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Long term home oxygen therapy for children is defined as oxygenotherapy outside hospital environment dedicated for patients with lung diseases, diseases of pulmonary vascular system and diseases of the thoracic wall (ventilation) suffering from chronic respiratory insufficiency of type 1. This review represents the second one of two articles on long-term home oxygen therapy (LTOT) in the Czech Republic, with a focus on the indication criteria for home oxygen therapy in children with chronic respiratory conditions. The review outlines the criteria based on the practice guidelines of the American Thoracic Society (ATS) and the British Thoracic Society (BTS), as well as specific indication criteria in the Czech Republic recommended by health insurance companies. Additionally, the review addresses practical aspects of LTOT, including the types of home oxygen devices, at-home patient follow-up, and indications for weaning off LTOT. [ABSTRACT FROM AUTHOR]

There is a lack of effective therapeutic drugs for pulmonary arterial hypertension. Previous studies have demonstrated the positive cardiovascular system protective effects of the new peptide ACTY116. However, its stability in ordinary aqueous solution injections is poor and its half‐life in the body is short, which has hindered the development of preparations. This study aimed to prepare in situ forming implants (ISFIs) of the peptide ACTY116 and investigate its impact on pulmonary arterial hypertension. We prepared ISFIs using NMP/TA as a solvent and PLGA as a polymer. These ISFIs exhibited low viscosity, low toxicity and sustained release properties. In a mouse model of pulmonary hypertension induced by SU5416/hypoxia, both ISFIs and ACTY116 peptides effectively reduced pulmonary hypertension, cardiac hypertrophy and pulmonary blood vessel wall thickness. In conclusion, this study highlights the potential of ACTY116 as a treatment for pulmonary arterial hypertension and suggests that incorporating it into an in‐situ gel implant could be a promising option. [ABSTRACT FROM AUTHOR]

Migration is a rare but serious complication of the etonogestrel contraceptive implant, and little is known about its extent. To document and characterise cases of etonogestrel contraceptive implant migration in the scientific literature. A systematic review of Medline, Embase and Global Health databases was carried out between January 2000 and January 2023 to identify articles presenting implant migrations. Narrative reviews, conference abstracts and articles not written in English or French were excluded. Forty-five articles, mostly published since 2016, were identified (eight case series and 37 case reports), for a total of 148 independent cases of migration: in pulmonary blood vessels (n = 74), in non-pulmonary blood vessels (n = 16) and extravascular (n = 58). Many patients are asymptomatic and migration is often an incidental finding. A non-palpable implant and symptoms related to implant location (intra- or extra-vascular) may be indicative of migration. Inadequate insertion and normal or underweight appear to increase the risk of migration. Scientific societies and authors offer practical strategies to deal with implant migration. Professionals who insert and remove contraceptive implants must be adequately trained. They need to be on the lookout for implant migration, and promptly refer patients to appropriate care if migration is suspected. This systematic review documents and characterises 148 cases of vascular and extravascular etonogestrel contraceptive implant migration. Healthcare professionals must be aware of this rare but serious complication and be adequately trained to insert and remove contraceptive implants. [ABSTRACT FROM AUTHOR]

The fact that some SARS-CoV-2 pneumonia patients benefit from changing body position, and some from continuous positive airways pressure (CPAP), indicates the functional character of hypoxia. We hypothesize that such effects could be explained by the closure of small airways. To prove the hypothesis, we evaluated the patency of small airways in 30 oxygen-dependent, spontaneously breathing patients with SARS-CoV-2 pneumonia during their hospital stay using the FOT method and then compared the results with data obtained three months later. During the acute period, total resistance (R5) and peripheral resistance (R5-20) rose above the upper limit of normal (ULN) in 28% and 50% of all patients, respectively. Reactance indices X5, AX and Fres exceeded ULN in 55%, 68% and 66% of cases. Significant correlations were observed between PaO2/FiO2, the time spent in the hospital and R5, X5, AX and Fres. After 3 months, 18 patients were re-examined. During the hospital stay, 11 of them had risen above the upper limit of normal (ULN), for both resistance (R5-20) and reactance (X5, AX) values. Three months later, ULN for R5-20 was exceeded in only four individuals, but ULN for X5 and AX was exceeded in five individuals. Lung function examination revealed a combined restrictive/obstructive ventilatory failure and reduced CO transfer factor. We interpret these changes as lung tissue remodeling due to the process of fibrosis. We conclude that during acute period of SARS-CoV-2 pneumonia, dilated pulmonary blood vessels and parenchymal oedema induce functional closure of small airways, which in turn induce atelectasis with pulmonary right-to-left shunting, followed by the resulting hypoxemia. [ABSTRACT FROM AUTHOR]

The article presents a case study of a 29-year-old man with Behcet's disease experiencing dyspnea, revealing cardiovascular limitations and impaired O2 extraction. Topics discussed include cardiovascular contributors to dyspnea, peripheral O2 extraction impairment, and the importance of invasive exercise tests for comprehensive evaluation.

Background: Hydrops fetalis (HF) is fluid accumulation in fetus body cavities and subcutaneous tissue. The condition has been described in various farm and companion animal species, including dogs. Most of cases result from a heart defect. Exact nature of this defect is rarely clarified. Case presentation: A newborn, male French bulldog puppy with severe HF underwent a full anatomopathological examination to diagnose the primary cause of HF. Based on the anatomopathological examination, fetal ultrasound, and micro-computed tomography, transposition of the great arteries with hypoplasia of the ascending aorta, aortic arch interruption, ostium secundum atrial septal defect, severe tricuspid valve dysplasia, as well as hypoplasia of pulmonary vessels and lungs were diagnosed. Conclusions: This is the first report of HF caused by severe, complex congenital heart defects with concurrent pulmonary vessel and lung hypoplasia. [ABSTRACT FROM AUTHOR]

To evaluate the effect of aging on pulmonary vessels based on computed tomography (CT) quantification and analyse the correlation between quantitative pulmonary vascular volume and pulmonary function during aging. A total of 330 healthy adult volunteers, including 161 men (53 aged 20–39 years, 61 aged 40–59 years, and 47 aged ≥60 years) and 169 women (53 aged 20–39 years, 63 aged 40–59 years, and 53 aged ≥60 years) were recruited in this study. AVIEW software was used to quantitatively measure pulmonary vascular volume, including pulmonary total blood vessel volume (TBV) and small blood vessel volume with a cross-sectional area of <5 mm2 (BV5). Pulmonary vascular volume parameters were standardised using the ratio of vascular volume to the body surface area (BSA; TBV/BSA and BV5/BSA). Subsequently, the effect of aging on the pulmonary vessels was analysed. The pulmonary vascular volume parameters TBV/BSA and BV5/BSA of the whole lung, right lung, and left lung decreased significantly with increasing age (p< 0.05). Additionally, TBV/BSA and BV5/BSA of the whole lung were higher in men than in women. The declining trend of pulmonary vascular volume was consistent in men and women and increased with age. The pulmonary vascular volume parameters, TBV/BSA and BV5/BSA, decreased with age and were weakly positively correlated with pulmonary function. • Aging affects the pulmonary vascular structure. • With the increase in age, the pulmonary vascular volume decreased significantly. • The declining trend of the pulmonary vascular volume was consistent in both sexes. • The pulmonary vascular volume was weakly correlated with pulmonary function. [ABSTRACT FROM AUTHOR]

Patent ductus arteriosus (PDA) is a cardiac anomaly where the ductus arteriosus, a blood vessel connecting the pulmonary artery and the aorta, fails to close completely after birth. Anesthesia management during bedside PDA ligation in the Neonatal Intensive Care Unit (NICU) presents unique challenges and higher risks compared to the operating room environment. Manual cardiovascular and respiratory monitoring may be inefficient and challenging for the anesthesiologists. This case report aims to discuss the anesthetic management of a one month and four days old male infant, who presented with respiratory distress since birth, was diagnosed with moderate PDA, respiratory distress syndrome, and in need of surfactant therapy. This report focuses on the utilization of total intravenous anesthesia (TIVA) without inhalation anesthesia for PDA ligation via left posterolateral thoracotomy performed at the bedside in the NICU [ABSTRACT FROM AUTHOR]

Hypoxia, centralization of blood in pulmonary vessels, and increased cardiac output during physical exertion are the pathogenetic pathways of acute pulmonary edema observed during exposure to extraordinary environments. This study aimed to evaluate the effects of breath-hold diving at altitude, which exposes simultaneously to several of the stimuli mentioned above. To this aim, 11 healthy male experienced divers (age 18-52y) were evaluated (by Doppler echocardiography, lung echography to evaluate ultrasound lung B-lines (BL), hemoglobin saturation, arterial blood pressure, fractional NO (Nitrous Oxide) exhalation in basal condition (altitude 300m asl), at altitude (2507m asl) and after breath-hold diving at altitude. A significant increase in E/e' ratio (a Doppler-echocardiographic index of left atrial pressure) was observed at altitude, with no further change after the diving session. The number of BL significantly increased after diving at altitude as compared to basal conditions. Finally, fractional exhaled nitrous oxide was significantly reduced by altitude; no further change was observed after diving. Our results suggest that exposure to hypoxia may increase left ventricular filling pressure and, in turn, pulmonary capillary pressure. Breath-hold diving at altitude may contribute to interstitial edema (as evaluated by BL score), possibly because of physical efforts made during a diving session. The reduction of exhaled nitrous oxide at altitude confirms previous reports of nitrous oxide reduction after repeated exposure to hypoxic stimuli. This finding should be further investigated since reduced nitrous oxide production in hypoxic conditions has been reported in subjects prone to high-altitude pulmonary edema. [ABSTRACT FROM AUTHOR]

The pulmonary vascular system plays a crucial role in maintaining normal physiological functions, and perturbations in this network often serve as indicators for various fatal diseases. Thus, accurate mapping and assessment of the intricate anatomical details of pulmonary vasculature is essential for the investigation of the underlying mechanism of these diseases. Yet it is considered a tough challenge as traditional imaging techniques offer limited representations of the vasculature network in the lung, while optical imaging methods face limitations from tissue depth. To overcome these obstacles, in this study, an AIENP‐reinforced DISCO method, for whole‐tissue 3D reconstruction of pulmonary capillaries is presented. Combining AIENPs, hydrogel‐enhanced scaffolds, and solvent‐based DISCO procedures, the method successfully visualizes the entire network of mouse pulmonary capillaries with a significantly shortened timeframe and cost. The whole process including labeling and clearing takes 6 days and it costs ≈ 5 USD to stain the lung vasculature of an adult mouse. Moreover, the study provides valuable insights for detecting pulmonary vascular abnormalities. This fast and cost‐effective technique opens new avenues for developing better fluorophores compatible with tissue optical clearing and offers insights for in‐depth research on pulmonary pathophysiology. [ABSTRACT FROM AUTHOR]

Pulmonary hypertension (PH) is a malignant disease with progressive increase of pulmonary vascular pressure, which eventually leads to right heart failure. More and more evidences show that immune cells and inflammation play an important role in the occurrence and development of PH. In the context of pulmonary vascular diseases, immune cells migrate into the walls of the pulmonary vascular system. This leads to an increase in the levels of cytokines and chemokines in both the bloodstream and the surrounding tissues of the pulmonary vessels. As a result, new approaches such as immunotherapy and anti-inflammatory treatments are being considered as potential strategies to halt or potentially reverse the progression of PH. We reviewed the potential mechanisms of immune cells, cytokines and chemokines in PH development. The potential relationship of vascular cells or bone morphogenetic protein receptor 2 (BMPR2) in immune regulation was also expounded. The clinical application and future prospect of immunotherapy were further discussed. [ABSTRACT FROM AUTHOR]

Background and Aim: COPD has significant impacts on cardiac functions, affecting the right ventricle, left ventricle, and pulmonary blood vessels. Cardiac involvement is a significant factor contributing to the increased mortality associated with COPD. Echocardiography is a valuable tool for quickly and accurately assessing cardiac changes. It is a noninvasive and portable method that provides reliable results. Our study aimed to evaluate the cardiac changes associated with COPD using echocardiography. Additionally, we sought to determine the relationship between echocardiographic findings and the varying degrees of COPD severity. Material and Methods: A study was conducted on 100 patients with COPD who received treatment at a Tertiary Care Teaching Institute in India from January 2022 to January 2023. A group of 100 COPD patients underwent spirometry to determine their stage, and echocardiography was used to evaluate their condition. The ECHO report assessed several parameters, including RV enlargement, tricuspid regurgitation, RA enlargement, pulmonary arterial hypertension, and LV function as indicated by LV ejection fraction. Results: In our study, we found that the percentages of patients with mild, moderate, severe, and very severe COPD were 4%, 28%, 58%, and 10%, respectively. During the evaluation of COPD using echocardiography, it was found that 24% of cases had normal echocardiographic parameters. In 70 out of 100 cases, pulmonary hypertension was observed. The prevalence of mild, moderate, and severe PH in these cases were 0%, 50%, 79.3%, and 100%, respectively. In 46% of patients, the ECHO revealed an enlargement of the right ventricle. In 14% of patients, the ECHO revealed an enlargement of the right atrium. Tricuspid regurgitation (TR) was found in 72% of the cases, as determined by measurements. Conclusion: The presence of pulmonary arterial hypertension, right ventricular enlargement, right atrial enlargement, and tricuspid regurgitation on echocardiography is closely associated with the severity of COPD. These conditions become more prevalent as the severity of COPD increases. It is worth noting that the risk of cardiac dysfunction tends to rise as COPD becomes more severe. Echocardiography can be a valuable tool for examining the cardiac complications associated with COPD. [ABSTRACT FROM AUTHOR]

A mild pneumocoelom was diagnosed by computed tomography in a stranded juvenile loggerhead sea turtle (Caretta caretta). After gas extraction by ultrasound-guided puncture, the animal did not improve and was subjected to hyperbaric oxygen therapy (HBOT). After HBOT, the turtle developed marked subcutaneous emphysema and was found dead the following morning. Gross lesions included a distended right atrium with numerous gas bubbles within the epicardium, gas bubbles in the hepatic, gastric and mesenteric veins, a small gas-filled bulla in the left lung and diffuse haemorrhages in the encephalon. Histological lesions included gas-like emboli in the lumen of the right atrium with myocardial necrosis, gas-like emboli in the lumina of intestinal, pulmonary and renal blood vessels and severe meningeal haemorrhages. From a forensic pathology perspective, the subcutaneous emphysema of immediate onset after HBOT and the greater severity of the histological lesions in blood vessels, heart, lung and brain differentiate this case from other cases of gas embolism in turtles due to incidental capture. Two factors contributed to this outcome: the existence of a probably unresolved pneumocoelom and the application of HBOT without an initial diagnosis that accurately indicated its use. Therefore, as in human medicine, the use of HBOT in sea turtles with lung lesions and pneumocoelom is discouraged. This is the first description of an iatrogenic gas embolism in a sea turtle. [Display omitted] [ABSTRACT FROM AUTHOR]

Purpose: Acute lung injury (ALI) is a severe pulmonary disease characterized by damage to the alveoli and pulmonary blood vessels, leading to severe impairment of lung function. Studies on the effect of capsaicin (8-methyl-N-geranyl-6-nonamide, CAP) on lipopolysaccharide (LPS)-induced ALI in bronchial epithelial cells transformed with Ad12-SV40 2B (BEAS-2B) are still limited. This study aimed to investigate the effect and specific mechanism by which CAP improves LPS-induced ALI.Methods: The present study investigated the effect of CAP and the potential underlying mechanisms in LPS-induced ALI in vitro and vivo via RNA sequencing, Western blotting (WB), quantitative real-time reverse transcription PCR (qRT‒PCR), enzyme-linked immunosorbent assay (ELISA), and transmission electron microscopy (TEM). The TRPV1 inhibitor AMG9810 and the AKT agonist SC79 were used to confirm the protective effect of the TRPV1/AKT axis against ALI. The autophagy agonist rapamycin (Rapa) and the autophagy inhibitors 3-methyladenine (3-MA) and bafilomycin A1 (Baf-A1) were used to clarify the characteristics of LPS-induced autophagy.Results: Our findings demonstrated that CAP effectively suppressed inflammation and autophagy in LPS-induced ALI, both in vivo and in vitro. This mechanism involves regulation by the TRPV1/AKT signaling pathway. By activating TRPV1, CAP reduces the expression of P-AKT, thereby exerting its anti-inflammatory and inhibitory effects on pro-death autophagy. Furthermore, prior administration of CAP provided substantial protection to mice against ALI induced by LPS, reduced the lung wet/dry ratio, decreased proinflammatory cytokine expression, and downregulated LC3 expression.Conclusion: Taken together, our results indicate that CAP protects against LPS-induced ALI by inhibiting inflammatory responses and autophagic death through the TRPV1/AKT signaling pathway, presenting a novel strategy for ALI therapy. [ABSTRACT FROM AUTHOR]

Measles is an acute respiratory infectious disease caused by the measles virus. It leads to respiratory involvement with manifestations such as pneumonia, laryngobronchitis, pneumonitis, etc. It can also cause secondary bacterial and fungal infections. Aminophylline is a methylxanthine bronchodilator composed of theophylline and ethylenediamine. Airway blockage is reversed by bronchial smooth muscle relaxation, increased myosin light chain kinase activity, and decreased intracellular calcium concentration. It relaxes the smooth muscle of the bronchial airways and pulmonary blood vessels, reducing airway responsiveness to histamine, methacholine, adenosine, and allergens. Allergic skin reactions secondary to aminophylline administration have been rarely seen. Aminophylline can be given orally as well as intravenously. A seven-month-old male infant presented with a lower respiratory tract infection and a maculopapular rash involving the face and trunk. A history of contact with measles was present. Intravenous aminophylline was administered for persistent wheezing. The infant developed a generalised erythematous papular rash with a more widespread distribution than before within one hour of administration. The child was treated with antihistamines for the same. After a detailed physical examination, looking at the pattern of the rash and excluding other causes like environmental factors and drug history, the diagnosis of an allergic reaction to aminophylline was made. Early identification of allergic reactions is paramount, as prompt cessation of the offending agent and initiation of appropriate medical interventions can significantly mitigate the severity of the reaction and prevent potential life-threatening complications. [ABSTRACT FROM AUTHOR]

Rationale: The increase in the incidence and the diagnostic limitations of pneumoconiosis have emerged as a public health concern. This study aimed to conduct a computed tomography (CT)- based quantitative analysis to understand differences in imaging results of pneumoconiosis according to disease severity. Methods: According to the International Labor Organization (ILO) guidelines, coal workers’ pneumoconiosis (CWP) are classified into five categories. CT images were obtained only at full inspiration and were quantitatively evaluated for airway structural variables such as bifurcation angle (θ), hydraulic diameter (Dh), wall thickness (WT), and circularity (Cr). Parenchymal functional variables include abnormal regions (emphysema, ground–glass opacities, consolidation, semi consolidation, and fibrosis) and blood vessel volume. Through the propensity score matching method, the confounding effects were decreased. Results: Category 4 demonstrated a reduced θ in TriLUL, a thicker airway wall in both the Trachea and Bronint compared to Category 0, and a decreased Cr in Bronint. Category 4 presented with higher abnormal regions except for ground–glass opacity and a narrower pulmonary blood vessel volume. A negative correlation was found between abnormal areas with lower Hounsfield units (HU) than the normal lung and the ratio of forced expiratory volume in 1 s/ forced vital capacity, with narrowed pulmonary blood vessel volume which is positively correlated with abnormal areas with upper HU than the normal lung. Conclusion: This study provided valuable insight into pneumoconiosis progression through a comparison of quantitative CT images based on severity. Furthermore, as there has been paucity of studies on the pulmonary blood vessel volume of the CWP, in this study, a correlation between reduced pulmonary blood vessel volume and regions with low HU values holds significant importance. [ABSTRACT FROM AUTHOR]

Activators of hypoxia inducible factors (HIFs), such as roxadustat, are promising agents for anemia treatment. However, since HIFs are also involved in the regulation of the pulmonary circulation, we hypothesized that roxadustat increases pulmonary vascular resistance and vasoconstrictor reactivity. Using isolated, cell-free solution perfused rat lungs, we found perfusion pressure-flow curves to be shifted to higher pressures by 2 weeks of roxadustat treatment (10 mg/kg every other day), although not as much as by chronic hypoxic exposure. Vasoconstrictor reactivity to angiotensin II and acute hypoxic challenges was not altered by roxadustat. Since roxadustat may inhibit angiotensin-converting enzyme 2 (ACE2), we also tested a purported ACE2 activator, diminazene aceturate (DIZE, 0.1 mM). It produced paradoxical, unexplained pulmonary vasoconstriction. We conclude that the risk of serious pulmonary hypertension is not high when roxadustat is given for 14 days, but monitoring is advisable. [ABSTRACT FROM AUTHOR]

• Mixed pulmonary hypertension in patients with left heart disease from chronic heart failure is related to a constellation of underlying pathologies: left ventricular dysfunction, valvular heart disease, and chronic pressure/volume overload. • Recently, several biomarkers with potential diagnostic and prognostic significance in pulmonary arterial hypertension have been identified, encompassing heart failure indicators, endothelial and platelet function impairment, cardiac myocyte harm, and oxidative stress. • Current methods of assessing pulmonary hypertension reversal may prohibit suitable candidates from being considered for heart transplantation and routed toward left ventricular assist device placement. • Future optimization may include the use of combination therapy with temporary mechanical circulatory support at home and concomitant medical therapy. Pulmonary arterial hypertension (PAH) is characterized by persistently increased pressure in the pulmonary arteries. New defining criteria for the different hemodynamic types of pulmonary hypertension (PH) that occur with left heart disease have been proposed by the task force on PH. After consideration of the changes in the general definition of PH in left heart disease, the proposed hemodynamic definition was: (1) isolated postcapillary PH: pulmonary artery wedge pressure >15 mm Hg and mean pulmonary arterial pressure (mPAP) >20 mm Hg and pulmonary vascular resistance (PVR) <3 Woods units (WU); and (2) combined post- and precapillary PH: pulmonary artery wedge pressure >15 mm Hg, mPAP >20 mm Hg, and PVR ≥3 WU. Secondary PH is initially reversible, but eventually, it can become fixed because of the remodeling process of the pulmonary vascular system. Limitations in defining both the time for and amount of reversibility lack clarity. We discuss a case of PH as a framework to better understand these key principles in addressing patients' candidacy for heart or heart-lung transplantation. We performed a literature search for all available contemporary data with the following terms: "pulmonary hypertension," "reversal," "Impella 5.5," "temporary mechanical support," and "LVAD" using the National Library of Medicine – PubMed and PubMed Central between 2019 and 2023. A total of 14 published papers were found with these search. From these, 3 addressed the issue of PH and reversibility in the setting of LHD after durable LVAD placement. No papers were found using Impella 5.5 and PH during this timeframe. Given the paucity of data in the field regarding temporary mechanical circulatory support and pulmonary hypertension, we present a case-based discussion to guide the reader in understanding the potential impact of this method in patients with WHO Class 2 Pulmonary hypertension. A 49-year-old woman with a medical history of acute on chronic biventricular systolic and diastolic heart failure, American College of Cardiology stage D, Stevenson profile C, New York Heart Association class IV (ejection fraction 18%) secondary to nonischemic cardiomyopathy after cardiac resynchronization therapy, pulmonary hypertension, bilateral deep vein thrombosis, and segmental pulmonary embolism presented for heart transplant evaluation. Her cardiac output and central hemodynamics were measured, and she was found to have a pulmonary artery (PA) pressure of 78/38 with a mean PA pressure of 51, pulmonary capillary wedge pressure (PCWP) 30, transpulmonary pressure gradient (TPG) 21, thermodilution cardiac output (CO) 3.35 L/min, and cardiac input (CI) 1.75 L/min/m2. Her PVR was 6.2 WU. Provocative pharmacologic testing for reversibility of PH was performed using sodium nitroprusside, which resulted in a blood pressure of 83/57 (92), heart rate 92/min, and PA pressure of 71/31, with a mean PA pressure of 44 PCWP 22, TPG 22, CO 4.8 L/min, and CI of 2.48 L/min/m2 with a PVR of 4.5 WU. Following this, the patient underwent Impella 5.5 placement through the right axillary artery to optimize afterload reduction and improve end-organ perfusion. Post-Impella hemodynamics on milrinone 0.5 mcg/kg/min demonstrated the following: blood pressure 90/66 (74), heart rate 53/min, and PA pressure of 56/29, with a mean PA pressure of 38, PCWP 24, TPG 14, CO 6 L/min, and CI of 2.9 L/min/m2 with a PVR of 2.3 WU. Left ventricular assist device support with Impella 5.5 is associated with a reduction in mPAP and PVR over weeks to months and thus plays a crucial role as a bridge to transplant. Our case and this review highlights the characteristics of PH resulting from heart failure with reduced ejection fraction and discusses the important clinical issues related to the treatment of these patients. We have shown that left ventricular assist device therapy with Impella 5.5 can effectively reduce left-sided filling pressures and lead to PH improvement. We demonstrate the potential benefits of Impella 5.5 in the management of patients with WHO 2 PH and cardiogenic shock with impaired hemodynamics. [ABSTRACT FROM AUTHOR]

A male Korean raccoon dog of unknown age was rescued and placed at the Daejeon Wildlife Rescue Center, Korea. Physical examination revealed severe emaciation and dehydration, as well as thick crusts and alopecia over most of the body. During medical care, the animal died and was submitted for postmortem examination. Firm, brown-red lesions of various sizes were observed on the surface of the lungs. In cross-sections of the lungs, pulmonary vessels were thickened and dilated, with white irregular papillary luminal projections. Histologically, pulmonary blood vessels were severely hyperplastic, characterized by thickened dilated walls and fibrous papillary projections covered with a single layer of endothelial cells (ECs). Hyperplastic fibrous connective tissue was confirmed by Masson trichrome staining. The ECs expressed CD31. We diagnosed the lesion as intravascular papillary endothelial hyperplasia, a unique non-neoplastic reactive process that has not been reported previously in pulmonary vessels of canids, equids, or felids, to our knowledge. [ABSTRACT FROM AUTHOR]

Simple Summary: Proper development of the fetal lung is vital to the survival and healthy growth of pigs after birth, but many factors can disturb the normal growth of the fetal pig lung. In the previous study, we found that the Hoxa1 mutation of g.50111251 G > TC resulted in the congestion and edema of fetal lungs, and all neonatal Hoxa1−/− piglets died of respiratory failure during the suckling period. The results of this study showed that supplementing all-trans retinoic acid (ATRA) to pregnant sows alleviated the dyspnea of neonatal Hoxa1−/− piglets by increasing the IFN-γ concentration (p < 0.05), airspace area (p < 0.01) and pulmonary microvessel density (p < 0.01); increasing the expression of VEGFD (p < 0.01), PDGFD (p < 0.01), KDR (p < 0.01), ID1 (p < 0.01), and NEDD4 (p < 0.01); and decreasing the septal wall thickness (p < 0.01) and the expression of SFTPC (p < 0.01) and FOXO3 (p < 0.01). Neonatal Hoxa1−/− piglets were characterized by dyspnea owing to the Hoxa1 mutation, and maternal administration with ATRA alleviated the dyspnea of neonatal Hoxa1−/− piglets. The purpose of this experiment was to explore how maternal ATRA administration rescued the abnormal fetal lungs of Hoxa1−/− piglets. Samples of the lungs were collected from neonatal Hoxa1−/− and non-Hoxa1−/− piglets delivered by sows in the control group, and from neonatal Hoxa1−/− piglets born by sows administered with ATRA at 4 mg/kg body weight on dpc 12, 13, or 14, respectively. These were used for the analysis of ELISA, histological morphology, immunofluorescence staining, immunohistochemistry staining, and quantitative real-time PCR. The results indicate that the Hoxa1 mutation had adverse impacts on the development of the alveoli and pulmonary microvessels of Hoxa1−/− piglets. Maternal administration with ATRA at 4 mg/kg body weight on dpc 14 rescued the abnormal lung development of Hoxa1−/− piglets by increasing the IFN-γ concentration (p < 0.05), airspace area (p < 0.01) and pulmonary microvessel density (p < 0.01); increasing the expression of VEGFD (p < 0.01), PDGFD (p < 0.01), KDR (p < 0.01), ID1 (p < 0.01), and NEDD4 (p < 0.01); and decreasing the septal wall thickness (p < 0.01) and the expression of SFTPC (p < 0.01) and FOXO3 (p < 0.01). Maternal administration with ATRA plays a vital role in rescuing the abnormal development of lung of Hoxa1−/− fetal piglets. [ABSTRACT FROM AUTHOR]

The respiratory system is the main target of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the cause of coronavirus disease 19 (COVID-19) where acute respiratory distress syndrome is considered the leading cause of death. Changes in pulmonary blood vessels, among which an endothelialitis/endotheliitis has been particularly emphasized, have been suggested to play a central role in the development of acute lung injury. Similar vascular changes are also observed in animal models of COVID-19. The present study aimed to determine whether the latter are specific for SARS-CoV-2 infection, investigating the vascular response in the lungs of mice infected with SARS-CoV-2 and other respiratory viruses (influenza A and murine gammaherpesvirus) by in situ approaches (histology, immunohistology, morphometry) combined with RNA sequencing and bioinformatic analysis. Non-selective recruitment of monocytes and T and B cells from larger muscular veins and arteries was observed with all viruses, matched by a comparable transcriptional response. There was no evidence of endothelial cell infection in any of the models. Both the morphological investigation and the transcriptomics approach support the interpretation that the lung vasculature in mice mounts a stereotypic response to alveolar and respiratory epithelial damage. This may have implications for the treatment and management of respiratory disease in humans. [ABSTRACT FROM AUTHOR]

We investigated the hemodynamic parameters of pediatric PDA patients and focused on the influence of PDA size on pulmonary arterial pressure and the prevalence of pulmonary hypertension. A total of 52 patients aged between 2 months and 20 years who received transcatheter closure of a PDA from January 2018 to June 2022 in our institution were retrospectively recruited. Their hemodynamic parameters collected both by echocardiography and by cardiac catheterization were analyzed to delineate the influence of PDA size on the pulmonary vascular system. The echocardiographic-based ductal size and indexed PDA size were 1.93 mm (1.15–6 mm) and 4.05 mm/m2 (2.03–25.47 mm/m2), respectively. The pulmonary artery pressure measured was 20.83 mmHg (8–45 mmHg). We found a positive correlation between indexed PDA size and mean pulmonary arterial pressure (mPAP) (Pearson correlation coefficient = 0.47, p < 0.001). A subgroup analysis showed that 28 patients (53.8%) developed pulmonary hypertension (PH) (defined as mPAP > 20 mmHg). The median age of the PH group was 1.02 years [range: 0.19–8.64], which was significantly younger than the non-PH group's median age of 3.43 years [range: 0.42–19.96] (p = 0.001). The indexed PDA size for the PH group, 4.69 mm/m2, was significantly higher than that of the non-PH group, 3.2 mm/m2 (p = 0.004). The major risk factor for patients with PH was the PDA/BSA index, with an OR of 2.181 (95% CI, 1.224–3.887). Our demographic data showed younger patients with a higher PDA/BSA index are more likely to develop pulmonary hypertension. [ABSTRACT FROM AUTHOR]

This article discusses a case report of a patient with pulmonary veno-occlusive disease (PVOD) who underwent lung transplantation despite not showing hemodynamic changes. The patient had radiographic findings consistent with PVOD but did not have low oxygen levels or abnormal pulmonary vascular resistance. The patient's condition worsened quickly, leading to lung transplantation before respiratory failure. The article highlights the importance of early referral for transplantation in suspected cases of PVOD, even without hemodynamic changes. It also covers the radiographic findings, diagnostic methods, and treatment options for sarcoidosis-associated PVOD. The text emphasizes the need to consider PVOD in patients with a history of sarcoidosis, even without active sarcoidosis markers. [Extracted from the article]

Intimal sarcomas (IS) are rare malignant mesenchymal tumors arising in large blood vessels of the systemic and pulmonary circulation and also in the heart. They are morphologically similar to other spindle cell, poorly differentiated sarcomas. The prognosis is poor and depends mainly on surgical options. Three cases of IS were collected from two institutions. Clinical data were retrieved and histological study was performed. A wide immunohistochemical panel was analyzed. FISH of MDM2 gene was performed, and a molecular study with NGS was implemented in all cases. The mean age of our cases was 54 years. Histologically, the tumors presented a diffuse growth pattern with heterogeneous atypical epithelioid or spindle cells and extensive thrombosed areas. All cases presented intense immunoexpression for MDM2, CDK4, CD117, c-myc, PDGFRA, and p16. PDGFRA, HTERT, and pan-TRK gained expression, while p16 lost intensity, being weaker in both the local recurrences and xenografts. The three cases showed amplification of MDM2 by FISH. NGS analysis revealed amplifications in the CDK4, PDGFRA, and KIT genes, together with BRAF mutation and KRAS amplification. P16 was expressed in all cases, losing intensity in local recurrence and xenografts. Two new alterations, a BRAF mutation and a KRAS amplification, were detected by NGS in different tumors, opening up new therapeutic options for these patients. [ABSTRACT FROM AUTHOR]

Absorption-based clinical computed tomography (CT) is the current imaging method of choice in the diagnosis of lung diseases. Many pulmonary diseases are affecting microscopic structures of the lung, such as terminal bronchi, alveolar spaces, sublobular blood vessels or the pulmonary interstitial tissue. As spatial resolution in CT is limited by the clinically acceptable applied X-ray dose, a comprehensive diagnosis of conditions such as interstitial lung disease, idiopathic pulmonary fibrosis or the characterization of small pulmonary nodules is limited and may require additional validation by invasive lung biopsies. Propagation-based imaging (PBI) is a phase sensitive X-ray imaging technique capable of reaching high spatial resolutions at relatively low applied radiation dose levels. In this publication, we present technical refinements of PBI for the characterization of different artificial lung pathologies, mimicking clinically relevant patterns in ventilated fresh porcine lungs in a human-scale chest phantom. The combination of a very large propagation distance of 10.7 m and a photon counting detector with 100 μ m pixel size enabled high resolution PBI CT with significantly improved dose efficiency, measured by thermoluminescence detectors. Image quality was directly compared with state-of-the-art clinical CT. PBI with increased propagation distance was found to provide improved image quality at the same or even lower X-ray dose levels than clinical CT. By combining PBI with iodine k-edge subtraction imaging we further demonstrate that, the high quality of the calculated iodine concentration maps might be a potential tool for the analysis of lung perfusion in great detail. Our results indicate PBI to be of great value for accurate diagnosis of lung disease in patients as it allows to depict pathological lesions non-invasively at high resolution in 3D. This will especially benefit patients at high risk of complications from invasive lung biopsies such as in the setting of suspected idiopathic pulmonary fibrosis (IPF). [ABSTRACT FROM AUTHOR]

Several recent studies assessed the PE prediction tools in COVID-19 patients, finding overall poor ability to discriminatively identify patients with COVID-19-associated PE using the common PE clinical decision tools. SP 29,30 sp The CHOD score (C reactive protein, heart rate, oxygen saturation, D-dimer) had the highest performance among all current models in determining which patients may require a CTPA for PE evaluation in the setting of COVID-19.[31] The CHOD decision tool uses a score of 0 to 7 points broken down into low-risk (4.5% incidence), moderate-risk (36.8% incidence), and high-risk categories (100% incidence).[31] While promising for use in COVID-19 patients, it has yet to be externally validated and should not be used as an isolated tool at this time. B AUTHORS b B Michael DeFilippo, DO b , Columbia University Medical Center, New York, NY B Cameron Callipari, MD b , Columbia University Medical Center, New York, NY B Jimmy Truong, DO b , Assistant Professor, Emergency Medicine, Columbia University Medical Center, New York, NY B PEER REVIEWER b B Steven M. Winograd, MD, FACEP, b Brookdale Emergency Department, Brooklyn, NY; Samaritan Emergency Department, Albany, NY EXECUTIVE SUMMARY Pulmonary embolism can present with chest pain (usually pleuritic), hemoptysis, dyspnea (most common), syncope/hypotension, and sudden death. In the Western hemisphere, PE remained the third most common inciting factor of cardiovascular death in hospitalized patients, surpassed only by acute myocardial infarctions and strokes. SP 3-6 sp Certain studies report that the 30-day mortality rate is as high as 30% in those with a high-risk PE and about 15% in those with intermediate-risk PEs.[3] Patients who survive a PE still face significant morbidity, since long-lasting sequelae can afflict these patients. [Extracted from the article]

This study aimed to investigate the role of the phosphatidylinositol 3-kinase/protein kinase B (PI3K/Akt) signaling pathway in the pulmonary vascular remodeling (PVR) of pulmonary arterial hypertension (PAH) in rats. A PAH model in rats was established through a left pneumonectomy and monocrotaline (MCT) injection, using the transglutaminase 2 (TG2) inhibitor cystamine dihydrochloride for intervention. Thirty healthy male Sprague Dawley rats were randomized into a control group, a model group, and an intervention group (n = 10 for each group). The mean pulmonary arterial pressure (mPAP) was measured in all groups after 35 days, and the right ventricular hypertrophy index (RVHI) was calculated. Hematoxylin and eosin and lung elastic-fiber staining were used on the rats' lung tissue in all three groups. The changes in pulmonary blood vessels and lung tissue force and the percentage of medial hypertrophy of small pulmonary arteries (WT%), vessel wall area to total area ratio (WA%), and the neointimal proliferation degree were observed. The Akt messenger RNA (mRNA) expression levels of lung tissues in all three groups were measured using a real-time polymerase chain reaction (RT-PCR) assay, and the protein expression levels of Akt and phosphorylated Akt (p-Akt) in all three groups were measured using aWestern blot assay. The results indicated that the PI3K/Akt signaling pathway might play a substantial role in inhibiting pulmonary vascular remodeling (PVR) following intervention with a TG2 inhibitor. [ABSTRACT FROM AUTHOR]

SARS-CoV-2-infected symptomatic patients often suffer from high fever and loss of appetite which are responsible for the deficit of fluids and of protein intake. Many patients admitted to the emergency room are, therefore, hypovolemic and hypoproteinemic and often suffer from respiratory distress accompanied by ground glass opacities in the CT scan of the lungs. Ischemic damage in the lung capillaries is responsible for the microscopic hallmark, diffuse alveolar damage (DAD) characterized by hyaline membrane formation, fluid invasion of the alveoli, and progressive arrest of blood flow in the pulmonary vessels. The consequences are progressive congestion, increase in lung weight, and progressive hypoxia (progressive severity of ARDS). Sequestration of blood in the lungs worsens hypovolemia and ischemia in different organs. This is most probably responsible for the recruitment of inflammatory cells into the ischemic peripheral tissues, the release of acute-phase mediators, and for the persistence of elevated serum levels of positive acute-phase markers and of hypoalbuminemia. Autopsy studies have been performed mostly in patients who died in the ICU after SARS-CoV-2 infection because of progressive acute respiratory distress syndrome (ARDS). In the death certification charts, after respiratory insufficiency, hypovolemic heart failure should be mentioned as the main cause of death. [ABSTRACT FROM AUTHOR]

Biomarkers are non-invasive tools, which can be very useful in diagnosis and prognosis of a specific disease. Pulmonary hypertension (PH) is a serious health condition, characterized by increased pulmonary arterial pressure, elevated pulmonary vascular resistance often leading to right heart failure. If not treated properly, it can significantly reduce patients' quality of life and even lead to death. Nowadays, there is an increasing interest on PH markers and more specifically how they can contribute to the diagnosis, prognosis, and monitoring of the development of this disease. Recent studies on biomarkers in PH suggest several novel and promising molecules, which can be potentially useful in PH work-up and follow-up strategies. This review focuses on biomarkers for diagnosis and prognosis of PH via well-known and some novel cardiovascular disease (CVD) indicators associated with heart failure, myocardial remodelling, and injury. Current thinking holds that CVD biomarkers can detect not only heart abnormalities but also pulmonary vascular system damage. [ABSTRACT FROM AUTHOR]

Pulmonary hypertension (PH) is a broad term describing the mean pulmonary artery pressure, as measured by right heart catheterization, exceeds 20mmHg. Pulmonary arterial hypertension (PAH) exists when PH is accompanied by a normal wedge pressure and elevated pulmonary vascular resistance. PAH is typified by dysmorphic and dysfunctional pulmonary arterial vasculature. Attempting to restore the functionality of the pulmonary artery is a hallmark of care to the PAH patient. Riociguat is a powerful stimulator of soluble guanylate cyclase and increases blood flow through the pulmonary arteries by dilating vascular smooth muscle cells. This review examines the pharmacology of riociguat, the fundamental clinical trials applying it to PAH patients, practical aspects when selecting its use, and future directions for its utilization. [ABSTRACT FROM AUTHOR]

Objective. The study aimed to evaluate the value of bedside echocardiography (TTE) and lower extremity blood vessels in diagnosis and prognosis of acute pulmonary embolism (APE). Methods. A retrospective study was performed on 53 patients with APE diagnosed by CT pulmonary angiography (CTPA) (systemic systolic blood pressure was >90 mmHg at time of consultation, and systemic systolic blood pressure decreased by <40 mmHg compared with basic value in those with hypertension). All patients underwent TTE examination before treatment. The high-risk factors, clinical manifestations, laboratory tests, and prognosis were retrospectively analyzed. Results. The rate of PE-related deterioration (cardiopulmonary resuscitation, tracheal intubation, cardiogenic shock, and death) within 14 days of hospitalization in RVD was 28%, and mortality rate (sudden death) was 20%, compared with non-RVD (both 0%). TTE examination showed that RVD as a predictor of pulmonary embolism-related death had a sensitivity of 100%, a specificity of 58%, a positive predictive value of 20%, and a negative predictive value of 100%. Conclusions. (1) TTE has increasingly shown obvious advantages in diagnosis of APE. It can detect direct or indirect signs of pulmonary embolism, confirm diagnosis or suspected diagnosis, and noninvasively and dynamically observe hemodynamic changes of heart in patients with acute PTE before and after treatment.. (2) The PE-related exacerbation rate (28%) or mortality (20%) of APE patients in normotensive with RVD was higher without RVD (0%). RVD is an independent predictor of poor prognosis in normotensive acute PTE. TTE tests allow people to identify people at risk of early death. The short-term prognosis of patients without RVD was better (14 days). [ABSTRACT FROM AUTHOR]

Airway epithelial cells represent the main target of SARS-CoV-2 replication but several pieces of evidence suggest that endothelial cells (ECs), lining pulmonary blood vessels, are key players in lung injury in COVID-19 patients. Although in vivo evidence of SARS-CoV-2 affecting the vascular endothelium exists, in vitro data are limited. In the present study, we set up an organotypic model to dissect the crosstalk between airway epithelium and pulmonary endothelial cells during SARS-CoV-2 infection. We showed that SARS-CoV-2 infected airway epithelium triggers the induction of endothelial adhesion molecules in ECs, suggesting a bystander effect of dangerous soluble signals from the infected epithelium. The endothelial activation was correlated with inflammatory cytokines (IL-1β, IL-6, IL-8) and with the viral replication in the airway epithelium. Interestingly, SARS-CoV-2 infection determined a modulation of endothelial p21, which could be partially reversed by inhibiting IFN-β production from ECs when co-cultured with HAE. Altogether, we demonstrated that SARS-CoV-2 infected epithelium triggers activation/senescence processes in ECs involving type I IFN-β production, suggesting possible antiviral/damage mechanisms occurring in the endothelium. [ABSTRACT FROM AUTHOR]

This study was aimed to explore the effect of CT image feature extraction of pulmonary nodules based on an artificial intelligence algorithm and the image performance of benign and malignant pulmonary nodules. In this study, the CT images of pulmonary nodules were collected as the research object, and the lung nodule feature extraction model based on expectation maximization (EM) was used to extract the image features. The Dice similarity coefficient, accuracy, benign and malignant nodule edges, internal signs, and adjacent structures were compared and analyzed to obtain the extraction effect of this feature extraction model and the image performance of benign and malignant pulmonary nodules. The results showed that the detection sensitivity of pulmonary nodules in this model was 0.955, and the pulmonary nodules and blood vessels were well preserved in the image. The probability of burr sign detection in the malignant group was 73.09% and that in the benign group was 8.41%. The difference was statistically significant (P < 0.05). The probability of malignant component leaf sign (69.96%) was higher than that of a benign component leaf sign (0), and the difference was statistically significant (P < 0.05). The probability of cavitation signs in the malignant group (59.19%) was higher than that in the benign group (3.74%), and the probability of blood vessel collection signs in the malignant group (74.89%) was higher than that in the benign group (11.21%), with statistical significance (P < 0.05). The probability of the pleural traction sign in the malignant group was 17.49% higher than that in the benign group (4.67%), and the difference was statistically significant (P < 0.05). In summary, the feature extraction effect of CT images based on the EM algorithm was ideal. Imaging findings, such as the burr sign, lobulation sign, vacuole sign, vascular bundle sign, and pleural traction sign, can be used as indicators to distinguish benign and malignant nodules. [ABSTRACT FROM AUTHOR]

Pulmonary arterial hypertension is a multifactorial, chronic disease process that leads to pulmonary arterial endothelial dysfunction and smooth muscular hypertrophy, resulting in impaired pliability and hemodynamics of the pulmonary vascular system, and consequent right ventricular dysfunction. Existing treatments target limited pathways with only modest improvement in disease morbidity, and little or no improvement in mortality. Ongoing research has focused on the molecular basis of pulmonary arterial hypertension and is going to be important in the discovery of new treatments and genetic pathways involved. This review focuses on the molecular pathogenesis of pulmonary arterial hypertension. [ABSTRACT FROM AUTHOR]

There is a need for clinical trial end-points to better assess how patients feel and function, so that interventions can be developed which alleviate symptoms and improve quality of life. Use of 6-min walk test (6MWT) outcomes as a primary end-point in interstitial lung disease (ILD) trials is growing, particularly for drugs targeting concurrent pulmonary hypertension. However, 6MWT outcomes may be influenced differentially by interstitial lung and pulmonary vascular components of ILD, making interpretation complicated. We propose that using 6MWT outcomes, including 6-min walk distance or oxygen desaturation, as primary end-points should depend upon the study population (how advanced the ILD is; whether vasculopathy is significant), the degree of disease progression, and, importantly, the effect of study treatment expected. We argue that the 6MWT as a single outcome measure is suitable as a primary end-point if the treatment goal is to improve functional performance or prevent disease progression within a study population of patients with advanced ILD or those with ILD and co-existent vasculopathy. In addition, we discuss the potential of composite primary end-points incorporating 6MWT outcomes, outlining important considerations to ensure that they are appropriate for the study population and treatment goals. [ABSTRACT FROM AUTHOR]

In an unsteady pulsatile non-Newtonian fluid past a tube with a thin wall layer, the dispersion of a narrow uniform slug of injected solute over a cross-section is examined. At the interface between the mobile fluid phase and the immobile wall phase, both irreversible and reversible reactions have been adopted. The Carreau–Yasuda model is used to describe the fluid's rheology. The impacts of fluid rheology and reaction parameters on the concentration profiles in the fluid- and wall-phases and the three transport coefficients, viz, the depletion coefficient (K0) , the convection coefficient (K1) , the dispersion coefficient (K2) in the fluid phase are predicted numerically. A considerable shift in the behaviour of K1 and K2 with a higher reaction rate may be observed in the transient stage. The axial dispersion of mobile-phase concentration in the unsteady Carreau–Yasuda II fluid model is significantly larger than in Poiseuille and steady Carreau–Yasuda II fluid models, and flow pulsatility on the immobile-phase concentration is prominent upstream at a longer time. In addition, the peak value of the mobile-phase section-mean concentration is consistently lower than in other fluid models. This study could help researchers to understand the drug delivery in blood vessels and pulmonary mechanical ventilation. [ABSTRACT FROM AUTHOR]

The aortopulmonary window (APW) is a rare congenital abnormality referring to communication between the main pulmonary artery and ascending aorta. To avoid irreversible pulmonary vascular disease, this type of congenital abnormalities should be repaired whenever it is diagnosed. The recommended timing for the surgery, in common practice, is three months of age. In older patients, the outcome is determined by pulmonary vascular resistance at the time of surgical repair. In this report, we present our five years old patient who underwent a valvular and supravalvular aortic surgery and concomitantly closure of APW successfully. [ABSTRACT FROM AUTHOR]

Objective: To study the therapeutic effect of Feixintong on rats with chronic pulmonary heart disease (CPHD), and to explore the effects of its treatment on pulmonary hypertension, hemodynamics and pulmonary vascular remodeling in rats with chronic pulmonary heart disease. Methods: 30 Wistar rats were randomly divided into normal control group, model group and Feixintong group. Rats in the model group and Feixintong group were intraperitoneally injected with monocrotaline to establish a CPHD model. The CPHD rats in the Feixintong group were given Feixintong via intragastric administration for 3 weeks. After 3 weeks of treatment, the FEV0.3, FVC, LVEF, LVEDD, IVST, LVPWT, WBHSV, WBLSV, pv, HT and pulmonary vascular remodeling related indicators in the three groups of rats were measured. Results: Compared with the model group rats, the Feixintong group rats' activity, diet and water consumption and body weight were significantly increased, and symptoms such as breathing and tongue color were all improved. After 3 weeks of Feixintong treatment, the pulmonary function indexes FEV0.3, FVC and FEV0.3/FVC of CPHD rats increased significantly(P<0.05), and the cardiac function structural indexes LVEF, LVEDD, IVST and LVPWT all increased significantly(P<0.05), the hemodynamic indexesPASP, PADP and mPAP were all significantly reduced(P<0.05), and the pulmonary vascular remodeling indexes MA, WT and WA were all significantly reduced(P<0.05), while the pulmonary vascular remodeling index NMA was significantly increased(P<0.05). Conclusion: Feixintong has a good therapeutic effect on chronic pulmonary heart rats, which can significantly reduce pulmonary hypertension in chronic pulmonary heart rats, improve its hemodynamic changes and help rebuild pulmonary blood vessels. [ABSTRACT FROM AUTHOR]

Despite intense investigation, the pathogenesis of COVID-19 and the newly defined long COVID-19 syndrome are not fully understood. Increasing evidence has been provided of metabolic alterations characterizing this group of disorders, with particular relevance of an activated tryptophan/kynurenine pathway as described in this review. Recent histological studies have documented that, in COVID-19 patients, indoleamine 2,3-dioxygenase (IDO) enzymes are differentially expressed in the pulmonary blood vessels, i.e., IDO1 prevails in early/mild pneumonia and in lung tissues from patients suffering from long COVID-19, whereas IDO2 is predominant in severe/fatal cases. We hypothesize that IDO1 is necessary for a correct control of the vascular tone of pulmonary vessels, and its deficiency in COVID-19 might be related to the syndrome's evolution toward vascular dysfunction. The complexity of this scenario is discussed in light of possible therapeutic manipulations of the tryptophan/kynurenine pathway in COVID-19 and post-acute COVID-19 syndromes. [ABSTRACT FROM AUTHOR]

Background: Severe leptospirosis is challenging as it could evolve rapidly and potentially fatal if appropriate management is not performed. An understanding of the progression and pathophysiology of Leptospira infection is important to determine the early changes that could be potentially used to predict the severe occurrence of leptospirosis. This study aimed to understand the kinetics pathogenesis of Leptospira interrogans strain HP358 in the hamster model and identify the early parameters that could be used as biomarkers to predict severe leptospirosis. Methodology/Principal findings: Male Syrian hamsters were infected with Leptospira interrogans strain HP358 and euthanized after 24 hours, 3, 4, 5, 6 and 7 days post-infection. Blood, lungs, liver and kidneys were collected for leptospiral detection, haematology, serum biochemistry and differential expression of pro- and anti-inflammatory markers. Macroscopic and microscopic organ damages were investigated. Leptospira interrogans strain HP358 was highly pathogenic and killed hamsters within 6–7 days post-infection. Pulmonary haemorrhage and blood vessel congestion in organs were noticed as the earliest pathological changes. The damages in organs and changes in biochemistry value were preceded by changes in haematology and immune gene expression. Conclusion/Significance: This study deciphered haemorrhage as the earliest manifestation of severe leptospirosis and high levels of IL-1β, CXCL10/IP-10, CCL3/MIP-α, neutrophils and low levels of lymphocytes and platelets serve as a cumulative panel of biomarkers in severe leptospirosis. Author summary: As the severe form of leptospirosis could progress rapidly and be potentially fatal if not treated earlier, deciphering the pathophysiology kinetics of infection is crucial to determine the parameters of disease severity. To understand this, we challenged hamsters with the highly virulent Leptospira interrogans strain HP358. Pulmonary haemorrhage was observed as the earliest pathological change followed by liver and kidneys damages. The increased expression of IL-1β, CXCL10/IP-10, CCL3/MIP-α, high neutrophils and low lymphocytes and platelets production observed in the present study indicate that these parameters could serve as a cumulative panel of biomarkers in severe leptospirosis. [ABSTRACT FROM AUTHOR]

Pulmonary hypertension (PAH) is a proliferative disease of pulmonary blood vessels, but the pathogenesis of pulmonary hypertension is still unclear. This article explores the role of tumor necrosis factor-α (TNF-α), tissue factor (TF), and coagulation function (CF) in the pathogenesis of PAH. PAH is often accompanied by vascular intima injury and muscular arterial media thickening. Coupled with the wide application of nanotargeted drugs in recent years, a targeted nanocarrier encapsulating sildenafil was prepared in this study. The particle size, PDI, zeta potential, drug loading, and encapsulation efficiency were 194.32 ± 17.31 nm , 0.28 ± 0.02 , − 6.34 ± 0.33 , 24.61%, and 70.52%. The monocrotaline PAH rat model was constructed, and it was found that the levels of TNF-α, TF, and CF in the peripheral blood of PAH rats were abnormally increased. 30 PAH rats were randomly divided into 5 groups and injected with saline (NS group), sildenafil (sildenafil group), target the nanoempty carrier (TNC-E group), ordinary nanocarrier encapsulated sildenafil (CNC-sildenafil group), and targeted nanocarrier encapsulate sildenafil (TNC-sildenafil group). Compared with the NS group, the mean pulmonary artery pressure in the TNC-sildenafil group was lower (P < 0.05). Compared with the normal rat group, the pulmonary small blood vessel media thickness, TNF-α level, TF level, and the area of myocardial cells were increased in the NS group, sildenafil group, TNC-E group, and CNC-sildenafil group (P < 0.05). Compared with the NS group, the pulmonary small blood vessel media thickness, myocardial cell area, and the levels of TNF-α and TF in the TNC-sildenafil group were reduced (P < 0.05). Targeting nanocarrier encapsulation of sildenafil can obviously reduce the average pulmonary artery pressure in rats with pulmonary hypertension, improve pulmonary vascular media proliferation and myocardial hypertrophy, and restore the levels of TNF-α, TF, and CF to a normal state. [ABSTRACT FROM AUTHOR]

Severe hypoxia due to coronavirus disease 2019 (COVID-19) is challenging in the intensive care unit (ICU). It is often unresponsive to mechanical ventilation at high positive end-expiratory pressure and the fraction of inspired oxygen combination. The cause of such worsening hypoxia may be microvascular thrombosis in the pulmonary vascular system because of the procoagulant nature of COVID-19 infection. Confirming the diagnosis with computed tomographic pulmonary angiography is not always possible, as the patients are too sick to be shifted. Tissue plasminogen activator (tPA) is recommended for pulmonary thromboembolism with hypotension and worsening hypoxia, as confirmed by computed tomography pulmonary angiography. However, its role in worsening hypoxia because of presumed microthrombi in the pulmonary vasculature in COVID-19 is unclear. We present six cases from our ICU where we used low-dose tPA in COVID-19 refractory hypoxia with presumed microthrombi in the pulmonary vasculature (oligemic lung field, refractory hypoxia, increased D dimer, electrocardiographic features of pulmonary embolism, and right ventricular strain on echocardiography). Oxygenation improved within 6 h and was maintained for up to 48 h in all patients. Therefore, there is a possible role of microthrombi in the mechanism of hypoxia in this setting. An early decision to start low-dose tPA may improve the outcome. However, all patients finally succumbed to sepsis and multiorgan failure later in their course. A systematic review of the literature has also been performed on the mechanism of thrombosis and the use of tPA in hypoxia due to COVID-19. [ABSTRACT FROM AUTHOR]

This commentary will discuss the use of advanced non-invasive imaging methodology for the pulmonary vascular system with special attention to a rubric for the imaging and clinical team to use for any particular clinical situation. [ABSTRACT FROM AUTHOR]

Pulmonary hypertension (PH) is a cardiovascular disorder characterized by substantial morbidity and mortality rates. It is a chronic condition characterized by intricate pathogenesis and uncontrollable factors. We summarized the pathological effects of estrogen, genetics, neuroinflammation, intestinal microbiota, metabolic reorganization, and histone modification on PH. PH is not only a pulmonary vascular disease, but also a systemic disease. The findings emphasize that the onset of PH is not exclusively confined to the pulmonary vasculature, consequently necessitating treatment approaches that extend beyond targeting pulmonary blood vessels. Hence, the research on the pathological mechanism of PH is not limited to target organs such as pulmonary vessels, but also focuses on exploring other fields (such as estrogen, genetics, neuroinflammation, intestinal microbiota, metabolic reorganization, and histone modification). [Display omitted] [ABSTRACT FROM AUTHOR]

Spontaneous migration of placental trophoblasts into maternal blood vessels and embolization to other organs (ie, lung, adrenal gland, spleen, and liver) occurs in women and certain animals with hemochorial placentation. Although considered incidental in most species, increased incidence and numbers of trophoblast emboli are reported in women with gestational diseases with arterial hypertension (pre-eclampsia and eclampsia). To the best of our knowledge, trophoblast emboli have not been reported in lagomorphs. This case report describes the identification of trophoblast emboli in the lung of a wild snowshoe hare (Lepus americanus). Death of this hare was attributed to pulmonary hemorrhages and hemothorax, but a definitive cause for the hemorrhages was not determined. It is unclear whether trophoblast embolism normally occurs in this species and represents an incidental finding, or whether it possibly contributed to rupture of pulmonary or thoracic blood vessels leading to hemorrhage. [ABSTRACT FROM AUTHOR]

The differential diagnosis between pulmonary tuberculous nodules and solid lung cancer nodules is difficult and easy to be misdiagnosed in clinic. The data of clinic and image features of Chest CT with 70 cases of non-calcified pulmonary tuberculous nodules and 198 cases of solid lung cancer nodules confirmed by pathology in the Department of Thoracic Surgery or Respiratory and Critical Care Medicine, the First Affiliated Hospital of Chongqing Medical University from January to September 2020 were collected retrospectively. The characteristics of clinical and chest CT were compared between pulmonary tuberculous nodules and solid lung cancer nodules. The sensitivity, specificity, accuracy and negative predictive value in the two groups were compared between Artificial Intelligence assisted diagnosis system and manual image reading. The results found that the mean age, past tumor history, family history of tumor, CT image features of nodules includes mean diameter, short burr, blood vessel crossing in the pulmonary tuberculous nodules group were lower than those in the solid lung cancer group (p < 0.05). In 35 cases of pulmonary tuberculous nodules group and 63 cases of solid lung cancer nodules group with Dicom format thin-slice chest CT, the sensitivity of AI-assisted diagnosis was 98.98 %. The diagnosis specificity, accuracy and negative predictive value in the AI group (80.61 %, 92.06 %, 60.00 %) were much higher than these in the intermediate respiratory physicians (62.24 %, 76.19 %, 37.14 %, p = 0.004, 0.015, 0.044) respectively, and there was no significant difference between AI and senior radiologists. There are many similarities in clinical and CT image features between pulmonary tuberculous nodules and solid lung cancer nodules. The ability of AI-assisted diagnosis system is better than that of intermediate physicians, reaching the diagnostic level of senior physicians, which is conducive to homogenization and improvement of the differential diagnosis ability of physicians. [ABSTRACT FROM AUTHOR]