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Multimedia Manual of Cardiothoracic... May 2024A 72-year-old male with a history of a triple-vessel coronary artery bypass graft years ago presented with a DeBakey type 2 aortic dissection and an aorto-left atrial...
A 72-year-old male with a history of a triple-vessel coronary artery bypass graft years ago presented with a DeBakey type 2 aortic dissection and an aorto-left atrial fistula with patent bypass grafts (left internal mammary artery and saphenous vein grafts). He developed pulmonary oedema and required intubation. The right axillary artery was cannulated. After the ascending aorta and left internal mammary artery were clamped, the aorta was transected, leaving aortic tissue around two saphenous vein grafts as two separate patches. An entry tear was found adjacent to the proximal anastomosis of the saphenous vein graft to the posterior descending artery. A fistula, which was located between a false lumen in the non-coronary sinus and the dome of the left atrium, was primarily closed. Because the adventitia was thinned out in the non-coronary sinus due to aortic dissection, partial aortic root remodelling was performed with resuspension of the commissures. Hemiarch repair was performed under moderate hypothermia and unilateral antegrade cerebral perfusion. After systemic perfusion was resumed, the locations of the saphenous vein graft buttons were determined. The ascending graft was cross-clamped again; the saphenous vein graft to the obtuse marginal branch graft was reimplanted using the Carrel patch technique while a saphenous vein graft to the posterior descending artery required interposition of a 10-mm Dacron graft to accommodate the length.
Topics: Humans; Male; Aged; Heart Atria; Aortic Dissection; Coronary Artery Bypass; Vascular Fistula; Fistula; Reoperation; Aortic Aneurysm, Thoracic; Saphenous Vein
PubMed: 38695663
DOI: 10.1510/mmcts.2024.002 -
Annals of the Rheumatic Diseases Apr 2024Giant cell arteritis (GCA), the most common systemic vasculitis, is characterised by aberrant interactions between infiltrating and resident cells of the vessel wall.... (Review)
Review
Giant cell arteritis (GCA), the most common systemic vasculitis, is characterised by aberrant interactions between infiltrating and resident cells of the vessel wall. Ageing and breach of tolerance are prerequisites for GCA development, resulting in dendritic and T-cell dysfunction. Inflammatory cytokines polarise T-cells, activate resident macrophages and synergistically enhance vascular inflammation, providing a loop of autoreactivity. These events originate in the adventitia, commonly regarded as the biological epicentre of the vessel wall, with additional recruitment of cells that infiltrate and migrate towards the intima. Thus, GCA-vessels exhibit infiltrates across the vascular layers, with various cytokines and growth factors amplifying the pathogenic process. These events activate ineffective repair mechanisms, where dysfunctional vascular smooth muscle cells and fibroblasts phenotypically shift along their lineage and colonise the intima. While high-dose glucocorticoids broadly suppress these inflammatory events, they cause well known deleterious effects. Despite the emerging targeted therapeutics, disease relapse remains common, affecting >50% of patients. This may reflect a discrepancy between systemic and local mediators of inflammation. Indeed, temporal arteries and aortas of GCA-patients can show immune-mediated abnormalities, despite the treatment induced clinical remission. The mechanisms of persistence of vascular disease in GCA remain elusive. Studies in other chronic inflammatory diseases point to the fibroblasts (and their lineage cells including myofibroblasts) as possible orchestrators or even effectors of disease chronicity through interactions with immune cells. Here, we critically review the contribution of immune and stromal cells to GCA pathogenesis and analyse the molecular mechanisms by which these would underpin the persistence of vascular disease.
PubMed: 38684323
DOI: 10.1136/ard-2023-225270 -
Gastrointestinal Endoscopy Apr 2024
PubMed: 38657841
DOI: 10.1016/j.gie.2024.04.023 -
Vascular Apr 2024Assessment of plaque stenosis severity allows better management of carotid source of stroke. Our objective is to create a deep learning (DL) model to segment carotid...
OBJECTIVES
Assessment of plaque stenosis severity allows better management of carotid source of stroke. Our objective is to create a deep learning (DL) model to segment carotid intima-media thickness and plaque and further automatically calculate plaque stenosis severity on common carotid artery (CCA) transverse section ultrasound images.
METHODS
Three hundred and ninety images from 376 individuals were used to train (235/390, 60%), validate (39/390, 10%), and test (116/390, 30%) on a newly proposed CANet model. We also evaluated the model on an external test set of 115 individuals with 122 images acquired from another hospital. Comparative studies were conducted between our CANet model with four state-of-the-art DL models and two experienced sonographers to re-evaluate the present model's performance.
RESULTS
On the internal test set, our CANet model outperformed the four comparative models with Dice values of 95.22% versus 90.15%, 87.48%, 90.22%, and 91.56% on lumen-intima (LI) borders and 96.27% versus 91.40%, 88.94%, 91.19%, and 92.88% on media-adventitia (MA) borders. On the external test set, our model still produced excellent results with a Dice value of 92.41%. Good consistency of stenosis severity calculation was observed between CANet model and experienced sonographers, with Intraclass Correlation Coefficient (ICC) of 0.927 and 0.702, Pearson's Correlation Coefficient of 0.928 and 0.704 on internal and external test set, respectively.
CONCLUSIONS
Our CANet model achieved excellent performance in the segmentation of carotid IMT and plaques as well as automated calculation of stenosis severity.
PubMed: 38656244
DOI: 10.1177/17085381241246312 -
Revista Da Associacao Medica Brasileira... 2024
Topics: Humans; Adventitia; Cysts; Popliteal Artery
PubMed: 38656014
DOI: 10.1590/1806-9282.20231482 -
Journal of Veterinary Diagnostic... Jul 2024A 57-y-old male yellow-naped parrot () was presented because of lethargy, inappetence, and weight loss. Hematology and serum biochemistry were unremarkable, and imaging...
A 57-y-old male yellow-naped parrot () was presented because of lethargy, inappetence, and weight loss. Hematology and serum biochemistry were unremarkable, and imaging revealed a mass in the distal esophagus at the coelomic inlet. The luminal diameter of the esophagus was reduced in this area, and passage of ingesta was limited. Following gavage feeding, the patient died and was submitted for autopsy. At postmortem examination, the noted mass effect was a thickening of the distal esophagus with adherent, coalescing, soft, pale-tan plaques on the mucosal surface. Additional gross findings included pale-tan, opaque feed material oozing from the dorsum of the lungs and covering the cranial air sacs. Histology of the esophagus, esophageal-proventricular junction, and proximal proventriculus revealed an unencapsulated, infiltrative, transmural neoplasm that extended from the mucosal surface deep into the muscularis, almost to the adventitia. The neoplasm was composed of cuboidal cells arranged in islands and tubules, consistent with an adenocarcinoma, a rarely reported entity in the esophagus of psittacine birds and to our knowledge not reported previously at the esophageal-proventricular junction.
Topics: Animals; Male; Bird Diseases; Esophageal Neoplasms; Adenocarcinoma; Fatal Outcome; Proventriculus; Amazona; Parrots; Esophagus
PubMed: 38653775
DOI: 10.1177/10406387241247282 -
Current Medical Imaging Apr 2024The incidence of stroke is rising, and it is the second major cause of mortality and the third leading cause of disability around the globe. The goal of this study was...
BACKGROUND AND OBJECTIVE
The incidence of stroke is rising, and it is the second major cause of mortality and the third leading cause of disability around the globe. The goal of this study was to rapidly and accurately identify carotid plaques and automatically quantify plaque burden using our automated tracking and segmentation US-video system.
METHODS
We collected 88 common carotid artery transection videos (11048 frames) with a history of atherosclerosis or risk factors for atherosclerosis, which were randomly divided into training, test, and validation sets using a 6:3:1 ratio. We first trained different segmentation models to segment the carotid intima and adventitia, and calculate the maximum plaque burden automatically. Finally, we statistically analyzed the plaque burden calculated automatically by the best model and the results of manual labeling by senior sonographers.
RESULTS
Of the three Artificial Intelligence (AI) models, the Robust Video Matting (RVM) segmentation model's carotid intima and adventitia Dice Coefficients (DC) were the highest, reaching 0.93 and 0.95, respectively. Moreover, the RVM model has shown the strongest correlation coefficient (0.61±0.28) with senior sonographers, and the diagnostic effectiveness between the RVM model and experts was comparable with paired-t test and Bland-Altman analysis [P= 0.632 and ICC 0.01 (95% CI: -0.24~0.27), respectively].
CONCLUSION
Our findings have indicated that the RVM model can be used in ultrasound carotid video. The RVM model can automatically segment and quantify atherosclerotic plaque burden at the same diagnostic level as senior sonographers. The application of AI to carotid videos offers more precise and effective methods to evaluate carotid atherosclerosis in clinical practice.
PubMed: 38639284
DOI: 10.2174/0115734056296233240401061756 -
Frontiers in Physiology 2024Redox processes can modulate vascular pathophysiology. The endoplasmic reticulum redox chaperone protein disulfide isomerase A1 (PDIA1) is overexpressed during vascular...
Redox processes can modulate vascular pathophysiology. The endoplasmic reticulum redox chaperone protein disulfide isomerase A1 (PDIA1) is overexpressed during vascular proliferative diseases, regulating thrombus formation, endoplasmic reticulum stress adaptation, and structural remodeling. However, both protective and deleterious vascular effects have been reported for PDIA1, depending on the cell type and underlying vascular condition. Further understanding of this question is hampered by the poorly studied mechanisms underlying PDIA1 expression regulation. Here, we showed that PDIA1 mRNA and protein levels were upregulated (average 5-fold) in the intima and media/adventitia following partial carotid ligation (PCL). Our search identified that miR-204-5p and miR-211-5p (miR-204/211), two broadly conserved miRNAs, share PDIA1 as a potential target. MiR-204/211 was downregulated in vascular layers following PCL. In isolated endothelial cells, gain-of-function experiments of miR-204 with miR mimic decreased PDIA1 mRNA while having negligible effects on markers of endothelial activation/stress response. Similar effects were observed in vascular smooth muscle cells (VSMCs). Furthermore, PDIA1 downregulation by miR-204 decreased levels of the VSMC contractile differentiation markers. In addition, PDIA1 overexpression prevented VSMC dedifferentiation by miR-204. Collectively, we report a new mechanism for PDIA1 regulation through miR-204 and identify its relevance in a model of vascular disease playing a role in VSMC differentiation. This mechanism may be regulated in distinct stages of atherosclerosis and provide a potential therapeutic target.
PubMed: 38638277
DOI: 10.3389/fphys.2024.1327794 -
Cardiovascular Pathology : the Official... 2024Exertional dyspnea has been documented in US military personnel after deployment to Iraq and Afghanistan. We studied whether continued exertional dyspnea in this patient...
Exertional dyspnea has been documented in US military personnel after deployment to Iraq and Afghanistan. We studied whether continued exertional dyspnea in this patient population is associated with pulmonary vascular disease (PVD). We performed detailed histomorphometry of pulmonary vasculature in 52 Veterans with biopsy-proven post-deployment respiratory syndrome (PDRS) and then recruited five of these same Veterans with continued exertional dyspnea to undergo a follow-up clinical evaluation, including symptom questionnaire, pulmonary function testing, surface echocardiography, and right heart catheterization (RHC). Morphometric evaluation of pulmonary arteries showed significantly increased intima and media thicknesses, along with collagen deposition (fibrosis), in Veterans with PDRS compared to non-diseased (ND) controls. In addition, pulmonary veins in PDRS showed increased intima and adventitia thicknesses with prominent collagen deposition compared to controls. Of the five Veterans involved in our clinical follow-up study, three had borderline or overt right ventricle (RV) enlargement by echocardiography and evidence of pulmonary hypertension (PH) on RHC. Together, our studies suggest that PVD with predominant venular fibrosis is common in PDRS and development of PH may explain exertional dyspnea and exercise limitation in some Veterans with PDRS.
Topics: Humans; Male; Pulmonary Artery; Adult; Hypertension, Pulmonary; Middle Aged; Female; Afghan Campaign 2001-; Iraq War, 2003-2011; Pulmonary Veins; Dyspnea; Veterans; Case-Control Studies; Veterans Health; Biopsy; Fibrosis
PubMed: 38604505
DOI: 10.1016/j.carpath.2024.107640 -
American Journal of Respiratory and... Apr 2024Idiopathic Pulmonary Arterial Hypertension (IPAH) is characterized by extensive pulmonary vascular remodeling due to plexiform and obliterative lesions, media...
RATIONALE
Idiopathic Pulmonary Arterial Hypertension (IPAH) is characterized by extensive pulmonary vascular remodeling due to plexiform and obliterative lesions, media hypertrophy, inflammatory cell infiltration, and alterations of the adventitia.
OBJECTIVE
Test the hypothesis that microscopic IPAH vascular lesions express unique molecular profiles, which collectively are different from control pulmonary arteries.
METHODS
We used digital spatial transcriptomics to profile the genome-wide differential transcriptomic signature of key pathological lesions (plexiform, obliterative, intima+media hypertrophy, and adventitia) in IPAH lungs (n= 11) and compared these data to the intima+media and adventitia of control pulmonary artery (n=5).
RESULTS
We detected 8273 transcripts in the IPAH lesions and control lung pulmonary arteries. Plexiform lesions and IPAH adventitia exhibited the greatest number of differentially expressed genes when compared with intima-media hypertrophy and obliterative lesions. Plexiform lesions in IPAH showed enrichment for (i) genes associated with TGFβ-signaling and (ii) mutated genes affecting the extracellular matrix and endothelial-mesenchymal transformation. Plexiform lesions and IPAH adventitia showed upregulation of genes involved in immune and interferon signaling, coagulation, and complement pathways. Cellular deconvolution indicated variability in the number of vascular and inflammatory cells between IPAH lesions, which underlies the differential transcript profiling.
CONCLUSIONS
IPAH lesions express unique molecular transcript profiles enriched for pathways involving pathogenetic pathways, including genetic disease drivers, innate and acquired immunity, hypoxia sensing, and angiogenesis signaling. These data provide a rich molecular-structural framework in IPAH vascular lesions that inform novel biomarkers and therapeutic targets in this highly morbid disease.
PubMed: 38568479
DOI: 10.1164/rccm.202307-1310OC