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Extracranial carotid and vertebral artery dissection is an important cause of stroke, especially in young people. In some observational studies it has been associated with a high risk of recurrent stroke. Both antiplatelet drugs and anticoagulant drugs are used to reduce risk of stroke but whether one treatment strategy is more effective than the other is unknown. We compared their efficacy in the Cervical Artery Dissection in Stroke Study (CADISS), with the additional aim of establishing the true risk of recurrent stroke. We did this randomised trial at hospitals with specialised stroke or neurology services (39 in the UK and seven in Australia). We included patients with extracranial carotid and vertebral dissection with onset of symptoms within the past 7 days. Patients were randomly assigned (1:1) by an automated telephone randomisation service to receive antiplatelet drugs or anticoagulant drugs (specific treatment decided by the local clinician) for 3 months. Patients and clinicians were not masked to allocation, but investigators assessing endpoints were. The primary endpoint was ipsilateral stroke or death in the intention-to-treat population. The trial was registered with EUDract (2006-002827-18) and ISRN (CTN44555237). We enrolled 250 participants (118 carotid, 132 vertebral). Mean time to randomisation was 3·65 days (SD 1·91). The major presenting symptoms were stroke or transient ischaemic attack (n=224) and local symptoms (headache, neck pain, or Horner's syndrome; n=26). 126 participants were assigned to antiplatelet treatment versus 124 to anticoagulant treatment. Overall, four (2%) of 250 patients had stroke recurrence (all ipsilateral). Stroke or death occurred in three (2%) of 126 patients versus one (1%) of 124 (odds ratio [OR] 0·335, 95% CI 0·006–4·233; p=0·63). There were no deaths, but one major bleeding (subarachnoid haemorrhage) in the anticoagulant group. Central review of imaging failed to confirm dissection in 52 patients. Preplanned per-protocol analysis excluding these patients showed stroke or death in three (3%) of 101 patients in the antiplatelet group versus one (1%) of 96 patients in the anticoagulant group (OR 0·346, 95% CI 0·006–4·390; p=0·66). We found no difference in efficacy of antiplatelet and anticoagulant drugs at preventing stroke and death in patients with symptomatic carotid and vertebral artery dissection but stroke was rare in both groups, and much rarer than reported in some observational studies. Diagnosis of dissection was not confirmed after review in many cases, suggesting that radiographic criteria are not always correctly applied in routine clinical practice. Stroke Association.

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.

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.

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.

Acute Type A aortic dissection (ATAAD) is a catastrophic cardiovascular emergency with high mortality and few treatment options. Diagnostic biomarkers or targeted treatments remain in the rudimentary stage, complicating early detection and intervention. The aim is to discover novel diagnostic and therapeutic biomarkers for ATAAD through integrated bioinformatics and experimental validation. Differentially expressed genes (DEGs) were identified using the \"limma\" package in R, applying the combined, normalized, and batch-effect-corrected microarray datasets GSE52093 and GSE98770. Functional enrichment analyses (GO and KEGG), protein-protein interaction (PPI) network construction, and weighted gene coexpression network analysis (WGCNA) were performed to identify key genes. Key genes were validated by qPCR, immunofluorescence, and functional assays in human aortic smooth muscle cells (HASMCs) and an independent dataset (GSE153434). There were 441 DEGs with 164 upregulated and 277 downregulated genes. These hub genes also overlapped with four key genes (DPT, ITGA5, HGF, and PLAUR) in the key WGCNA module. Of these, DPT was downregulated compared with ATAAD tissues. DPT knockdown induced HASMC migration and inhibited HASMC proliferation, as assessed by functional assays. The diagnostic potential of these genes, especially of DPT, was confirmed using ROC analysis. DPT is a promising diagnostic and therapeutic biomarker for ATAAD. Downregulation may also disturb extracellular matrix homeostasis and smooth muscle cell function, leading to aortic wall instability. These findings provide a foundation for future research on DPT-targeted interventions for ATAAD.

Background During total aortic arch replacement surgery (TARS) for patients with acute type A aortic dissection, the organs in the lower body, such as the viscera and spinal cord, are at risk of ischemia even when antegrade cerebral perfusion (ACP) is performed. Combining ACP with retrograde inferior vena caval perfusion (RIVP) during TARS may improve outcomes by providing the lower body with oxygenated blood. Methods This study is designed as a multicenter, computer-generated, randomized controlled, assessor-blind, parallel-group study with a superiority framework in patients scheduled for TARS. A total of 636 patients will be randomized on a 1:1 basis to a moderate hypothermia circulatory arrest (MHCA) group, which will receive selective ACP with moderate hypothermia during TARS; or to an RIVP group, which will receive the combination of RIVP and selective ACP under moderate hypothermia during TARS. The primary outcome will be a composite of early mortality and major complications, including paraplegia, postoperative renal failure, severe liver dysfunction, and gastrointestinal complications. All patients will be analyzed according to the intention-to-treat protocol. Discussion This study aims to assess whether RIVP combined with ACP leads to superior outcomes than ACP alone for patients undergoing TARS under moderate hypothermia. This study seeks to provide high-quality evidence for RIVP to be used in patients with acute type A aortic dissection undergoing TARS. Trial registration Clinicaltrials.gov, ID: NCT03607786 . Registered on 30 July 2018.

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.

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.

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.