Background To investigate the prognostic importance of functional capacity and exercise behavior in patients with metastatic non-small cell lung cancer (NSCLC). Patients and methods Using a prospective design, 118 consecutive participants with histologically confirmed metastatic (inoperable) NSCLC and Eastern Cooperative Oncology group (ECOG) 0–3 completed a six-minute walk test to assess functional capacity and questionnaire that assessed self-reported exercise behavior. Cox proportional models were used to estimate the risk of all-cause mortality according to six-minute walk distance (6MWD) (<358.5 m, 358.5–450 m, ≥450 m) and exercise behavior (MET-hrs wk−1) categories with adjustment for important covariates. Results Median follow-up was 26.6 months; 77 deaths were reported during this period. Functional capacity was an independent predictor of survival (Ptrend = 0.003) and added incremental prognostic value beyond that provided by PS plus other traditional markers of prognosis (Ptrend = 0.025). Compared with patients achieving a 6MWD <358.5 m, the adjusted hazard ratio (HR) for all-cause mortality was 0.61 (95% CI, 0.34–1.07) for a 6MWD of 358.5–450 m, and 0.48 (95% CI, 0.24–0.93) for a 6MWD >450 m. In unadjusted analysis, there was a borderline significant effect of exercise behavior on survival (p = 0.052). Median survival was 12.89 months (95% CI, 9.11–21.05 months) for those reporting <9 MET-hrs wk−1 compared with 25.63 months (95% CI, 11.28 to ∞ months) for those reporting ≥9 MET-hrs wk−1. Conclusions Functional capacity is a strong independent predictor of survival in advanced NSCLC that adds to the prediction of survival beyond traditional risk factors. This parameter may improve risk stratification and prognostication in NSCLC.

A 58-year-old woman presented to a pulmonology clinic for evaluation of bilateral pulmonary nodules. Two years previously, she had presented with atrioventricular nodal reentrant tachycardia. During evaluation for her tachyarrhythmia, transthoracic echocardiogram (TTE) revealed a large, homogenous, highly mobile right atrial and ventricular mass. She underwent electrophysiologic ablation, tricuspid valve annular ring replacement, and resection of the mass, which pathology confirmed to be a myxoma. Now, a recent abdomen and pelvis CT study obtained for history of nephrolithiasis incidentally noted bilateral lower lobe pulmonary nodules. Follow-up noncontrast chest CT confirmed bilateral peribronchovascular solid pulmonary nodules up to 8 mm in diameter throughout all lobes. The nodules appeared contiguous with the segmental and subsegmental bronchovascular bundles, and many occurred at branch points. There was no mediastinal or hilar lymphadenopathy. To evaluate the pulmonary nodules, she was referred to a pulmonology clinic. She reported only stable, nonlimiting dyspnea on exertion. She did not have a cough. She denied a history of fevers, weight loss, or night sweats. She had no rash or skin changes, visual changes, joint pain or swelling, or palpitations. She had no history of oropharyngeal or genital ulcerations. Social history was notable for a 40-pack-year smoking history, with quit date 2 years prior. She had no risk factors for TB exposure and no exposures to sandblasting, stone cutting, or other environmental risk factors for silicosis. Family history was negative for autoimmune conditions, sarcoidosis, and lymphoproliferative disorders.

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In the over 100 years since the recognition of pulmonary hypertension (PH), immense progress and significant achievements have been made with regard to understanding the pathophysiology of the disease and its treatment. These advances have been mostly in idiopathic pulmonary arterial hypertension (IPAH), which was classified as Group 1 Pulmonary Hypertension (PH) at the Second World Symposia on PH in 1998. However, the pathobiology of PH due to chronic lung disease, classified as Group 3 PH, remains poorly understood and its treatments thus remain limited. We review the history of the classification of the five groups of PH and aim to provide a state-of-the-art review of the understanding of the pathogenesis of Group 1 PH and Group 3 PH including insights gained from novel high-throughput omics technologies that have revealed heterogeneities within these categories as well as similarities between them. Leveraging the substantial gains made in understanding the genomics, epigenomics, proteomics, and metabolomics of PAH to understand the full spectrum of the complex, heterogeneous disease of PH is needed. Multimodal omics data as well as supervised and unbiased machine learning approaches after careful consideration of the powerful advantages as well as of the limitations and pitfalls of these technologies could lead to earlier diagnosis, more precise risk stratification, better predictions of disease response, new sub-phenotype groupings within types of PH, and identification of shared pathways between PAH and other types of PH that could lead to new treatment targets.

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