Thoracic and abdominal aortic dissection in a hypertensive hyperthyroid cat

Evolving Experience of Percutaneous Management of Type B Aortic Dissection

Genetics of Thoracic and Thoracoabdominal Aortic Dissections and Aneurysms.

This study aims to investigate the relationship between the development of aortic dissections and aneurysms with the polymorphisms of angiotensin converting enzyme gene, methylenetetrahydrofolate reductase gene, plasminogen activator inhibitor-1 gene, and nitric oxide synthase gene. Between April 2009 and July 2014, 38 patients with aortic dissections (28 males, 10 females; mean age 55.1±10.7 years; range, 30 to 78 years) and 67 patients with aortic aneurysms (57 males, 10 females; mean age 63.0±11.4 years; range, 31 to 82 years) were included in this cross-sectional study. The control group consisted of 60 healthy volunteers (41 males, 19 females; mean age 56.3±11.2 years; range, 30 to 82 years) without an aortic aneurysm or dissection, as assessed by thoracoabdominal computed tomography. The prespecified four genes were genotyped with competitive allelespecific polymerase chain reaction. The aortic dissection group had higher nitric oxide synthase-3 (4b/4b) expression levels, compared to the control group. The aortic aneurysm group had also higher nitric oxide synthase-3 (4b/4a) expression levels, compared to the control group. Compared to the control group, a higher rate of angiotensin converting enzyme I/D gene polymorphism was detected in the aneurysm group, while higher D/D polymorphism rates were found in the dissection group; although not statistically significant. Our study results suggest that the nitric oxide synthase-3 intron 4b/4b and nitric oxide synthase-3 intron 4b/4a gene polymorphisms can be used as a predictor of aortic dissection and aneurysm development.

To explore the safety and feasibility of endograft repair in refractory aortic dissection and dissecting aneurysm. The clinical data of 13 refractory cases of aortic dissection and dissecting aneurysm, 11 males and 2 females, aged 52 (38-82), out of the 68 consecutive patients with aortic dissection and dissecting aneurysm who underwent endograft repair from Jan 2001 to Oct 2004, were analyzed. Nine of the 13 cases were diagnoses as with aortic dissection and dissecting aneurysm of Stanford type A, 3 of which had tears in the ascending aorta (DeBakey type I), 3 had tears in aortic arch, and 3 had tears on the distal aortic arch with ascending aorta involved; and the other four out of the 13 cases were diagnosed as Stanford type B, one with Marfan's syndrome. Eight of the 13 cases had more than 2 entries, 3 of which had suffered from shock and hemathorax due to rupture preoperatively. Follow-up ranging 2 months to 3 years was carried out after the operation. Transluminal placement of stentgratf was technically successful in all patients. Three patients with DeBakey type I dissections received stent-grafts introduced through the left common carotid or right femoral artery, of which one case died from gastrointestinal hemorrhage 1 month postoperatively. For the patients with tears in aortic arch preliminary Y type bypass from ascending aorta to left common carotid artery and left subclivian artery was performed in 2 cases, and carotid-carotid artery bypass was performed in one case, and then stent-grafts were deployed through right femoral artery. The 3 cases with tears in the distal arch and ruptured aneurysm, received stent-grafts implantation through the femoral artery emergently, and closed thoracic drainage and anti-shock treatment, one of which died from another aneurysm rupture 27 hours postoperatively. Out of the 4 cases with Stanford type B dissection with multiple tear entries, 3 underwent multiple stent-grafts repair and 1 underwent emergent abdominal-bilateral iliac arteries Y-type graft bypass due to rupture of iliac dissecting aneurysm. During the follow-up CT, MRI and color Doppler sonography showed that all 11 patients remained healthy with the former tears well closed and thrombosis in the false lumen. Endograft repair for refractory aortic dissecting aneurysm is feasible and technically successful, especially for the patients with tears in the ascending aorta or aortic arch.

Aortic dissection (AD) and aortic aneurysm (AA) are acute aortic syndromes associated with high mortality, requiring rapid recognition and accurate differentiation from each other and from healthy individuals. While imaging remains the diagnostic gold standard, hematological indices and inflammatory biomarkers may provide fast and accessible adjunctive tools in emergency settings. This retrospective comparative study, conducted at 2 tertiary centers, included 576 participants after exclusions: 213 patients with AD, 178 with AA, and 185 healthy controls. Demographic, clinical, and laboratory data were collected at admission. Hematological indices, including the neutrophil-to-lymphocyte ratio (NLR), platelet-to-lymphocyte ratio, platelet-to-neutrophil ratio, derived NLR (dNLR), systemic immune-inflammation index, fibrinogen-to-C-reactive protein ratio, and fibrinogen-to-d-dimer ratio, together with conventional inflammatory markers such as C-reactive protein, fibrinogen, and d-dimer, were analyzed. Receiver operating characteristic curve analysis and multivariable logistic regression were used to assess diagnostic performance. Compared with controls, patients with AD and AA exhibited significantly higher inflammatory indices (all P < .001). Neutrophil-to-lymphocyte ratio showed the highest diagnostic accuracy in distinguishing AD from controls (area under the curve [AUC] = 0.933, sensitivity 90.1%, specificity 89.7%), whereas platelet-to-neutrophil ratio and systemic immune-inflammation index also demonstrated considerable discriminative ability. For AA versus controls, NLR (AUC = 0.846) and platelet-to-neutrophil ratio (AUC = 0.838) were the most predictive parameters. For AD versus AA, fibrinogen-to-d-dimer ratio exhibited the best performance (AUC = 0.898, sensitivity 77.0%, specificity 83.7%). Multivariable logistic regression models combining clinical factors such as hypertension, sex, diabetes, and coronary artery disease with hematological indices achieved excellent discrimination (AUCs = 0.938 for AD vs controls, 0.870 for AA vs controls, and 0.944 for AD vs AA). Simple hematological ratios, particularly NLR and the novel fibrinogen-to-d-dimer ratio index, provide strong diagnostic and discriminative value in acute aortic syndromes. Integrating these biomarkers with clinical risk factors may enhance early triage and differential diagnosis, especially when advanced imaging modalities are delayed or unavailable.

<h2>Abstract</h2><h3>Background</h3> Thoracic aortic aneurysms (TAA) and aortic dissections (AD) are recognized as one of the leading causes of death in developed countries. Although mortality decreases if at-risk individuals are diagnosed early on through screening, many fail to seek the proper preventive interventions timely. Genetic predisposition, smoking, and hypertension are well-known risk factors for highly lethal aortic aneurysmal rupture or dissection. Hypothyroidism has also been extensively described in the literature as a possible risk factor directly related to the origin of thoracic aortic aneurysm and dissection. Numerous studies have proposed a pathophysiological role for hypothyroidism in the development of TAA and AD, although this role is still not fully understood. <h3>Objective</h3> This scoping review sought human and animal studies to examine the relationship between hypothyroidism and thoracic aortic diseases. <h3>Methods</h3> A search in PubMed, Web of Science, and Scopus using the terms "aortic dissection," "aorta," "aortic aneurysm," and "hypothyroidism" yielded 907 articles, and only nine were relevant to this study topic and criteria. <h3>Results</h3> The included articles discuss thoracic aortic diseases as potential risk factors for thoracic aortic aneurysm and dissection. A low thyroid hormone level might be a negative prognostic indicator after acute aortic dissection. <h3>Conclusion</h3> Establishing a link between hypothyroidism and thoracic aortic diseases could improve clinical practice through the development of screening strategies for thyroid function in patients with thoracic aortic diseases, thereby reducing postoperative mortality rates.

Introduction: Aortic dissection and aortic aneurysm represent significant health risk as they are associated with very high mortality. Incidence of aortic dissection is low and estimated to be 5-30/100,000 hospitalized patients. Similarly, aortic aneurysms have low incidence (depending upon location) and high mortality (over 80%). Combined mortality associated with aortic aneurysm or dissection and its contemporary trends in the U.S. are not well known. Methods: In this retrospective study death certificate data were retrieved from the Centers for Disease Control and Prevention’s Wide-Ranging Online Data for Epidemiologic Research (WONDER) database for 1999-2018. Mortality for aortic aneurysm and dissection ICD-10 code-I71 as an underlying cause of death were queried from 1999-2018. This duration was further stratified into five-year periods. WONDER database is publicly available de-identified data collected by CDC that reports the underlying cause of death across the United States. Crude mortality rate and age-adjusted mortality rate per 100,000 were calculated in four U.S census regions (CR1 Northeast, CR2 Midwest, CR3 South, CR4 West). Results: From 1999-2018 AAMR for aortic aneurysm and dissection showed a downward trajectory. Regional variations were observed and are illustrated in figure 1. For Northeast (CR-1) AAMR declined by 54%, for Midwest (CR-2) it declined by 48%; for South (CR-3) it declined by 53%, and for West (CR-4) it declined by 52%. (Table-1) Conclusions: Our study shows a downward trajectory of AAMR for aortic aneurysm and dissection. Which reinforces the continuation of guideline based screening.

Recent years have witnessed the emergence of novel technologies that enable less invasive endovascular treatment of descending thoracic aortic disease (TAD). This has occurred against a backdrop of improved identification of various disease processes and better results with open surgical repair. The natural history of the specific acute aortic syndromes that affect the descending thoracic aorta has also been described with more clarity and has become more commonly recognized. This is in part secondary to the widespread availability and application of advanced imaging technologies that permit precise diagnoses. As data are accumulating, these pathological processes involving the descending thoracic aorta are no longer thought of as simply variants of one another but as distinct entities with well-defined clinical behavior. As the technology for endovascular repair continues to mature and its utilization increases, there is a need for a careful assessment of the current state of medical management, traditional open therapy, and evolving endovascular treatment of distinct thoracic aortic pathologies. The purpose of this scientific statement is to present a contemporary review of the various pathological processes that affect the descending thoracic aorta: Aneurysms, dissections, intramural hematomas (IMHs), penetrating atherosclerotic ulcers (PAUs), and aortic transections. These disorders will be considered in detail, with an exploration of the natural history, available treatment options, and controversies regarding management. Current intervention criteria will be reviewed with respect to both open surgical repair and endovascular treatment. Our goal is to provide the healthcare professional with a better understanding of the pathophysiology of the various disease processes that involve the descending thoracic aorta and to review current outcomes and technical pitfalls associated with these therapies to facilitate strong, evidence-based decision making in the care of these patients. Treatment of descending TAD involves complex, exigent decision making in an era of evolving technology. Survival data for nonoperative …

Increased Tissue Microarray Matrix Metalloproteinase Expression Favors Proteolysis in Thoracic Aortic Aneurysms and Dissections

Feline systemic arterial hypertension (SHT) is associated with a wide spectrum of left ventricular (LV) geometric patterns as well as diastolic, and to a lesser extent, systolic myocardial dysfunction. However, little is known about SHT-related cardiac changes in dogs. SHT in dogs is responsible for morphological and functional cardiac alterations. Thirty dogs with spontaneous untreated SHT and 28 age- and body weight-matched healthy dogs as controls. Prospective observational study. Conventional echocardiography and 2-dimensional color tissue Doppler imaging were performed in SHT dogs by trained observers and compared with controls. Forty-seven percent of SHT dogs (14/30) had diffuse concentric hypertrophy. None had left atrial dilatation and 10/30 (33%) had aortic insufficiency (AoI) associated with proximal aortic dilatation. Longitudinal diastolic left ventricular free wall (LVFW) motion was altered in all SHT dogs at the base (early to late diastolic wave ratio, E/A = 0.5 ± 0.1 versus 1.3 ± 0.3 for controls, P < .0001) and the apex (E/A = 1.6 ± 1.7 versus 3.9 ± 3.1, P < .05). Longitudinal motion of the interventricular septum at the base (E/A = 0.7 ± 0.4 versus 1.1 ± 0.1, P < .01) and radial LVFW motion in the subendocardium (E/A = 0.9 ± 0.5 versus 1.6 ± 0.3, P < .01) were also altered in dogs with SHT. Longitudinal LVFW systolic velocities and gradients were also significantly decreased (P < .05) in SHT dogs. As in SHT in cats, SHT in dogs is associated with myocardial dysfunction independently of the presence of myocardial hypertrophy. However, unlike feline SHT, it results in a homogeneous LV geometric pattern with a relatively high prevalence of AoI.

Previous data suggest women are at increased risk of death from aortic dissection. Therefore, we analyzed data from the GenTAC registry, the NIH-sponsored program that collects information about individuals with genetically triggered thoracic aortic aneurysms and cardiovascular conditions. We performed cross-sectional analyses in adults with Marfan syndrome (MFS), familial thoracic aortic aneurysm or dissection (FTAAD), bicuspid aortic valve (BAV) with thoracic aortic aneurysm or dissection, and subjects under 50 years of age with thoracic aortic aneurysm or dissection (TAAD <50 years). Women comprised 32% of 1,449 subjects and were 21% of subjects with BAV, 34% with FTAAD, 22% with TAAD <50 years, and 47% with MFS. Thoracic aortic dissections occurred with equal gender frequency yet women with BAV had more extensive dissections. Aortic size was smaller in women but was similar after controlling for BSA. Age at operation for aortic valve dysfunction, aneurysm or dissection did not differ by gender. Multivariate analysis (adjusting for age, BSA, hypertension, study site, diabetes, and subgroup diagnoses) showed that women had fewer total aortic surgeries (OR = 0.65, P < 0.01) and were less likely to receive angiotensin converting enzyme inhibitors (ACEi; OR = 0.68, P < 0.05). As in BAV, other genetically triggered aortic diseases such as FTAAD and TAAD <50 are more common in males. In women, decreased prevalence of aortic operations and less treatment with ACEi may be due to their smaller absolute aortic diameters. Longitudinal studies are needed to determine if women are at higher risk for adverse events.

Transforming growth factor (TGF)-β/Smad signaling pathway in aortic dissection patients and normal subjects has not been previously described. The present study was designed to evaluate the TGF-β/Smad signaling expressions in the patients with acute type A aortic dissection in comparison with those in the patients with thoracic aortic aneurysm and with coronary artery disease, and (or) the healthy subjects. Consecutive surgical patients for acute type A aortic dissection (20 patients), aortic aneurysm (nine patients) or coronary artery disease (20 patients) were selected into this study. Blood samples (4 ml) were obtained from the right radial arterial indwelling catheter after systemic heparinization prior to the start of cardiopulmonary bypass in the operating room. Twenty-one young healthy volunteers without underlying health issues who donated forearm venous blood samples (4 ml) were taken as control. The surgical specimens of the aortic tissues were obtained immediately after they were severed during the operations of the replacement of the aorta in the patients with aortic dissection or aortic aneurysm. In patients receiving coronary artery bypass grafting, the tiny aortic tissues were taken when the punch holes of the proximal anastomosis on the anterior wall of the ascending aorta were made. The aortic tissues were for RNA, protein, or supernatant preparations until detection of TGF-β1 mRNA by quantitative real-time reverse transcription polymerase chain reaction, of TGF-β1, TGF-β receptor I, Smad2/3, Smad4 and Smad7 by Western blot, and of TGF-β1 by enzyme-linked immunosorbent assay, respectively. In particular, the linear correlations of the relative grayscales between different proteins of each group, and those correlations between the quantitative TGF-β1 by enzyme-linked immunosorbent assay and the time interval from the onset to surgery or the maximal dimensions of the aorta of the aortic dissection group were assessed. Quantitative real-time reverse transcription polymerase chain reaction showed that TGF-β1 mRNA were upregulated in all surgical groups (1.59 ± 0.33 vs. 1.45 ± 0.34 vs. 1.48 ± 0.48, P > 0.05). Western blot revealed that the expressions of TGF-β1, TGF-β receptor I, Smad2/3, Smad4 and Smad7 were positive in the aortic tissues of all three investigated groups. Of the quantitative relative grayscales, a significant reverse correlation was noted between TGF-β1 and Smad2/3 (Y = -0.8552X + 1.6417, r = -0.759, P < 0.0001), and a close direct correlation between Smad4 and Smad7 (Y = 0.5905X + 0.2805, r = 0.781, P < 0.0001) in the Aortic Dissection Group. In the Aortic Aneurysm Group, Smad4 and Smad7 were also closely correlated (Y = 0.5228X + 0.1642, r = 0.727, P = 0.026), and in the Coronary Artery Disease Group, TGF-β1 and Smad7 were much significantly correlated (Y = 0.5301X + 0.5758, r = 0.917, P = 0.004). By enzyme-linked immunosorbent assay, TGF-β1 level of the aortic tissue was lower in the aortic dissection than in the aortic aneurysm and coronary artery disease groups with no statistical significance (319.52 ± 129.21 pg/mg protein vs. 324.09 ± 49.70 pg/mg protein vs. 304.15 ± 29.39 pg/mg protein, P > 0.05). The plasma TGF-β1 levels were 1158.30 ± 11.54 pg/ ml, 1170.27 ± 8.26 pg/ml, 1225.00 ± 174.42 pg/mL and 1160.25 ± 13.01 pg/mL in the four groups, respectively, showing significant intergroup differences (P < 0.05). No significant correlation was found between the aortic or plasma TGF-β1 levels and the time interval from the onset to surgery or the maximal dimensions of the aorta in the patients of the aortic dissection group. Aortic dissection, aortic aneurysm and atheroslerosis might be associated with an enhanced TGF β/Smad signaling function, with aortic dissection exhibiting a less prominent upregulation. It might have implications for downstream signal activation presumably translating into matrix degradation in the condition of aortic dissection in comparison to matrix deposition in aortic aneurysm and coronary artery disease.

Commentary: We still do not know what we do not know

Introduction: Marfans (MFS) and Ehlers Danlos syndrome (EDS) predispose patients to acute aortic dissections and aneurysms. Given their low incidence, there are limited large cohort data on mortality. Hypothesis: Type of connective tissue disorder will predict mortality in patients with Marfans or Ehlers Danlos Syndrome. Methods: The National Inpatient Sample (NIS) was reviewed for adults (&gt;18 years) with MFS and EDS between 2010-2017 via ICD9 and 10 diagnosis codes. Procedure codes were used to distinguish patients undergoing open aortic repair or TEVAR (thoracic endovascular aortic repair) for either a type A aortic dissection or an aortic aneurysm. NIS weights were used to project the 20% NIS volume to national volumes. Univariable logistic regression was used to determine independent predictors of mortality. Results: A total of 19,567 patients were identified. The incidence of MFS and EDS was 18 and 22.4 per 100k, respectively. After applying the inclusion criteria, there were 2,553 MFS and 180 EDS patients. EDS patients were more likely older (50 vs 42, P&lt;0.001) and women (47% vs 33%, P&lt;0.001). MFS patients were more likely to have a type A aortic dissection (44% vs 31%, P&lt;0.001). However, in the total cohort, aortic aneurysm was more frequent (56%). EDS patients were more likely to undergo TEVAR (2.8% vs 1.0%, P=0.03). MFS patients were more likely to have a complication of acute kidney injury (P=0.02) whereas EDS patients were more likely to have bowel ischemia (P=0.05). The majority of patients (89%) were treated at urban teaching hospitals. There was no statistical difference in mortality between the MFS and EDS cohorts (4.6% vs 2.8%, P=0.26). In logistic regression for death, aortic aneurysm (HR 0.14, P&lt;0.001) and elective admission (OR 0.28, P=0.003) were protective for death whereas aortic dissection was a predictor for mortality (OR 7.31, P&lt;0.001). Type of connective tissue disease or sex were not significant predictors. Conclusions: National level estimates show low mortality for patients with MFS and EDS presenting to the hospital with an aortic dissection or aneurysm. Differences in age and sex can guide aortic surveillance for these patient populations, leading to potentially decreased risk of acute aortic dissections and hospital mortality.

Vascular endothelial growth factor pathway inhibitors (VPIs) pose a concern for aortic aneurysm (AA) and aortic dissection (AD), signaling potential vascular disease development. To investigate VPI-associated AA and AD. This case-control study with a nested design used full population data from a national claims database in Taiwan between 2011 and 2019. Eligible participants were aged 20 years or older with kidney, hepatic, gastrointestinal, or pancreatic cancer diagnosed between January 1, 2012, and December 31, 2019. The first cancer diagnosis date was defined as the cohort entry date. Cases were patients who received a diagnosis of AA or AD in hospitalizations or emergency visits between the cohort entry date and December 31, 2019. Controls were matched by ratio (up to 1:5) based on age, sex, cancer type, cohort entry date, and the index date (ie, the first AA or AD event date). Data analysis was performed between January 2022 and December 2023. Use of the oral VPIs sorafenib, sunitinib, and pazopanib between cohort entry date and index date. In the primary analysis, AA and AD were evaluated compositely, while in the secondary analyses, they were evaluated separately. Adjusted odds ratios (aORs) were calculated using conditional logistic regression to assess the association with VPI use (sorafenib, sunitinib, and pazopanib) considering various VPI exposure windows and cumulative use. A total of 1461 cases were included (mean [SD] age, 73.0 [12.3] years; 1118 male patients [76.5%]), matched to 7198 controls. AA or AD risk increased with a VPI exposure of 100 days or less before the index date (aOR, 2.10; 95% CI, 1.40-3.15), mainly from VPI-associated AD (aOR, 3.09; 95% CI, 1.77-5.39). Longer VPI duration (68 days or more: aOR, 2.64; 95% CI, 1.66-4.19) and higher cumulative dose (61 or more defined daily doses: aOR, 2.65; 95% CI, 1.66-4.23) increased the risk. The use of the 3 study VPIs (sorafenib, sunitinib, and pazopanib) was associated with an increased risk of AA and AD in patients with cancer, essentially all of the risk from VPI-associated AD. Future studies are needed to determine the risk factors of VPI-associated AA and AD, as well as to establish a class effect.