the optimal approach must be decided on a case-by-case basis, considering the benefits and drawback of each treatment option. CONCLUSION: A high index of suspicion and a comprehensive history is required to effectively diagnose and manage infection and inflammation of the thoracic aorta. Differentiating between infectious and inflammatory cases is crucial for management planning, as infectious causes typically require antibiotics and surgical intervention. Over the years, the post treatment results have shown significant improvement due to earlier diagnosis, advancement in surgical options and increasingly specific microbial therapy.

Genetics and mechanisms of thoracic aortic disease.

Aortic disease has many forms including aortic aneurysm and dissection, aortic coarctation or abnormalities in aortic function, such as loss of aortic distensibility. Genetic analysis in humans is one of the most important experimental approaches in uncovering disease mechanisms, but the relative infrequency of thoracic aortic disease compared with other cardiovascular conditions such as coronary artery disease has hindered large-scale identification of genetic associations. In the past decade, advances in machine learning technology coupled with large imaging datasets from biobank repositories have facilitated a rapid expansion in our capacity to measure and genotype aortic traits, resulting in the identification of dozens of genetic associations. In this Review, we describe the history of technological advances in genetic discovery and explain how newer technologies such as deep learning can rapidly define aortic traits at scale. Furthermore, we integrate novel genetic observations provided by these advances into our current biological understanding of thoracic aortic disease and describe how these new findings can contribute to strategies to prevent and treat aortic disease.

MDCT Imaging of Non-Traumatic Thoracic Aortic Emergencies and Its Impact on Diagnosis and Management-A Reappraisal.

Non-traumatic thoracic aorta emergencies are associated with significant morbidity and mortality. Diseases of the intimomedial layers (aortic dissection and variants) have been grouped under the common term of acute aortic syndrome because they are life-threatening conditions clinically indistinguishable on presentation. Patients with aortic dissection may present with a wide variety of symptoms secondary to the pattern of dissection and end organ malperfusion. Other conditions may be seen in patients with acute symptoms, including ruptured and unstable thoracic aortic aneurysm, iatrogenic or infective pseudoaneurysms, aortic fistula, acute aortic thrombus/occlusive disease, and vasculitis. Imaging plays a pivotal role in the patient's management and care. In the emergency room, chest X-ray is the initial imaging test offering a screening evaluation for alternative common differential diagnoses and a preliminary assessment of the mediastinal dimensions. State-of-the-art multidetector computed tomography angiography (CTA) provides a widely available, rapid, replicable, noninvasive diagnostic imaging with sensitivity approaching 100%. It is an impressive tool in decision-making process with a deep impact on treatment including endovascular or open surgical or conservative treatment. Radiologists must be familiar with the spectrum of these entities to help triage patients appropriately and efficiently. Understanding the imaging findings and proper measurement techniques allow the radiologist to suggest the most appropriate next management step.

Sarcopenia predicts for long-term survival in patients with thoracoabdominal aortic aneurysms undergoing operative and nonoperative management.

OBJECTIVE: Sarcopenia, defined as a loss of muscle mass or poor muscle quality, is a syndrome associated with poor surgical outcomes. The prognostic value of sarcopenia in patients with thoracoabdominal aortic aneurysms (TAAAs) is unknown. The present study was designed to define sarcopenia in this patient population and assess its impact on survival among patients who had undergone operative and nonoperative management of TAAAs. METHODS: We retrospectively reviewed all patients with a diagnosis of a TAAA at an academic hospital between 2009 and 2017 who had been selected for operative and nonoperative management. Sarcopenia was identified by measuring the total muscle area on a single axial computed tomography image at the third lumbar vertebra. The muscle areas were normalized by patient height, and cutoff values for sarcopenia were established at the lowest tertile of the normalized total muscle area. Long-term patient survival was assessed using Kaplan-Meier and Cox regression models. RESULTS: A total of 295 patients were identified, of whom 199 had undergone operative management and 96 nonoperative management for TAAAs. The patients selected for nonoperative management were more likely to be women and to have chronic kidney disease, coronary artery disease, cerebrovascular disease, a higher modified frailty index, and a larger aortic diameter. The Kaplan-Meier analyses revealed significantly lower long-term survival for the patients with and without sarcopenia in the operative and nonoperative groups. In Cox regression analyses, sarcopenia was a significant predictor of shorter survival for both operative (hazard ratio, 0.96; 95% confidence interval, 0.94-0.99; P = .006) and nonoperative (hazard ratio, 0.95; 95% confidence interval, 0.90-1.00; P = .05) groups after adjusting for age, race, sex, maximum aortic diameter, modified frailty index, chronic kidney disease, and active smoking. Additionally, age was a significant predictor of shorter survival in the operative group, and smoking and aortic diameter were significant in the nonoperative group. CONCLUSIONS: In our cohort of patients who had received operative and nonoperative management of TAAAs, the patients with sarcopenia had had significantly lower long-term survival, regardless of whether surgery had been performed. These data suggest that sarcopenia could be used as a predictor of survival for patients with TAAAs and might be useful for risk stratification and decision making in the management of TAAAs.

Mesenchymal Stem Cells Alter MicroRNA Expression and Attenuate Thoracic Aortic Aneurysm Formation.

BACKGROUND: Thoracic aortic aneurysms (TAA) are a progressive disease characterized by inflammation, smooth muscle cell activation and matrix degradation. We hypothesized that mesenchymal stem cells (MSCs) can immunomodulate vascular inflammation and remodeling via altered microRNA (miRNAs) expression profile to attenuate TAA formation. MATERIALS AND METHODS: C57BL/6 mice underwent topical elastase application to form descending TAAs. Mice were also treated with MSCs on days 1 and 5 and aortas were analyzed on day 14 for aortic diameter. Cytokine array was performed in aortic tissue and total RNA was tagged and hybridized for miRNAs microarray analysis. Immunohistochemistry was performed for elastin degradation and leukocyte infiltration. RESULTS: Treatment with MSCs significantly attenuated aortic diameter and TAA formation compared to untreated mice. MSC administration also attenuated T-cell, neutrophil and macrophage infiltration and prevented elastic degradation to mitigate vascular remodeling. MSC treatment also attenuated aortic inflammation by decreasing proinflammatory cytokines (CXCL13, IL-27, CXCL12 and RANTES) and upregulating anti-inflammatory interleukin-10 expression in aortic tissue of elastase-treated mice. TAA formation demonstrated activation of specific miRNAs that are associated with aortic inflammation and vascular remodeling. Our results also demonstrated that MSCs modulate a different set of miRNAs that are associated with decrease leukocyte infiltration and vascular inflammation to attenuate the aortic diameter and TAA formation. CONCLUSIONS: These results indicate that MSCs immunomodulate specific miRNAs that are associated with modulating hallmarks of aortic inflammation and vascular remodeling of aortic aneurysms. Targeted therapies designed using MSCs and miRNAs have the potential to regulate the growth and development of TAAs.

Epidemiology of thoracoabdominal aortic aneurysms.

Thoracoabdominal aortic aneurysms, although rare, continue to be associated with high morbidity and mortality in the modern era of vascular surgery, and knowledge of this disease is essential for those in clinical practice. Given the clinically silent nature of the disease, it is difficult to determine disease incidence, with most epidemiologic recommendations not made based on evidence regarding those diagnosed with the disease, but extrapolated from data on surgical outcomes. It appears that although men are more likely to develop thoracoabdominal aortic aneurysms, the distribution is not as skewed as in abdominal aortic aneurysms. Current evidence suggests that Black and Hispanic patients continue to have disproportionately poor disease outcomes, mostly attributed to later presentation and undergoing interventions at lower-volume centers. Although select patients meet criteria for disease screening based on personal or family history of aneurysmal disease, general population screening has not been recommended by any professional organization to date. Vascular surgeons need to continue to be at the forefront of thoracoabdominal aortic aneurysm management, especially as care becomes centered around comprehensive "aortic care centers" and as more endovascular therapies become available.

Moderate aerobic exercise prevents matrix degradation and death in a mouse model of aortic dissection and aneurysm.

Thoracic aortic aneurysm and dissection (TAAD) is a deadly disease characterized by intimal disruption induced by hemodynamic forces of the circulation. The effect of exercise in patients with TAAD is largely unknown. ß-Aminopropionitrile (BAPN) is an irreversible inhibitor of lysyl oxidase that induces TAAD in mice. The objective of this study was to investigate the effect of aerobic exercise on BAPN-induced TAAD. Upon weaning, mice were given either BAPN-containing water or standard drinking water and subjected to either conventional cage activity (BAPN-CONV) or forced treadmill exercise (BAPN-EX) for up to 26 wk. Mortality was 23.5% (20/85) for BAPN-CONV mice versus 0% (0/22) for BAPN-EX mice (hazard ratio 3.8; P = 0.01). BAPN induced significant elastic lamina fragmentation and intimal-medial thickening compared with BAPN-untreated controls, and aneurysms were identified in 50% (5/10) of mice that underwent contrast-enhanced CT scanning. Exercise significantly decreased BAPN-induced wall thickening, calculated circumferential wall tension, and lumen diameter, with 0% (0/5) of BAPN-EX demonstrating chronic aortic aneurysm formation on CT scan. Expression of selected genes relevant to vascular diseases was analyzed by qRT-PCR. Notably, exercise normalized BAPN-induced increases in TGF-ß pathway-related genes Cd109, Smad4, and Tgfßr1; inflammation-related genes Vcam1, Bcl2a1, Ccr2, Pparg, Il1r1, Il1r1, Itgb2, and Itgax; and vascular injury- and response-related genes Mmp3, Fn1, and Vwf. Additionally, exercise significantly increased elastin expression in BAPN-treated animals compared with controls. This study suggests that moderate aerobic exercise may be safe and effective in preventing the most devastating outcomes in TAAD.NEW & NOTEWORTHY Moderate aerobic exercise was shown to significantly reduce mortality, extracellular matrix degradation, and thoracic aortic aneurysm and dissection formation associated with lysyl oxidase inhibition in a mouse model. Gene expression suggested a reversal of TGF-ß, inflammation, and extracellular matrix remodeling pathway dysregulation, along with augmented elastogenesis with exercise.

Insights on the Pathogenesis of Aneurysm through the Study of Hereditary Aortopathies.

Thoracic aortic aneurysms (TAA) are permanent and localized dilations of the aorta that predispose patients to a life-threatening risk of aortic dissection or rupture. The identification of pathogenic variants that cause hereditary forms of TAA has delineated fundamental molecular processes required to maintain aortic homeostasis. Vascular smooth muscle cells (VSMCs) elaborate and remodel the extracellular matrix (ECM) in response to mechanical and biochemical cues from their environment. Causal variants for hereditary forms of aneurysm compromise the function of gene products involved in the transmission or interpretation of these signals, initiating processes that eventually lead to degeneration and mechanical failure of the vessel. These include mutations that interfere with transduction of stimuli from the matrix to the actin-myosin cytoskeleton through integrins, and those that impair signaling pathways activated by transforming growth factor-ß (TGF-ß). In this review, we summarize the features of the healthy aortic wall, the major pathways involved in the modulation of VSMC phenotypes, and the basic molecular functions impaired by TAA-associated mutations. We also discuss how the heterogeneity and balance of adaptive and maladaptive responses to the initial genetic insult might contribute to disease.

Stent-assisted balloon dilatation of chronic aortic dissection.

BACKGROUND: The treatment of complicated chronic aortic dissection remains controversial. We previously reported encouraging early results with the stent-assisted balloon-induced intimal disruption and relamination of aortic dissection (STABILISE) technique for treating complicated acute aortic dissections. However, to date there have been no specific reports on the treatment of complicated chronic aortic dissections with this technique. The aim of this study was to assess the results of the STABILISE technique to treat complicated chronic aortic dissection. METHODS: A single-center prospectively maintained database enrolled all patients hospitalized for aortic dissection at our institution. Inclusion criteria for the STABILISE procedure at the chronic stage of dissection (>3 months) were postdissection aneurysm with a diameter >55 mm or rapid aortic diameter growth >5 mm/6 months. We reviewed all patients treated for complicated chronic aortic dissection with the STABILISE technique. Patients were monitored at 3, 6, and 12 months and annually thereafter with clinical, imaging, and laboratory studies. Outcome analyses included survival, rupture, spinal cord ischemia, endoleak, morbidity (cardiac, renal, or pulmonary), reinterventions, false lumen patency, and aneurysm growth. RESULTS: Between September 2015 and December 2018, 17 patients underwent a STABILISE procedure for complicated chronic aortic dissection of the descending aorta. Fifteen patients were treated for remaining chronic distal thoracoabdominal aortic dissection after acute DeBakey type I aortic dissection repair, and 2 patients were treated for chronic type B aortic dissection. The median patient age was 61 years (range, 46-67 years). The median interval between the onset of acute symptoms and the procedure was 9 months (range, 3-67 months). Indications for the STABILISE procedure were a rapidly growing dissected aortic diameter >5 mm/6 months in 13 patients and aneurysmal evolution of the descending thoracic aorta >55 mm in 4 patients. There were no cases of in-hospital death, stroke, spinal cord ischemia, ischemic colitis, or renal failure necessitating dialysis. The median duration of follow-up was 17 months (range, 5-28.5 months). At the last computed tomography scan, 15 patients (88%) had complete false lumen thrombosis of the treated thoracoabdominal aorta down to the renal arteries. None of the patients had aortic growth at treated thoracoabdominal aorta level. One patient developed a proximal type 1 endoleak and required reintervention. Regarding the untreated aortoiliac level below the renal arteries, 11 patients had persistent false lumen patency, and 1 patient developed a common iliac artery aneurysm. All the other patients had stable infrarenal aortoiliac diameters. No late deaths were reported during follow-up. CONCLUSIONS: The STABILISE technique is a safe and effective means of performing immediate, complete aortic remodeling of the thoracoabdominal aorta in patients with complicated chronic aortic dissection, stabilizing the diameter of the dissected aorta.

Impact of Endovascular False Lumen Embolization on Thoracic Aortic Remodeling in Chronic Dissection.

BACKGROUND: Retrograde false lumen (FL) perfusion after thoracic endovascular aortic repair (TEVAR) for chronic dissection is a mode of treatment failure. Thrombosis of the FL is associated with favorable reverse remodeling. Objectives are to describe FL embolization (FLE) strategy and assess aortic remodeling and survival. METHODS: From January 2009 to December 2017, 51 patients with chronic dissection underwent FLE, most after previous TEVAR. Devices included a combination of iliac plug (29 patients), coils (19 patients), or nitinol plug (3 patients). Computed tomography was performed before discharge, at 3 months, and annually (median follow-up 2 years [range, 1 month to 7 years]). RESULTS: After FLE, mean maximum aortic diameter decreased (64.2 ± 12 mm to 61.0 ± 13 mm; P = .03), true lumen diameter increased (24.7 ± 10 mm to 33.7 ± 8 mm; P < .001), and FL diameter decreased (36.7 ± 12 mm to 25.6 ± 15 mm, P < .001). For reverse remodeling, FL thrombosis with ≥10% decrease in diameter and ≥10% increase in true lumen diameter was achieved in 20 (39.2%; 16 primarily, 4 secondarily). Nine patients progressed after the first FLE: persistent FL flow with increase in aortic diameter and underwent repeat FLE with complete thrombosis (n = 4) or open thoracoabdominal completion (n = 5). A total of 26 patients had indeterminate response (FL thrombosis without change in maximum diameter), and none have required reoperation. Six patients had complete obliteration of the entire FL. At last follow-up, 42 (82%) patients were alive. Three deaths were related to aortic pathology. CONCLUSIONS: FLE is an important endovascular adjunct to TEVAR promoting reverse aortic remodeling in select patients with chronic aortic dissection and persistent retrograde FL perfusion.