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Interdisciplinary Cardiovascular and... Jun 2024Postoperative air leakage is a major complication of lung resection, particularly right upper lobectomy. However, various surgical procedures can reduce postoperative...
OBJECTIVES
Postoperative air leakage is a major complication of lung resection, particularly right upper lobectomy. However, various surgical procedures can reduce postoperative complications and shorten the drainage period. The current study aimed to analyze the utility of bronchus-first right upper lobectomy as an alternative routine procedure.
METHODS
We retrospectively analyzed the data of 225 (53.7%) patients who underwent bronchus-first right upper lobectomy and 194 (46.3%) patients who underwent the conventional bronchus-last right upper lobectomy at our institution from 2015 to 2022. In patients with incomplete fissures who underwent bronchus-first right upper lobectomy, the bronchus was dissected firstly, followed by the pulmonary artery and vein, then, the interlobar fissure was divided. We compared the outcomes of two procedures and analyzed the surgical utility of bronchus-first right upper lobectomy.
RESULTS
The surgical outcomes and postoperative morbidity comparing bronchus-first and bronchus-last procedure were as followed: median operation time (min) 103/126 (p < 0.001), median bleeding amount (mL) 28/55 (p = 0.003), incomplete lobulation rate (%) 35.1/24.2 (p = 0.02), incidence of prolonged air leakage (%) 2.2/3.1 (p = 0.76) and rate of fellow surgeon's operation (%) 28.0/4.6 (p < 0.001). The procedure was associated with a decreased incidence of prolonged air leakage. The 4-year overall survival rates did not significantly differ between the two groups (p = 0.24).
CONCLUSIONS
Bronchus-first right upper lobectomy can prevent postoperative air leakage in patients with incomplete fissure. Additionally, as an alternative routine procedure, it is associated with a shorter surgical duration and a lower volume of blood loss regardless of interlobar fissure and operator's experience.
PubMed: 38913868
DOI: 10.1093/icvts/ivae114 -
Heliyon Jun 2024Inferior vena cava filters have been shown to be effective in preventing deep vein thrombosis and its secondary complication, pulmonary embolism, thereby reducing the...
BACKGROUND AND OBJECTIVE
Inferior vena cava filters have been shown to be effective in preventing deep vein thrombosis and its secondary complication, pulmonary embolism, thereby reducing the high mortality rate. Although inferior vena cava filters have evolved, specific complications like inferior vena cava thrombosis-induced deep vein thrombosis worsening and recurrent pulmonary embolism continue to pose challenges. This study analyzes the effects of geometric parameter variations of inferior vena cava filters, which have a significant impact on the thrombus formation inside the filter, the capture, dissolution, and hemodynamic flow of thrombus, as well as the shear stress on the filter and vascular wall.
METHODS
This study used computational fluid dynamic simulations with the carreau model to investigate the impact of varying inferior vena cava filter design parameters (number of struts, strut arm length, and tilt angle) on hemodynamics.
RESULTS
Recirculation and stagnation areas due to flow velocity and pressure, along with wall shear stress values, were identified as key factors. It is important to find a balance between wall shear stress high enough to aid thrombolysis and low enough to prevent platelet activation. The results of this paper show that the risk of platelet activation and thrombus filtration may be lowest when the wall shear stress of the filter ranges from 0 to 4 [Pa], minimizing stress concentration within the filter.
CONCLUSION
16 arm struts with a length of 20 mm and a tilt angle of 0° provide the best balance between thrombus capture and minimization of hemodynamic disturbance. This configuration minimizes the size of the stagnation and recirculation zones while maintaining sufficient wall shear stress for thrombus dissolution.
PubMed: 38912484
DOI: 10.1016/j.heliyon.2024.e32667 -
The Indian Journal of Radiology &... Jul 2024The aim of this study was to examine the imaging manifestations of post-endoscopic retrograde cholangiopancreatography (ERCP) specific complications by computed...
The aim of this study was to examine the imaging manifestations of post-endoscopic retrograde cholangiopancreatography (ERCP) specific complications by computed tomography to aid in its early and successful diagnosis and timely intervention. Forty-one cases of imaging having post-ERCP were complications were retrospectively collected and the spectrum of complications and their key imaging features and methods to improve their detection were analyzed. The most common complication detected in computed tomography (CT) post-ERCP was the presence of intra-abdominal collections seen in 21 patients (51.2%). Pancreatitis was seen in 20 of 41 patients (48.7%), while bowel perforation was present in 9 patients (21%). Pleural effusion was present in 8 patients (19.5%), liver abscess in 6 patients (14.6%), cholangitis in 4 patients (9.7%), gallbladder perforation in 4 patients (9.7%), displaced common bile duct stent in 3 patients (7.3%), possibility of main pancreatic duct cannulation in 2 patients (4.8%), vascular injury resulting in right hepatic artery pseudoaneurysm in 1 patient (2.4%), thrombosis of portal vein or its branches in 2 patients (4.8%), superior mesenteric vein thrombosis in 1 patient (2.4%), right hepatic vein thrombosis in 1 patient (2.4%), pulmonary thromboembolism in 2 patients (4.8%), duodenal inflammation in 1 patient (2.4%), bowel ileus in 4 patients (9.6%), and bowel obstruction in 1 patient (2.4%). Complications after ERCP can cause significant morbidity and mortality if not diagnosed early and treated appropriately. Familiarity with normal findings post-ERCP and knowledge of the imaging appearance of these complications are vital in the early management of these conditions.
PubMed: 38912237
DOI: 10.1055/s-0044-1779585 -
APL Bioengineering Jun 2024Previous lung-on-chip devices have facilitated significant advances in our understanding of lung biology and pathology. Here, we describe a novel lung-on-a-chip model in...
Previous lung-on-chip devices have facilitated significant advances in our understanding of lung biology and pathology. Here, we describe a novel lung-on-a-chip model in which human induced pluripotent stem cell-derived alveolar epithelial type II cells (iAT2s) form polarized duct-like lumens alongside engineered perfused vessels lined with human umbilical vein endothelium, all within a 3D, physiologically relevant microenvironment. Using this model, we investigated the morphologic and signaling consequences of the KRAS mutation, a commonly identified oncogene in human lung adenocarcinoma (LUAD). We show that expression of the mutant KRAS isoform in iAT2s leads to a hyperproliferative response and morphologic dysregulation in the epithelial monolayer. Interestingly, the mutant epithelia also drive an angiogenic response in the adjacent vasculature that is mediated by enhanced secretion of the pro-angiogenic factor soluble uPAR. These results demonstrate the functionality of a multi-cellular platform capable of modeling mutation-specific behavioral and signaling changes associated with lung adenocarcinoma.
PubMed: 38911024
DOI: 10.1063/5.0207228 -
BMC Cardiovascular Disorders Jun 2024Fibrosing mediastinitis (FM) is a rare disease characterized by excessive proliferation of fibrous tissue in the mediastinum and can cause bronchial stenosis, superior...
INTRODUCTION
Fibrosing mediastinitis (FM) is a rare disease characterized by excessive proliferation of fibrous tissue in the mediastinum and can cause bronchial stenosis, superior vena cava obstruction, pulmonary artery and vein stenosis, etc. CASE PRESENTATION: An aging patient with intermittent chest tightness and shortness of breath was diagnosed with FM associated pulmonary hypertension (FM-PH) by echocardiography and enhanced CT of the chest, and CT pulmonary artery (PA)/ pulmonary vein (PV) imaging revealed PA and PV stenosis. Selective angiography revealed complete occlusion of the right upper PV, and we performed endovascular intervention of the total occluded PV. After failure of the antegrade approach, the angiogram revealed well-developed collaterals of the occluded RSPV-V2b, so we chose to proceed via the retrograde approach. We successfully opened the occluded right upper PV and implanted a stent.
CONCLUSIONS
This report may provide new management ideas for the interventional treatment of PV occlusion.
Topics: Humans; Treatment Outcome; Stents; Pulmonary Veins; Chronic Disease; Pulmonary Veno-Occlusive Disease; Stenosis, Pulmonary Vein; Mediastinitis; Male; Phlebography; Angioplasty, Balloon; Aged; Hypertension, Pulmonary; Fibrosis; Collateral Circulation; Pulmonary Circulation; Female
PubMed: 38909188
DOI: 10.1186/s12872-024-03984-y -
Biomedicine & Pharmacotherapy =... Jun 2024Pulmonary hypertension (PH) is a life-threatening disease characterized by pulmonary vascular remodeling. Endothelial-to-mesenchymal transition (EndMT) is an important...
Pulmonary hypertension (PH) is a life-threatening disease characterized by pulmonary vascular remodeling. Endothelial-to-mesenchymal transition (EndMT) is an important manifestation and mechanism of pulmonary vascular remodeling. Resolvin D1 (RvD1) is an endogenous lipid mediator promoting the resolution of inflammation. However, the role of RvD1 on EndMT in PH remains unknown. Here, we aimed to investigate the effect and mechanisms of RvD1 on the treatment of PH. We showed that RvD1 and its receptor FPR2 expression were markedly decreased in PH patients and both chronic hypoxia-induced PH (CH-PH) and sugen 5416/hypoxia-induced PH (SuHx-PH) mice models. RvD1 treatment decreased right ventricular systolic pressure (RVSP) and alleviated right ventricular function, and reduced pulmonary vascular remodeling and collagen deposition in the perivascular of both two PH mice models. Then, RvD1 inhibited EndMT in both the lungs of PH mice models and primary cultured human umbilical vein endothelial cells (HUVECs) treated with TGF-β and IL-1β. Moreover, RvD1 inhibited EndMT by downregulating Smad2/3 phosphorylation in vivo and in vitro via FPR2. In conclusion, our date suggest that RvD1/FPR2 axis prevent experimental PH by inhibiting endothelial-mensenchymal-transition and may be a therapeutic target for PH.
PubMed: 38908199
DOI: 10.1016/j.biopha.2024.117023 -
Journal of Cardiothoracic Surgery Jun 2024Pulmonary arteriovenous malformation (PAVM), also known as pulmonary arteriovenous fistula, is a rare vascular developmental anomaly. Most cases of PAVM are associated... (Review)
Review
BACKGROUND
Pulmonary arteriovenous malformation (PAVM), also known as pulmonary arteriovenous fistula, is a rare vascular developmental anomaly. Most cases of PAVM are associated with hereditary hemorrhagic telangiectasia (HHT). Hemothorax associated with PAVM is even rarer, and management concerning this complication still challenges.
CASE PRESENTATION
A 55-year-old man with sudden onset of dyspnea and chest pain was admitted to our hospital. He had a medical history of epistaxis, intraperitoneal germ cell tumor and PAVM. Chest unenhanced CT revealed the left-sided pleural effusion together with partial passive atelectasis and gradual increase at the interval of six days. Diagnostic thoracocentesis further revealed hemorrhagic effusion. CT angiography (CTA) showed tortuously dilated lumen of the left lower pulmonary artery and PAVM with the formation of aneurysm. Due to his family's refusal of surgery, the patient underwent transcatheter embolization therapy. However, the left pleural effusion did not significantly reduce and there was a slow drop in hemoglobin value even after interventional treatment, indicating the possibility of ongoing active bleeding. Eventually, the patient received lobectomy of the left lower lobe with a satisfactory outcome.
CONCLUSIONS
Massive hemothorax resulting from PAVM rupture into the pleural space can lead to fatal outcomes. CTA can accurately diagnose this pathologic condition. Transcatheter embolization is frequently used in the treatment of PAVM, but it may be challenging to achieve the desirable effect in patients with hemothorax. Combined with our case and literature review, direct radical surgery can lead to a successful outcome when PAVM complicated with hemothorax and a large diameter of the draining vein.
Topics: Humans; Hemothorax; Male; Middle Aged; Pulmonary Artery; Pulmonary Veins; Arteriovenous Fistula; Arteriovenous Malformations; Computed Tomography Angiography; Embolization, Therapeutic; Rupture, Spontaneous; Tomography, X-Ray Computed
PubMed: 38907280
DOI: 10.1186/s13019-024-02867-9 -
Diabetes & Vascular Disease Research 2024A pharmacoepidemiological study to assess VTE risk factors in a diabetes-rich population.
A pharmacoepidemiological nested case-control study of risk factors for venous thromboembolism with the focus on diabetes, cancer, socioeconomic group, medications, and comorbidities.
OBJECTIVES
A pharmacoepidemiological study to assess VTE risk factors in a diabetes-rich population.
METHODS
The study comprised 299,590 individuals. We observed 3450 VTEs and matched them with 15,875 controls using a nested case-control approach and collected data on comorbidities and prescriptions. By multivariable conditional logistic regression, we calculated ORs with 95%CIs for comorbidities and medications to evaluate their associations with VTE.
RESULTS
Diabetes (aOR 2.16; 95%CI 1.99-2.34), inflammatory bowel disease (1.84; 1.27-2.66), and severe psychiatric disorders (1.72; 1.43-2.05) had the strongest associations among the non-cancer comorbidities. Pancreatic (12.32; 7.11-21.36), stomach (8.57; 4.07-18.03), lung and bronchus (6.26; 4.16-9.43), and ovarian (6.72; 2.95-15.10) cancers were ranked as high-risk for VTE. Corticosteroids, gabapentinoids, psychotropic drugs, risedronic acid, and pramipexole were most strongly associated (aOR exceeding 1.5) with VTE. Insulin (3.86; 3.33-4.47) and sulphonylureas (2.62; 2.18-3.16) had stronger associations than metformin (1.65; 1.49-1.83). Statins and lercanidipine (0.78; 0.62-0.98) were associated with a lowered risk of VTE.
CONCLUSIONS
In this cohort, with 50% diabetes prevalence, pancreatic, stomach, lung and bronchus, and ovarian cancers were strongly associated with VTE. Corticosteroids, gabapentinoids, and psychotropic medications had the strongest associations with VTE among medications. This may be valuable for generating hypotheses for the further research. Lercanidipine may be a novel protective medication against VTE.
Topics: Humans; Female; Risk Factors; Male; Case-Control Studies; Neoplasms; Middle Aged; Aged; Comorbidity; Venous Thromboembolism; Pharmacoepidemiology; Risk Assessment; Diabetes Mellitus; Adult; Socioeconomic Factors; Social Determinants of Health
PubMed: 38904171
DOI: 10.1177/14791641241236894 -
Indian Pacing and Electrophysiology... Jun 2024A 70-year-old man with hypertensive heart disease underwent catheter ablation of persistent atrial fibrillation. After completing the pulmonary vein isolation, atrial...
A 70-year-old man with hypertensive heart disease underwent catheter ablation of persistent atrial fibrillation. After completing the pulmonary vein isolation, atrial burst pacing induced an annular atrial tachycardia (AT). Overdrive pacing exhibited constant fusion, indicating a macroreentrant mechanism of the AT. However, the CARTO3 activation map created using the Octaray catheter (both Biosense Webster, Irvine, CA) exhibited a centrifugal spread with the earliest activation site at the 4 o'clock position of the tricuspid annulus. In contrast, the Ripple map revealed a clear reentrant circuit with its isthmus located at the 4-6 o'clock position of the tricuspid annulus. The local electrograms in these areas recorded systolic and diastolic potentials simultaneously, and the misannotation of the large far-field potentials caused this discrepant result. Handling low-amplitude complex fractionated electrograms remains a challenge in creating a precise activation mapping. The Ripple map, especially when combined with the Octaray catheter, was effective in dynamically visualizing all these electrograms and accurately delineating the reentrant circuit.
PubMed: 38901653
DOI: 10.1016/j.ipej.2024.06.004 -
Nature Communications Jun 2024Mutations in the FOXF1 gene, a key transcriptional regulator of pulmonary vascular development, cause Alveolar Capillary Dysplasia with Misalignment of Pulmonary Veins,...
Mutations in the FOXF1 gene, a key transcriptional regulator of pulmonary vascular development, cause Alveolar Capillary Dysplasia with Misalignment of Pulmonary Veins, a lethal lung disease affecting newborns and infants. Identification of new FOXF1 upstream regulatory elements is critical to explain why frequent non-coding FOXF1 deletions are linked to the disease. Herein, we use multiome single-nuclei RNA and ATAC sequencing of mouse and human patient lungs to identify four conserved endothelial and mesenchymal FOXF1 enhancers. We demonstrate that endothelial FOXF1 enhancers are autoactivated, whereas mesenchymal FOXF1 enhancers are regulated by EBF1 and GLI1. The cell-specificity of FOXF1 enhancers is validated by disrupting these enhancers in mouse embryonic stem cells using CRISPR/Cpf1 genome editing followed by lineage-tracing of mutant embryonic stem cells in mouse embryos using blastocyst complementation. This study resolves an important clinical question why frequent non-coding FOXF1 deletions that interfere with endothelial and mesenchymal enhancers can lead to the disease.
Topics: Forkhead Transcription Factors; Animals; Humans; Persistent Fetal Circulation Syndrome; Mice; Enhancer Elements, Genetic; Mesoderm; Lung; Endothelial Cells; Zinc Finger Protein GLI1; Embryonic Stem Cells; Pulmonary Alveoli
PubMed: 38898031
DOI: 10.1038/s41467-024-49477-6