Explore the vast range of titles available.

Objectives This study aims to retrospectively analyze the clinical features of Stanford type A acute aortic dissection (TAAAD) based on Sun’s modified classification, and to investigate whether the Sun’s modified classification can be used to assess the risk of preoperative rupture. Methods Clinical data was collected between January 2018 and June 2019. Data included patient demographics, history of disease, type of dissection according to the Sun’s modified classification, time of onset, biochemical tests, and preoperative rupture. Results A total of 387 patients with TAAAD who met the inclusion criteria of Sun’s modified classification were included. There were more complex types, with 75, 151 and 140 patients in the type A1C, A2C and A3C groups, respectively. The age of the entire group of patients was 51.46 ± 12.65 years and 283 (73.1%) were male. The time from onset to the emergency room was 25.37 ± 30.78 h. There were a few cases of TAAAD combined with stroke, pericardial effusion, pleural effusion, and lower extremity and organ ischemia in the complex type group. The white blood cell count (WBC), neutrophil count (NEC) and blood amylase differed significantly between the groups. Three independent risk factors for preoperative rupture were identified: neutrophil count, blood potassium ion level, and platelet count. Binary logistic regression analysis showed that the Sun’s modified classification could not be used to assess the risk of preoperative rupture in TAAAD. Conclusion TAAAD was classified as the complex type in most patients. WBC, NEC and blood amylase were significantly different between the groups. NEC and serum potassium ion level were independent risk factors for preoperative rupture of TAAAD, while platelet count was its protective factor. More samples are needed to determine whether Sun’s modified classification can be used to evaluate the risk of preoperative rupture.

Acute aortic dissection (AAD) is a life-threatening cardiovascular emergency characterized by aortic layer separation and false lumen formation, with high mortality rates. Emerging evidence highlights the critical role of innate immunity in AD pathogenesis. Innate immune activation drives AAD progression through multiple mechanisms, including macrophage polarization (M1/M2 imbalance), neutrophil extracellular trap (NET) formation, and inflammasome activation. These processes amplify vascular inflammation via cytokine storms (IL-1β, IL-6, TNF-α) and oxidative stress, further promoting matrix metalloproteinase activation and smooth muscle cell phenotypic switching. The cGAS-STING pathway, triggered by mitochondrial DNA release, and TLR signaling act as central hubs connecting vascular injury to innate immune responses. This review synthesizes recent advances in the molecular mechanisms of AAD, focusing on aortic wall structural alterations, dysregulated signaling pathway, including TGF-β, Ang II, STING, and TLR cascades, and immune-inflammatory responses mediated by innate immune components. A deeper understanding of these innate immune components may lead to improved diagnostic biomarkers and targeted therapies for AAD management.

Background Acute aortic dissection (AAD) is a life-threatening cardiovascular emergency frequently associated with misdiagnosis and delayed treatment. This paper aims to illustrate the diagnostic challenges of AAD in rehabilitation settings by presenting a case with atypical musculoskeletal symptoms and emphasize the importance of considering vascular emergencies with literature review. Methods A 46-year-old male presented to a rehabilitation center with migrating right shoulder pain and proximal weakness. Initial complaint suggested a musculoskeletal disorder; however, further evaluation revealed hypertension, tachycardia, and migratory, intensifying pain. A subsequent computed tomography angiography confirmed AAD. The patient underwent urgent Sun’s procedure, including ascending aorta and total arch replacement with stented elephant trunk implantation, which was followed by multidisciplinary rehabilitation due to the secondary ischemic stroke. Results The patient’s early symptoms closely mimicked musculoskeletal disorders, which delayed his prioritization of seeking medical service. After cardiovascular evaluation and successful aortic repair, the AAD was stabilized. However, he later developed right-sided hemiplegia as a secondary complication and was referred back for neurological rehabilitation, which included repetitive task training, robot-assisted therapy, and functional electrical stimulation. Three months post-surgery, he demonstrated significant functional recovery, with Fugl-Meyer Assessment scores improving from 12/66 to 58/66 for the upper extremity and from 17/34 to 32/34 for the lower extremity. Conclusion This case and literature review highlight the diagnostic challenges of AAD presenting as musculoskeletal pain and underscores the need for rehabilitation specialists to maintain a broad differential diagnosis. A high index of suspicion is essential for early recognition and timely referral, especially in patients with overlapping symptoms and vascular risk factors. Impact This case adds to the limited body of evidence on AAD presenting with musculoskeletal complaints and may serve to raise clinical awareness. Further studies, including case series and systematic investigations, are needed to better characterize such atypical presentations and guide diagnostic pathways in rehabilitation settings.

A congenitally malformed aortic valve, unicuspid (UAV), or bicuspid (BAV), occurs in about 1% of the population and is known to be more frequent in patients with aortic dissection. The clinical and operative findings in a series of 134 patients with spontaneous, acute type A aortic dissection were studied, comparing patients with normal and abnormal aortic valve morphology. The aortic valve was normal in 123 of 134 (92%) patients and abnormal in 11 of 134 (8%) patients: BAV in 10 of 134 (7.5%) and UAV in 1 of 134 (0.7%). Demographics were similar between groups, except for a lower frequency of systemic hypertension in the UAV/BAV group (46 vs 82%, p <0.01). The University of Pennsylvania malperfusion class stratification was also similar in the 2 groups. The UAV/BAV group had a greater frequency of aortic root aneurysm (64 vs 18%, p <0.01) and a larger median root diameter (5.7 vs 4.6 cm, p = 0.02). In the UAV/BAV group, the entry tear was more frequently in proximal (intrapericardial) zone 0 (91 vs 62%, p = 0.049). The frequency of abnormal aortic media histology was similar. The rate of root replacement was higher in the UAV/BAV group and early mortality was similar. The frequency of congenitally malformed aortic valve in this series was 8 times higher than in the normal population. The 1 UAV in the series was the only severely stenotic valve. In patients with type A aortic dissection with a congenitally malformed valve, aortic root aneurysm was more common and the entry tear was nearly always proximal.

Protein lactylation, a novel post-translational modification (PTM), has emerged as a critical factor in disease processes related to glycolysis and immune responses. However, its role in aortic dissection (AD) has yet to be thoroughly investigated. This study aimed to investigate the involvement of protein lactylation in AD and identify key lactylation-related genes as potential diagnostic biomarkers. Transcriptomic data from public databases were analyzed to identify differentially expressed lactylation-related genes in AD. Functional enrichment analyses were performed, and Weighted Gene Co-expression Network Analysis (WGCNA) was utilized to identify gene modules associated with AD. Machine learning methods, including LASSO and Random Forest, were employed to identify key diagnostic genes. Experimental validation was performed using human aortic tissues and an AD model. Bioinformatics analysis identified 11 lactylation-related differentially expressed genes (LR-DEGs) in AD. WGCNA and machine learning revealed two optimal feature genes, PGK1 and HMGA1, which were validated in an independent dataset and demonstrated high diagnostic accuracy (AUC: PGK1 = 1, HMGA1 = 0.94). Immune infiltration analysis indicated significant correlations between these genes and specific immune cell types, suggesting a role in immune regulation. Experimental validation in human and murine AD tissues confirmed the upregulation of PGK1 and HMGA1. This study underscores the importance of lactylation in the pathogenesis of AD and identifies PGK1 and HMGA1 as key biomarkers related to lactylation. These findings enhance our understanding of the metabolic and immune mechanisms involved in AD, thereby presenting new molecular targets for diagnosis and therapeutic intervention.

BackgroundAcute aortic dissection (AD) in pregnancy poses a lethal risk to both mother and fetus. However, well-established therapeutic guidelines are lacking. This study aimed to investigate clinical features, outcomes and optimal management strategies for pregnancy-related AD.MethodsWe conducted a retrospective multicentre cohort study including 67 women with acute AD during pregnancy or within 12 weeks postpartum from three major cardiovascular centres in China between 2003 and 2021. Patient characteristics, management strategies and short-term outcomes were analysed.ResultsMedian age was 31 years, with AD onset at median 32 weeks gestation. Forty-six patients (68.7%) had type A AD, of which 41 underwent immediate surgery. Overall maternal mortality was 10.4% (7/67) and fetal mortality was 26.9% (18/67). Compared with immediate surgery, selective surgery was associated with higher risk of composite maternal and fetal death (adjusted RR: 12.47 (95% CI 3.26 to 47.73); p=0.0002) and fetal death (adjusted RR: 8.77 (95% CI 2.33 to 33.09); p=0.001).ConclusionsImmediate aortic surgery should be considered for type A AD at any stage of pregnancy or postpartum. For pregnant women with AD before fetal viability, surgical treatment with the fetus in utero should be considered. Management strategies should account for dissection type, gestational age, and fetal viability.Trial registration number NCT05501145.

Currently, evidence concerning the link between maximal aortic diameter and in-hospital mortality in cases of acute type B aortic dissection (ATBAD) is insufficient. Thus, this study aimed to explore the relationship between the maximal aortic diameter at the time of admission and the early prognosis of patients diagnosed with ATBAD. A total of 678 patients with ATBAD were included between January 2016 and December 2018, during which their clinical data was gathered. The independent variable analyzed was the maximal diameter of the aorta, while the dependent variable was mortality during hospitalization. Factors considered in this analysis included the patients’ age, gender, body mass index (BMI), medical history of hypertension, stroke, diabetes, atherosclerosis, smoking habits, chronic kidney insufficiency, time until presentation, systolic and diastolic blood pressures, ejection fraction, presence of aortic regurgitation, symptoms, involvement of abdominal vessels, laboratory findings, and treatment approaches. Of these patients collected, the mean age was 56.03 ± 12.22 years, and approximately 82.45% of them were male. After analysis, it was found that the maximal aortic diameter of patients with ATBAD was positively correlated with in-hospital mortality (OR = 1.06, 95% CI 1.03 to 1.10). Surprisingly, a J curve relationship was detected between maximal aortic diameter (point 31 mm) and in-hospital death for patients with ATBAD. The effect sizes and confidence intervals of the right (maximal aortic diameter > 31 mm) and left (maximal aortic diameter ≤ 31 mm) aspects of the inflection point were 1.06 (1.02–1.11) and 1.03 (0.83–1.28), respectively. In addition, the stratified analysis showed a stable relationship between maximal aortic diameter and in-hospital mortality, while there was no significant difference in the interaction between different subgroups. In patients with ATBAD, a J-curve relationship was identified between the maximal aortic diameter and in-hospital mortality. Specifically, when the maximal aortic diameter exceeds 31 mm, a positive correlation with in-hospital death was observed.

Ascending thoracic aortic aneurysm (ATAA) remains a significant medical concern, with its asymptomatic nature posing diagnostic and monitoring challenges, thereby increasing the risk of aortic wall dissection and rupture. Current management of aortic repair relies on an aortic diameter threshold. However, this approach underestimates the complexity of aortic wall disease due to important knowledge gaps in understanding its underlying pathologic mechanisms.Since traditional risk factors cannot explain the initiation and progression of ATAA leading to dissection, local vascular factors such as extracellular matrix (ECM) and vascular smooth muscle cells (VSMCs) might harbor targets for early diagnosis and intervention. Derived from diverse embryonic lineages, VSMCs exhibit varied responses to genetic abnormalities that regulate their contractility. The transition of VSMCs into different phenotypes is an adaptive response to stress stimuli such as hemodynamic changes resulting from cardiovascular disease, aging, lifestyle, and genetic predisposition. Upon longer exposure to stress stimuli, VSMC phenotypic switching can instigate pathologic remodeling that contributes to the pathogenesis of ATAA.This review aims to illuminate the current understanding of cellular and molecular characteristics associated with ATAA and dissection, emphasizing the need for a more nuanced comprehension of the impaired ECM–VSMC network.

Background The purpose of this study was to assess the relationship between admission inflammatory indexes neutrophil-to-lymphocyte ratio (NLR), monocyte-to-lymphocyte ratio (MLR), and systemic immune-inflammation index (SII), and the risk of in-hospital all-cause mortality in acute aortic dissection (AAD) patients. Methods A retrospective analysis was conducted on 597 AAD patients (Stanford classification: Stanford type A 365 patients, Stanford type B 232 patients) at a single center. Outcomes were the incidence of in-hospital all-cause mortality. The risk of all-cause death was compared between the groups with low and high inflammatory indexes using the Kaplan-Meier curve. The association between admission inflammatory indexes and outcomes was evaluated using the Cox regression model and restricted cubic splines (RCS). Stratified analysis was performed based on AAD type, age (< 50 years or ≥ 50 years), and gender. Results The Kaplan-Meier curves revealed statistically significant differences in outcomes among the low and high inflammatory indexes groups. Cox regression analysis revealed that the in-hospital mortality risk was significantly high in the high inflammatory index groups. MLR was the strongest associated with in-hospital mortality risk. The RCS curve revealed that NLR was non-linearly and J-shaped correlated with in-hospital mortality, and MLR and SII were linearly correlated with in-hospital mortality. Stratified analysis showed interactions between NLR, MLR, and SII and AAD type and age for the risk of in-hospital mortality. Conclusion Admission high inflammatory indexes were independently associated with an increased risk of in-hospital all-cause mortality in AAD patients. The inflammatory indexes NLR, MLR, and SII may be useful indicators for predicting in-hospital all-cause mortality in AAD patients.

Objectives To investigate the short-term/long-term impact of pulmonary artery intramural hematoma (PA-IMH) in patients with acute Stanford type A aortic dissection (ATAAD) following surgical repair. Materials and methods Consecutive patients with ATAAD who received surgical repair at Beijing and Yunnan Fuwai Hospital in 2010–2021 were retrospectively reviewed. Patients with hemorrhage extending along the PA were identified as the PA-IMH group. Multivariable logistics regression was used to obtain the odds ratio (OR), and the Kaplan-Meier method was used to estimate the survival rate. Results Of the 2046 ATAAD patients, 324 (15.8%) patients were identified with PA-IMH, and 1722 (84.2%) were without PA-IMH. PA-IMH had a higher prevalence in patients with older age, female gender, aortic IMH, and type II aortic dissection. PA-IMH patients incurred excess early mortality compared with non-PA-IMH patients (9.3% vs. 5.6%, OR = 1.86, 95%CI 1.19–2.91, p  = 0.006). The results were stable in the subgroup analysis, with an increased risk in older (> 70 years) or DeBakey type II ATAAD patients. Notably, an increase in the degree and extent of PA-IMH exacerbated the risk of early mortality. However, after landmark analysis at 30-day postsurgery, no significant difference was noted in the long-term outcomes between PA-IMH and non-PA-IMH groups ( p  = 0.440). The 5-year survival rates were 87.1% (95%CI: 83.3%, 91.1%) and 90.1% (95%CI: 88.5%, 91.7%), respectively. Conclusions The presence of PA-IMH in ATAAD patients is common and is independently associated with increased early mortality after surgical repair, especially in those with older age (> 70) or type II dissection. However, such detrimental effects do not persist in the long-term follow-up among patients who survived hospital discharge. Clinical relevance statement We confirmed that PA-IMH significantly increases early postoperative mortality in patients with acute type A aortic dissection, especially in older patients or DeBakey type II dissection. This should prompt further investigation of the incremental role of PA-IMH in this pathology. Key Points Acute type A aortic dissection mortality gets worse when pulmonary artery intramural hematoma is present. Pulmonary artery-intramural hematoma increased the risk of early mortality but not affect long-term prognosis. Further research should investigate the effects of pulmonary artery intramural thrombus on aortic dissection.