Pulmonary Changes Research Articles

To study the pulmonary function changes in post-COVID-19 discharged patients and their correlation with disease severity

To study the pulmonary function changes in post-COVID-19 discharged patients and their correlation with disease severity

EUS for the evaluation of esophageal injury after catheter ablation for atrial fibrillation

Background & AimAtrial fibrillation (AF) ablation is an increasingly utilized rhythm control strategy that can damage adjacent structures in the mediastinum including the esophagus. Atrioesophageal fistulas and esophagopericardial fistulas are life-threatening complications that are thought to progress from early esophageal mucosal injury (EI). Endoscopic ultrasound (EUS) has been proposed as a superior method than EGD to survey EI and damage to deeper structures. We aim to evaluate the safety of EUS in categorizing post-ablation EI and quantify EUS-detected lesions and their correlation with injury severity and clinical course. Methods234 consecutive patients between 2006-2020 who underwent AF ablation followed by EUS for the purpose of EI screening were retrospectively reviewed. Kansas City Classification (KCC) was used to classify EI (Type 1, Type 2a/b, Type 3a/b). ResultsEUS identified pleural effusions (31.6%) of patients, mediastinal adventitia changes (22.2%), mediastinal lymphadenopathy (14.1%), pulmonary vein changes (10.6%), and esophageal wall changes (7.7%). EGD revealed 175 (75%) patients without and 59 (25%) with EI. Patients with Type 2a/b EI and no EI were compared with multivariate logistic regression, and the presence of esophageal wall abnormality on EUS with OR 72.85 (95% CI 13.9-380.7), female sex with OR 3.97 (95% CI 1.3-12.3), and number of energy deliveries with OR 1.01 (95% CI 1.003-1.03), were associated with the presence EI type 2a or 2b. Pre-ablation PPI use was not associated with decreased risk of EI. ConclusionsEUS safely assesses mediastinal damage after ablation for atrial fibrillation and may excel over EGD in evaluating mucosal lesions of uncertain significance, with reduced risk of gas embolization in the setting of a full thickness injury (entero-vascular fistula). We propose an EUS-first guided approach to post-AF ablation examination, followed by EGD if it is safe to do so.

Forsythiaside A ameliorates bleomycin-induced pulmonary fibrosis by inhibiting oxidative stress and apoptosis.

Pulmonary fibrosis (PF) is a common clinically critical disease characterized by high morbidity and high mortality. Forsythiaside A (FA) is a phenylethanol glycoside component in Forsythia suspensa, which has anti-inflammatory, antioxidant, and antiviral activities. However, the effects of FA on bleomycin (BLM)-induced PF are unclear. The present study explored the role of FA in the amelioration of oxidative stress and apoptosis in BLM-induced PF as well as the possible underlying mechanisms, in vivo and in vitro. Network pharmacology was used to collect the effects of FA on BLM-induced PF. Subsequently, further observation of the effects of FA on mice with PF by pulmonary pathological changes, transmission electron microscopy, real-time polymerase chain reaction, Western blot analysis, immunofluorescence, and immunohistochemistry. An in vitro model was constructed by inducing A549 with transforming growth factor beta-1 (TGF-β1) to observe the effect of FA on epithelial cell apoptosis. Network pharmacology predicted signaling pathways such as IL-17 signaling pathway and Relaxin signaling pathway. The results of in vivo studies showed that FA ameliorated BLM-induced PF through inhibition of fibrosis, modulation of apoptosis, and oxidative stress. In addition, FA promoted TGF-β1-induced apoptosis in A549 cells. The results of our study suggested that FA could protect mice against BLM-induced PF by regulating oxidative stress and apoptosis as well as the Epithelial mesenchymal transition pathway.

GABA-immunoreactivity in Neuroepithelial Bodies of Spontaneously Hypertensive Rats

Neuroepithelial bodies (NEBs) are complex sensory receptors dispersed throughout the intrapulmonary airways. They are composed of pulmonary neuroendocrine cells (PNECs) which have a large amount of dense-core vesicles containing calcitonin gene-related peptide (CGRP), serotonin (5HT), substance P (SP) and δ-aminobutyric acid (GABA). NEBs are densely innervated by vagal sensory terminals, dorsal root afferents and intrinsic motor fibres. Their location, neurochemical composition and dense innervation make NEBs a key component for the regulation of lung homeostasis. Pulmonary arterial hypertension is a rare disease characterized by morphological alterations in the microcirculation of the lungs causing a wide array of complications and high mortality. Spontaneously hypertensive rats (SHRs) are a common model for essential hypertension, that may develop secondary pulmonary hypertension and thus can be used as an animal model to study pulmonary pressure changes. The present study focuses on the immunohistochemical demonstration of GABA in the NEBs and its potential role in the regulation of the pulmonary pressure. Two groups of SHRs were used and age-matched normotensive Wistar Kyoto (WKY) rats served as controls. We found single PNECs and clusters of GABA-immunoreactive cells protruding into the lumen of the intrapulmonary airways in all examined groups of SHRs and in the normotensive WKY rats. However, the expressional levels statistically differed within the two age groups of SHRs and the controls. Specifically, the NEBs and PNECs in 1-month-old SHRs and particularly in 3-month-old SHRs showed more intense GABA-immunostaining compared to the WKY rats. In conclusion, NEBs and PNECs react to the alterations of the pulmonary pressure homeostasis by an increased GABA expression as a preventive or reactive regulation mechanism against developing pulmonary hypertension.

Concordance and Prognostic Relevance of Different Definitions of Systemic Sclerosis Interstitial Lung Disease Progression.

Interstitial lung disease (ILD) in systemic sclerosis (SSc) is a common complication that has varied progression rate and prognosis. Different progression definitions are available: include minimal clinically important worsening of forced vital capacity (FVC MCIW), EUSTAR (EUropean Scleroderma Trials and Research group) progression, OMERACT (Outcome Measures in Rheumatology Clinical Trials) progression, and Erice ILD working group progression. Pulmonary function and symptoms changes may act as specific confounding factors applying these definitions in SSc. To assess the concordance and prognostic value of four different definitions in SSc-ILD patients overall and specific clinical groups. Progression status in consecutive SSc-ILD patients was assessed over 24 months, 60-month disease-related mortality risk was compared between progressors and non-progressors using the four definitions. Among 245 patients, 26 SSc-related deaths were reported. Mortality was linked to progression for FVC MCIW (HR 2.27, 95% CI 1.03-4.97), OMERACT (HR 2.90, 95% CI 1.28-6.57), and Erice definitions (HR 11.02, 95% CI 2.38-51.08). The association between progression and mortality was poor in patients with disease duration ≥3 years, mild functional impairment, and pulmonary artery systolic pressure (PASP)≥40 mmHg. Erice criteria appeared superior in patients with duration ≥3 years, limited cutaneous variant, and PASP<40 mmHg. OMERACT criteria performed better in diffuse cutaneous variant patients with severe functional impairment. The four evaluated definitions of progression in SSc-ILD are not interchangeable, resulting in up to a third of cases being classified differently based on the adopted criteria, and presenting different prognostic values, particularly within specific clinical groups.

Correlation of high-resolution computed tomography and immunological bronchoalveolar lavage in interstitial lung disease at the onset of inflammatory rheumatic diseases: implications for diagnosis and therapeutic strategies

ObjectivesInflammatory rheumatic diseases (IRD) are often associated with interstitial lung disease (ILD). The aim of the present study was to establish a correlation between the findings on HRCT and the immunological bronchoalveolar lavage (BAL).MethodsThe study included 74 patients with newly diagnosed IRD and evidence of ILD on HRCT with the following pattern: ground-glass opacities (GGO), non-specific interstitial pneumonia (NSIP) and usual interstitial pneumonia (UIP). Patients with other HRCT pattern were excluded. No patient received any immunosuppressive therapy. In addition to HRCT, immunological BAL was performed and the American Thoracic Society clinical practice guideline were used to define BAL patterns (lymphocytic cellular pattern, neutrophilic cellular pattern, eosinophilic cellular pattern and unspecified pattern).ResultsThe main HRCT patterns were NSIP (47.3%), GGO (33.8%), and UIP (18.9%). BAL patterns showed the following distribution: 41.9% lymphocytic cellular pattern, 23.0% neutrophilic cellular pattern, 18.9% eosinophilic cellular pattern, and 16.2% unspecific cellular pattern. Placing these data in the context of the HRCT findings, the lymphocytic cellular BAL pattern (48%) was most commonly BAL pattern associated with GGO pattern in HRCT, whereas neutrophilic and lymphocytic cellular BAL patterns were the dominant feature in NSIP and UIP.ConclusionIn patients with new-onset IRD and ILD, inflammatory pulmonary changes are predominate, reflected by GGO on HRCT and a mainly lymphocytic cell profile in the immunological BAL. In NSIP or UIP on HRCT, the percentages of lymphocytes and neutrophils were higher in BAL fluid, representing a fibrotic component in addition to the inflammation. Consequently, patients with evidence of GGO on HRCT should primarily be treated with anti-inflammatory/immunosuppressive therapy, whereas in patients with NSIP and UIP a combination of anti-inflammatory and anti-fibrotic agents would be the appropriate treatment.

Japanese spotted fever complicated with pleural effusion in Zhejiang province, China: a case report and literature review.

Japanese spotted fever (JSF) mainly occurs in Japan; however, it has been increasingly reported in China. JSF is typically characterized by fever, rash, and eschar, in addition to non-specific symptoms. Yet, reports on the pulmonary indicators in JSF are limited. Herein, we report an unusual case of JSF associated with pleural effusion and pneumonia, in which the pathogen was identified via blood next-generation sequencing (NGS). We report a case of a 33-year-old woman who presented with fever for five days, rash for two days, and myalgia, fatigue, and edema for one day. She had recently been on vacation when an unknown insect bit her. The doctors at the local primary hospital considered a bacterial infection and administered dexamethasone, ceftriaxone, indomethacin, and anti-allergy agents, but the symptoms persisted. A rash without pruritus or pain developed gradually over the entire body and face. We considered rickettsial infection and administered doxycycline and levofloxacin. Metagenomic NGS from blood confirmed the presence of Rickettsia japonica (R. japonica). Abdominal computed tomography revealed bilateral pleural effusion with two atelectasis; patchy shadows with blurred edges, and uniform enhancement in both lower lungs. After several days of treatment, the symptoms and laboratory results improved. A literature review of the epidemiology of R. japonica and JSF in China, characteristics of JSF, and related pulmonary changes, and technology to diagnose JSF is provided. JSF has a variety of symptoms and is becoming increasingly popular in China. Clinical doctors need to identify it carefully.

Oral infection with periodontal pathogens induced chronic obstructive pulmonary disease-like lung changes in mice

BackgroundEpidemiological studies have demonstrated that periodontitis is an independent risk factor for chronic obstructive pulmonary disease (COPD). However, the mechanism underlying the association between these two diseases remains unclear. The lung microbiota shares similarities with the oral microbiota, and there is growing evidence to suggest that the lung microbiome could play a role in the pathogenesis of COPD. This study aimed to investigate whether periodontal pathogens could contribute to the pathogenesis of COPD in a mouse model.MethodsWe established mouse models with oral infection by typical periodontal pathogens, porphyromonas gingivalis (Pg group) or fusobacterium nucleatum (Fn group), over a three-month period. Mice that did not receive oral infection were set as the control group (C group). We assessed the level of alveolar bone resorption, lung function, and histological changes in the lungs of the mice. Additionally, we measured the levels of inflammatory factors and tissue damage associated factors in the lung tissues.ResultsLung function indices, including airway resistance, peak inspiratory/expiratory flow and expiratory flow-50%, were significantly reduced in the Fn group compared to the C group. Additionally, histological examination revealed an increased number of inflammatory cells and bullae formation in the lung tissue sections of the Fn group. Meanwhile, levels of inflammatory factors such as IL-1β, IL-6, IFN-γ, and TNF-α, as well as tissue damage associated factors like matrix metalloproteinase-8 and neutrophil elastase, were significantly elevated in the lung tissue of the Fn group in comparison to the C group. The Pg group also showed similar but milder lung changes compared to the Fn group. Pg or Fn could be detected in the lungs of both oral infected groups.ConclusionThe results indicated that oral periodontal pathogens infection could induce COPD-like lung changes in mice, and they may play a biological role in the association between periodontitis and COPD.

Hepatopulmonary Syndrome: A Comprehensive Review.

Hepatopulmonary syndrome (HPS) is defined by abnormally dilated blood vessels and shunts within the lungs, leading to impaired oxygen exchange. This condition results from intricate interactions between the liver, the gastrointestinal system, and the lungs. This complex system primarily affects pulmonary endothelial, immunomodulatory, and respiratory epithelial cells. Consequently, this contributes to pathological pulmonary changes characteristic of HPS. A classification system based on the severity of oxygen deficiency has been proposed for grading the physiological dysfunction of HPS. Contrast-enhanced echocardiography is considered the primary radiological evaluation for identifying abnormal blood vessel dilations within the lungs, which, combined with an elevated alveolar-arterial gradient, is essential for making the diagnosis. Liver transplantation is the sole effective definitive treatment that can reverse the course of the condition. Despite often being symptomless, HPS carries a significant risk of mortality before transplantation, regardless of the severity of liver disease. Meanwhile, there is varying data regarding survival rates following liver transplantation. The adoption of the model for end-stage liver disease (MELD) standard exception policy has notably improved the results for individuals with HPScompared to the period before MELD was introduced. This review offers a summary of the present understanding, highlighting recent advancements in the diagnosis and treatment of HPS. Furthermore, it aims to augment comprehension of the condition's fundamental mechanisms through insights derived from experimental models and translational research.

Breath assessment at with post-tuberculosis patients suffered new coronavirus infection

BACKGROUND: The possibility of mutual aggravation of post-tuberculosis and post-COVID respiratory pathologies requires additional consideration. AIM: To study some subjective breathing parameters at patients with post-tuberculosis pulmonary residual changes after a new coronavirus infection recovering. MATERIALS AND METHODS: The study included two groups: the main group — 14 patients with cured pulmonary tuberculosis, who had recovered from a new coronavirus infection, a comparison group — 52 patients with post-tuberculosis changes non-sick new coronavirus infection who were admitted to the tuberculosis sanatorium “Glukhovskaya” in 2020–2021. The severity of shortness of breath using the Modified Medical Research Council (mMRC) and Borg scales was assessed upon admission to the sanatorium and a month later. Results: The mMRC scale was 1.5 ± 1.4 and 2.1 ± 0.2 and the Borg scale was 1.5 ± 1.4 and 2.9 ± 0.2 before treatment respectively in the main group and the comparison group. According to the mMRC scale initially 14.3 and 11.5% of patients with pulmonary tuberculosis and the comparison group did not complain of shortness of breath and 50% of pulmonary tuberculosis patients and 42.4% of the comparison group defined it as severe. After a month there were 3 or 4 points on the mMRC scale among pulmonary tuberculosis patients. In the comparison group 3-point shortness of breath decreased by 11.2 times most often indicated shortness of breath with 2 score. According to the Borg scale dyspnea was initially assessed as 3 points at 71.5% pulmonary tuberculosis patients. In the comparison group 67.3% patients had grade 3 dyspnea and 11.5% noted 4–6 grade shortness of breath. After a month the proportion of patients with mild shortness of breath at the pulmonary tuberculosis and comparison groups increased by 4.5 and 3.3 times, respectively, and the frequency of 3-grade shortness of breath decreased by 5 and 3.9 times. CONCLUSIONS: Major post-tuberculosis changes, smoking and chronic obstructive pulmonary disease determine the severity of breathing discomfort to a greater extent than the experience of new coronavirus infection but rehabilitation treatment are leveled out these differences. It is advisable to study the state of the respiratory system at patients cured of pulmonary tuberculosis.

Pulmonary pathological changes in the patient undergoing lung transplantation after chronic graft-versus-host disease complicated by pulmonary infection post-hematopoietic stem cell transplantation: report of a case

Pulmonary pathological changes in the patient undergoing lung transplantation after chronic graft-versus-host disease complicated by pulmonary infection post-hematopoietic stem cell transplantation: report of a case

Impact of general anesthesia on the echocardiographic assessment of right ventricular function in pediatric patients with pulmonary arterial hypertension.

One of the great diagnostic challenges for children with pulmonary arterial hypertension is the need for general anesthesia (GA) to enable successful right heart catheterization. Here, for the first time, we describe how echocardiographic estimates of right ventricular function and pulmonary pressures change in pediatric patients during GA.

Unmasking the nature of granulomatosis with polyangiitis – a diagnostic odyssey revealed through a compelling case report

Introduction and aim. Granulomatosis with polyangiitis (GPA), formerly known as Wegener’s granulomatosis, presents a formidable challenge in the realm of autoimmune diseases. Granulomatosis, characterized by vasculitis and granuloma formation, exhibits diverse clinical manifestations. The rarity of GPA is evident, with an estimated incidence between 0.4 and 11.9 cases per 1 million person-years. The aim of this report is to show the complex diagnostic challenges inherent in GPA, demonstrating the diagnostic process from initial symptoms. Description of the case. This case report unfolds the diagnostic journey of a 52-year-old Caucasian male. The presented case, initially suspected as a respiratory infection, led to a comprehensive investigation owing to persistent symptoms, abnormal blood counts, and elevated inflammatory markers. This narrative aims to depict the patient’s diagnostic journey. Key diagnostic tools include ANCA testing, imaging studies, and tissue biopsy. Pulmonary nodules, lymphangitic changes, and renal involvement culminating in a GPA diagnosis confirmed by positive ANCA and anti-PR3 antibodies. The successful management of this case involved a tailored therapeutic regimen, including cyclophosphamide and methylprednisolone, addressing both vasculitic and renal components. Conclusion. This case contributes to the understanding of atypical presentations of GPA, emphasizing the importance of a holistic and dynamic diagnostic approach.

The impact of antifibrotic use on long-term clinical outcomes in the pulmonary fibrosis foundation registry

BackgroundIdiopathic pulmonary fibrosis (IPF) is a devastating interstitial lung disease (ILD) with a high mortality rate. The antifibrotic medications pirfenidone and nintedanib have been in use since 2014 for this disorder and are associated with improved rate of lung function decline. Less is known about their long-term outcomes outside of the clinical trial context.MethodsThe Pulmonary Fibrosis Foundation Patient Registry was used for this study. Patients with an IPF diagnosis made within a year of enrollment were included. The treated group was defined as patients receiving either pirfenidone or nintedanib for at least 180 days. The untreated group did not have any record of antifibrotic use. Demographic data, comorbidities, serial lung function, hospitalization, and vital status data were collected from the registry database. The primary outcomes were transplant-free survival, time to first respiratory hospitalization, and time to 10% absolute FVC decline. Time-to-event analyses were performed utilizing Cox proportional hazards models and the log-rank test. Model covariates included age, gender, smoking history, baseline lung function, comorbidities, and oxygen use.ResultsThe registry contained 1212 patients with IPF; ultimately 288 patients met inclusion criteria for the treated group, and 101 patients were designated as untreated. Patients treated with antifibrotics were significantly younger (69.8 vs. 72.6 years, p = 0.008) and less likely to have smoked (61.1% ever smokers vs. 72.3% never smokers, p = 0.04). No significant differences were seen in race, gender, comorbidities, or baseline pulmonary function between groups. The primary outcome of transplant-free survival was not significantly different between the two groups (adjusted HR 0.799, 95% CI 0.534–1.197, p = 0.28). Time to respiratory hospitalization was significantly shorter in the treated group (adjusted HR 2.12, 95% CI 1.05–4.30, p = 0.04). No significant difference in time to pulmonary function decline was seen between groups.ConclusionsThis multicenter study demonstrated 63% of newly diagnosed IPF patients had continuous antifibrotic usage. Antifibrotics were not associated with improved transplant-free survival or pulmonary function change but was associated with an increased hazard of respiratory hospitalization. Future studies should further investigate the role of antifibrotic therapy in clinically important outcomes in real-world patients with IPF and other progressive ILDs.

Effects of different nitric oxide synthases on pulmonary and systemic hemodynamics in hypoxic stress rat model.

Under hypoxia, exaggerated compensatory responses may lead to acute mountain sickness. The excessive vasodilatory effect of nitric oxide (NO) can lower the hypoxic pulmonary vasoconstriction (HPV) and peripheral blood pressure. While NO is catalyzed by various nitric oxide synthase (NOS) isoforms, the regulatory roles of these types in the hemodynamics of pulmonary and systemic circulation in living hypoxic animals remain unclear. Therefore, this study aims to investigate the regulatory effects of different NOS isoforms on pulmonary and systemic circulation in hypoxic rats by employing selective NOS inhibitors and continuously monitoring hemodynamic parameters of both pulmonary and systemic circulation. Forty healthy male Sprague-Dawley (SD) rats were randomly divided into four groups: Control group (NG-nitro-D-arginine methyl ester, D-NAME), L-NAME group (non-selective NOS inhibitor, NG-nitro-L-arginine methyl ester), AG group (inducible NOS inhibitor group, aminoguanidine), and 7-NI group (neurological NOS inhibitor, 7-nitroindazole). Hemodynamic parameters of rats were monitored for 10 min after inhibitor administration and 5 min after induction of hypoxia [15% O2, 2200 m a. sl., 582 mmHg (76.5 kPa), Xining, China] using the real-time dynamic monitoring model for pulmonary and systemic circulation hemodynamics invivo. Serum NO concentrations and blood gas analysis were measured. Under normoxia, mean arterial pressure and total peripheral vascular resistance were increased, and ascending aortic blood flow and serum NO concentration were decreased in the L-NAME and AG groups. During hypoxia, pulmonary arterial pressure and pulmonary vascular resistance were significantly increased in the L-NAME and AG groups. This compensatory mechanism activated by inducible NOS and endothelial NOS effectively counteracts the pulmonary hemodynamic changes induced by hypoxic stress. It plays a crucial role in alleviating hypoxia-induced pulmonary arterial hypertension.

The Lung in Rheumatoid Arthritis-Friend or Enemy?

Rheumatoid arthritis (RA) is a chronic autoimmune condition frequently found in rheumatological patients that sometimes raises diagnosis and management problems. The pathogenesis of the disease is complex and involves the activation of many cells and intracellular signaling pathways, ultimately leading to the activation of the innate and acquired immune system and producing extensive tissue damage. Along with joint involvement, RA can have numerous extra-articular manifestations (EAMs), among which lung damage, especially interstitial lung disease (ILD), negatively influences the evolution and survival of these patients. Although there are more and more RA-ILD cases, the pathogenesis is incompletely understood. In terms of genetic predisposition, external environmental factors act and subsequently determine the activation of immune system cells such as macrophages, neutrophils, B and T lymphocytes, fibroblasts, and dendritic cells. These, in turn, show the ability to secrete molecules with a proinflammatory role (cytokines, chemokines, growth factors) that will produce important visceral injuries, including pulmonary changes. Currently, there is new evidence that supports the initiation of the systemic immune response at the level of pulmonary mucosa where the citrullination process occurs, whereby the autoantibodies subsequently migrate from the lung to the synovial membrane. The aim of this paper is to provide current data regarding the pathogenesis of RA-associated ILD, starting from environmental triggers and reaching the cellular, humoral, and molecular changes involved in the onset of the disease.

Effect of Resected Lung Volume on Pulmonary Function and Residual Lung Volume in Patients Undergoing Segmentectomy: A Retrospective Study.

We elucidated the effects of planned resection volume on postoperative pulmonary function and changes in residual lung volume during segmentectomy. This study included patients who underwent thoracoscopic segmentectomy between January 2017 and December 2022 and met eligibility criteria. Pre- and post-resection spirometry and computed tomography were performed. Three-dimensional reconstructions were performed by using computed tomography images to calculate the volumes of the resected, remaining, and nonoperative side regions. Based on the resected region volume, patients were divided into the higher and lower volume segmentectomy groups. Changes in lung volume and pulmonary function before and after the surgery were comparatively analyzed. The median percentage of resected lung volume was 10.9%, forming the basis for categorizing patients into the two groups. Postoperative forced expiratory volume in 1 s (FEV1) and forced vital capacity (FVC) ratios to preoperative measurements in both groups did not differ significantly (FEV1, p = 0.254; FVC, p = 0.777). Postoperative FEV1 and FVC ratios to their predicted postoperative values were significantly higher in the higher volume segmentectomy group than in the lower volume segmentectomy group (FEV1, p = 0003; FVC, p < 0.001). The higher volume segmentectomy group showed significantly greater post-to-preoperative lung volume ratio in overall, contralateral, ipsilateral, residual lobe and residual segment than the lower volume segmentectomy group. Postoperative respiratory function did not differ significantly between the higher- and lower-volume segmentectomy groups, indicating improved respiratory function because of substantial postoperative residual lung expansion. Our findings would aid in determining the extent of resection during segmentectomy.

Follistatin-respiratory connection predicting all-cause mortality among community-dwelling middle-to-old age individuals: Results from the I-Lan Longitudinal Study

ObjectivesThe link between aging and pulmonary function decline is well-established, but the underlying mechanisms have yet to be fully revealed. Serum follistatin, a myokine implicated in muscle degeneration, may play a role in age-related pulmonary changes. This study aims to investigate the relationship between serum follistatin levels and pulmonary function decline in community-dwelling older adults, and evaluate their combined association with all-cause mortality. Research design and methodsThis longitudinal cohort study utilized data from 751 participants aged ≥50 years in the I-Lan Longitudinal Aging Study between 2018−2019. Serum follistatin levels, spirometry results, demographic and clinical data were retrieved. Participants were stratified based on their follistatin levels. Survival curves and group comparisons based on follistatin levels and decline in peak expiratory flow (PEF) using Kaplan-Meier analysis and log-rank tests. Multivariate Cox proportional hazards models were further used to identify independent predictors of all-cause mortality during the 52-month follow-up. ResultsElevated follistatin levels significantly correlated with worse pulmonary function, particularly decreased PEF (p = 0.030). Kaplan–Meier analysis revealed the combination of elevated follistatin levels and decreased PEF was associated with increased risk of all-cause mortality (Log-rank p = 0.023). Cox proportional hazards models further identified that concurrent presence of higher follistatin levels and decreased PEF predicted higher risk of all-cause mortality (adjusted HR 3.58, 95% CI: 1.22–10.53, p = 0.020). ConclusionHigher serum follistatin levels correlate with decreased pulmonary function, specifically PEF decline, in community-dwelling older adults. Furthermore, the coexistence of elevated follistatin levels and decreased PEF was associated with risk of all-cause mortality. Follistatin may serve as a biomarker for pulmonary aging and related adverse outcomes.

Clinical characteristics and risk factors of connective tissue disease complicated with bronchiectasis and pulmonary infection.

The clinical data from 118 CTD patients with bronchiectasis were collected and categorized into two groups: pulmonary infection present (n = 67) and absent (n = 51), for comparative analysis of characteristics and risk factors. Then, we analyzed and compared their demographics, disease characteristics, and risk factors for infection. Among the whole cohort (n = 118), the incidence of pulmonary infections was 56.78%. The occurrence of rheumatoid arthritis, systemic lupus erythematosus, and vasculitis was found to be associated with an increased risk of pulmonary infection. Sputum culture identified Pseudomonas aeruginosa and Klebsiella pneumoniae as the predominant pathogens in the infected group. Notably, symptoms such as joint pains (p = 0.018) and morning stiffness (p = 0.017) were significantly more common in the infected group compared to the noninfected group. Moreover, our findings revealed that elevated levels of C-reactive protein and complement C3, along with bronchial expansion observed on high-resolution computed tomography (HRCT), were significant independent factors in the infection group. Conversely, pulmonary interstitial changes identified through HRCT (OR: 0.135, 95% CI: 0.030-0.612, p = 0.009) were significantly associated with the non-infection group. Overall, this study provides valuable insights into managing CTD patients with bronchiectasis, emphasizing early detection and tailored approaches to prevent and treat pulmonary infections for better outcomes.

Prevalence of non pulmonary vein triggers and pulmonary pressure change in atrial fibrillation ablation for cardiac amyloidosis patients

Abstract Background Cardiac amyloidosis (CA) has been associated with an increased risk of atrial arrhythmias and high risk to develop pulmonary hypertension due to infiltration of the amyloid protein in the atrial wall. Though non-PV triggers are commonly seen in left atrium, they are also seen in the right side of the heart, so identifying them at the time of ablation is essential. Objective The study evaluates the prevalence of non-PV triggers during catheter ablation in atrial fibrillation (AF) patients affected by cardiac amyloidosis and how restoration of sinus rhythm affects pulmonary pressures. Methods This is a study including 74 consecutive patients with an established diagnosis of amyloidosis ATTR diagnosed with cardiac MRI or myocardial biopsy that underwent their first AF catheter ablation. All have a transthoracic echocardiogram before ablation. They underwent pulmonary vein (PV) isolation + isolation of left atrial posterior wall and superior vena cava. Additionally, extrapulmonary triggers, which are defined as ectopic triggers originating from sites other than PVs including left atrial appendage (LAA), coronary sinus (CS), interatrial septum, crista terminalis, mitral valve anulus were identified. Post procedure, patients were followed up routinely with ECG during office visits, echocardiogram, 7-day Holter monitor and event recorders during the first year followed by biannual checkups during the remaining part of the follow-up period. Student’s t-test was used to compare pulmonary pressure between the groups. Results Isoproterenol-challenge revealed non-PV triggers in 51 (68.9%) patients. These triggers were mostly mapped to LAA (39, 52.7%), CS (30, 40,5%), and crista terminalis (35, 47.3%). Besides, ectopic beats were seen originating from inter-atrial septum (19, 25.6%), mitral valve annulus (10, 13.5%). More than one trigger was found in (68%) patients. At 1-year after the ablation, 65 (87.8%) were arrhythmia-free off antiarrhythmic drugs. Moreover, in patients who maintained sinus rhythm post-ablation, there was either a non progression or a reduction in pulmonary pressures (PAPm before ablation: 44.8 ± 8.9 mmHg vs PAPm after ablation 45.1 ± 11.1 mmHg, P value =0.87). Conversely, those experiencing arrhythmic recurrences demonstrated an increase in pulmonary pressures (PAPm before ablation: 41.9 ± 7.7 mmHg vs PAPm after ablation 47.8 ± 10.2 mmHg, P value =0.019). Fig.1 Conclusion Our findings suggest that non-PV triggers are highly prevalent in cardiac amyloidosis AF patients including a high rate crista terminalis firing. Notably, restoration of sinus rhythm post-ablation was linked to stable or reduced pulmonary arterial pressures, whereas patients with arrhythmic recurrences experienced a significant increase.