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Objectives This study investigated whether pulmonary artery (PA) 18F-FDG uptake is associated with hypertension, and if it correlates to elevated pulmonary pressures. Background 18F-fluorodeoxyglucose (FDG) positron emission tomography (PET) combined with computed tomography or cardiac magnetic resonance (CMR) has been used to assess inflammation mostly in large arteries of the systemic circulation. Much less is known about inflammation of the vasculature of the pulmonary system and its relationship to pulmonary hypertension (PH). Methods In a single-center cohort of 175 patients with suspected cardiac sarcoidosis, who underwent hybrid thoracic PET/CMR, 18F-FDG uptake in the PA was quantified according to maximum standardized uptake value (SUVmax) and target-to-background ratio (TBR) and compared with available results from right heart catheterization (RHC) or transthoracic echocardiography (TTE). Results Thirty-three subjects demonstrated clear 18F-FDG uptake in the PA wall. In the subgroup of patients who underwent RHC (n = 10), the mean PA pressure was significantly higher in the group with PA 18F-FDG uptake compared with the group without uptake (34.4 ± 7.2 mm Hg vs 25.6 ± 9.3 mm Hg; P = 0.003), and 9 (90%) patients with PA 18F-FDG uptake had PH when a mean PA pressure cutoff of 25 mm Hg was used compared with 18 (45%) in the nonuptake group (P Conclusions We demonstrate that 18F-FDG uptake by PET/CMR in the PA is associated with PH and that its intensity correlates with PA pressure.

Background To evaluate the chest CT appearance of patients with a clinicopathologic diagnosis of hypersensitivity pneumonia. Methods IRB approval was obtained for a retrospective review of patients with a preoperative CT scan, a surgical pathology report from a transbronchial biopsy or wedge resection consistent with hypersensitivity pneumonitis, and a pulmonary consultation, which also supported the diagnosis. The pathology report was evaluated for granulomas, airway-centered fibrosis, microscopic honeycombing, and fibroblast foci. The medical records were reviewed for any known antigen exposure. Patients were separated into two groups; those with and without a known antigen exposure. The CT scans were assessed for distribution of fibrosis: upper lobe or lower lobe predominance, airway-centered versus peripheral distribution, three-density pattern, and honeycombing. Results 264 pathology reports included the term chronic hypersensitivity pneumonitis (CHP). Thirty-eight of the patients had a pulmonologist who gave the patient a working diagnosis of CHP. The average age of these patients was 64 years, and 21/38 were women. Seventeen of the 38 patients had at least one antigen exposure described in the medical records. All the patients had fibrosis along the airways on chest CT. Both known antigen exposure and no known antigen patients had upper and lower lung-predominant fibrosis. There were more patients with hiatal hernias in the unknown antigen group. Honeycombing was an uncommon finding. Conclusion Airway-centered fibrosis was present on chest CT in all 38 patients with CHP (100%), with or without known antigen exposure.

BACKGROUND Chest CT scans are routinely obtained to monitor disease progression in pulmonary fibrosis. However, radiologists do not employ a standardized system for quantitative description of the severity of the disease. Development and validation of a grading system offers potential for enhancing the information that radiologists provide clinicians. STUDY DESIGN AND METHODS Our retrospective review analyzed 100 sequential patients with usual interstitial pneumonitis (UIP) on HRCT scans from 2018 and 2019. A radiologic scoring system evaluated the percent of normal lung on the basis of a 0-5 point scale per lobe (findings for the right middle lobe were included in the right upper lobe score), yielding an overall additive numerical score on a scale of 20 (completely normal lung) to 0 (no normal lung). Two radiologists quantified the percentage of normal lung by consensus agreement. Percent DLCO as well as demographic data were obtained from the medical record. Statistical analysis was performed using Spearman correlation to assess correlation between grade and percent DLCO. RESULTS 96 patients met the inclusion criteria; average age was 71, 68% were male. Score on CT scan ranged from 18 to 4; average 10.9, SD 3.58. The single-breath diffusing capacity (percent DLCO) ranged from 88% to 17%; mean 44.5%, SD 14.3%. Spearman's correlation for CT score and percent DLCO was 0.622, P

Objective To determine the prevalence of osteophyte induced lung fibrosis (OIF) and its relationship to osteophyte size, location, and surrounding fat. Methods 94 CT scans of the chest were reviewed, size of the largest osteophyte and the presence of fibrosis were recorded. Results Presence of fibrosis was higher among patient with large (> 10 mm) osteophytes compared to those with small (1–10 mm) osteophytes. Age and presence of periosteophyte fat were significantly associated with presence of fibrosis. Conclusions As the size of an osteophyte increases, there is a greater likelihood of lung fibrosis. Subpleural fat protects the lung from OIF.

Background Early recognition of patients with interstitial lung disease (ILD) who have an increased risk of developing acute exacerbation (AE) or preclinical AE may be clinically useful, since AE is associated with poor outcome and preventive measures would be of interest to ILD researchers. This study evaluated the relationship between elevated serum D-dimer level (≥0.4 mcg/mL) and subsequent AE or preclinical AE in patients with ILD. Methods This single-center, retrospective study was performed from October 2009 through September 2015 in patients with ILD who were ≥18 years old and had idiopathic pulmonary fibrosis, other idiopathic interstitial pneumonias, chronic hypersensitivity pneumonitis, ILD related to collagen tissue disease, or combined pulmonary fibrosis/emphysema. The primary outcome measure was AE development within three months from each D-dimer measurement. The secondary outcome measures were respiratory-related hospitalization, all-cause hospitalization, venous thromboembolism (VTE), and all-cause mortality within three months. Results A total of 263 patients (mean age, 64.1 years) with 374 D-dimer measurements (median, 0.44 mcg/mL) were included. The risk of developing AE was significantly higher in patients with elevated serum D-dimer level (adjusted odds ratio: 10.46; 95% CI: 1.24–88.11; p = 0.03). Patients with elevated serum D-dimer level had increased risk for respiratory-related hospitalization, all-cause hospitalization, VTE, and all-cause mortality. The other factors predictive for AE were home oxygen therapy, increased serum lactate dehydrogenase, decreased FVC, and decreased FEV1.0. Conclusions Elevated serum D-dimer is associated with the risk of developing AE. Serum D-dimer may be used as a prognostic marker to predict AE or recognize preclinical AE.

The assessment of both the pattern and activity of myocardial injury has important implications for the clinical management of patients with cardiovascular disease. Comprehensive evaluation of these has previously been challenging using a single imaging modality. Cardiac magnetic resonance (CMR)

The idiopathic interstitial pneumonias (IIPs) are a group of diffuse lung diseases that share many similar radiologic and pathologic features. According to the revised 2013 American Thoracic Society-European Respiratory Society classification system, these entities are now divided into major IIPs (idiopathic pulmonary fibrosis, idiopathic nonspecific interstitial pneumonia, respiratory bronchiolitis-associated interstitial lung disease, desquamative interstitial pneumonia, cryptogenic organizing pneumonia, and acute interstitial pneumonia), rare IIPs (idiopathic lymphoid interstitial pneumonia, idiopathic pleuroparenchymal fibroelastosis), and unclassifiable idiopathic interstitial pneumonias. Some of the encountered radiologic and histologic patterns can also be seen in the setting of other disorders, which makes them a diagnostic challenge. As such, the accurate classification of IIPs remains complex and is best approached through a collaboration among clinicians, radiologists, and pathologists, as the treatment and prognosis of these conditions vary greatly.

Background Sarcoidosis-associated pulmonary hypertension (SAPH) is a common problem in patients with persistent dyspneic sarcoidosis. The objective of this study was to determine the effect of bosentan therapy on pulmonary arterial hemodynamics in patients with SAPH. Methods This 16-week study was a double-blind, placebo-controlled trial of either bosentan or placebo in patients with SAPH confirmed by right-sided heart catheterization. Patients were enrolled from multiple academic centers specializing in sarcoidosis care. They were stable on sarcoidosis therapy and were receiving no therapy for pulmonary hypertension. The cohort was randomized two to one to receive bosentan at a maximal dose of 125 mg or placebo bid for 16 weeks. Pulmonary function studies, 6-min walk test, and right-sided heart hemodynamics, including pulmonary artery mean pressure and pulmonary vascular resistance (PVR), were performed before and after 16 weeks of therapy. Results Thirty-five patients completed 16 weeks of therapy (23 treated with bosentan, 12 with placebo). For those treated with bosentan, repeat hemodynamic studies at 16 weeks demonstrated a significant mean ± SD fall in PA mean pressure (−4 ± 6.6 mm Hg, P = .0105) and PVR (−1.7 ± 2.75 Wood units, P = .0104). For the patients treated with placebo, there was no significant change in either PA mean pressure (1 ± 3.7 mm Hg, P > .05) or PVR (0.1 ± 1.42 Wood units, P > .05). There was no significant change in 6-min walk distance for either group. Two patients treated with bosentan required an increase of supplemental oxygen by > 2 L after 16 weeks of therapy. Conclusions This study demonstrated that bosentan significantly improved pulmonary hemodynamics in patients with SAPH. Trial registry ClinicalTrials.gov ; No: NCT00581607; URL: www.clinicaltrials.gov

Background The provision of effective palliative care is of great importance to patients awaiting lung transplantation. Although the prospect of lung transplantation provides hope to patients and their families, these patients are usually very symptomatic from their underlying disease. Methods An e-mail questionnaire was sent to members of the American College of Chest Physicians' Transplant NetWork and the Pulmonary Council of the International Society for Heart and Lung Transplantation (ISHLT). The survey included questions about barriers to providing palliative care, the availability of palliative care services, and recommended strategies to improve palliative care for lung transplant candidates. Results The 158 respondents represented approximately 65% of transplant programs in the ISHLT registry. Respondents were in practice a mean of 11.3 (± 9) years, 70% were pulmonologists, 17% were surgeons, and 13% were other care providers. Barriers were classified into domains including patient factors, family factors, physician factors, and institutional/transplant program/lung allocation system factors. Significant patient/family barriers included unrealistic patient/family expectations about survival, unwillingness to plan end-of-life care, concerns about abandonment or inappropriate care after enrollment in a palliative care program, and family disagreements about care goals. For institutional/program/allocation system barriers, only the requirement for weight loss or gain to meet program-specific BMI requirements was identified. Significant physician barriers included competing time demands and the seemingly contradictory goals of transplant vs palliative care. Strategies recommended to improve palliative care included routine advance care planning for patients awaiting transplantation, access to palliative care specialists, training of transplant physicians in symptom management, and regular meetings among transplant physicians, nurses, patients, and families. Conclusions Physicians providing care to lung transplant candidates reported considerable barriers to the delivery and acceptance of palliative care and identified specific strategies to improve palliative care for lung transplant candidates.

Inhaled asbestos induces accumulation of alveolar macrophages (AM) and polymorphonuclear leukocytes (PMN) in lung. Asbestos-enhanced production of superoxide anion (O2-) by AM and/or PMN may be involved in the pathogenesis of asbestos-induced fibrosis, either through direct effects on collagen synthesis or via mediation of tissue injury and repair. In in vivo experiments, bronchoalveolar lavage (BAL) 3 to 8 weeks following intratracheal asbestos injections showed increases in both PMN and AM, with AM representing 78 to 82% of cells recovered. Inhalation models, generally regarded as more analagous to human exposures, have confirmed AM as the predominant component of the cellular response to inhaled asbestos. In this study, the in vitro effects of asbestos fiber on O2- production by AM have been determined in cell populations derived from the Syrian golden hamster. AM for in vitro study were obtained by BAL. O2- production was monitored as superoxide dismutase (SOD) - inhibitable cytochrome c reduction. Significant rises in O2- release by AM were noted in the presence of 0.4 mg/ml crocidolite (2.53 +/- 0.33 nmole cytochrome c reduced/10(6) cells/30 min, 37 degrees C; controls 1.13 +/- 0.18 nmole; P less than 0.02). Chrysotile induced levels of O2- release in AM which were similar to those evoked by crocidolite.