Emerging evidence suggests a significant association between monocytes and the pathophysiology and prognosis of idiopathic pulmonary fibrosis (IPF). This review aims to systematically evaluate current knowledge regarding blood monocyte counts and their relationship with the etiology, progression, and prognosis of IPF. We conducted a systematic search in the PubMed database for articles published through 17 February 2025, using the MeSH terms “lung diseases, interstitial” and “monocytes,” which yielded 314 results. After filtering for full-text articles in English (n = 242), we included only studies focusing on blood monocyte counts with clinical implications in IPF. Articles relating to other cell types or non-IPF lung diseases were excluded. Our systematic search identified 12 relevant articles. Monocytes play an essential role in regulating inflammatory responses and resolution across multiple diseases, with established but incompletely understood contributions to lung fibrosis development in IPF. Correlations have been demonstrated between elevated blood monocyte counts and the following: (1) the presence and progression of interstitial lung abnormalities, (2) the progression from an indeterminate usual interstitial pneumonia (UIP) pattern on CT scans to definitive IPF, and (3) worse lung function parameters, an increased risk of acute exacerbations, and reduced overall survival in IPF patients. Monocytes serve as critical orchestrators throughout IPF’s natural history—from early interstitial changes to disease progression and acute exacerbations. Targeting monocyte recruitment pathways and reprogramming their differentiation represents a promising therapeutic approach, while circulating monocyte counts offer potential as accessible biomarkers for disease progression and treatment response. Future research should characterize stage-specific monocyte phenotypes to enable precision-targeted interventions.

Background: Estimated plasma volume status (ePVS) correlates with intravascular congestion and prognosis in patients with heart failure. The ePVS relationship with invasive hemodynamic profiling and clinical outcomes in patients with liver cirrhosis (LC) remains unclear.Methods: This single‐center retrospective cohort study included LC patients who underwent right heart catheterization (RHC) between 2018 and 2023. Estimated plasma volume status (ePVS) was calculated using the Strauss‐derived Duarte formula, with patients classified into high (> 5.5%) and low‐ePVS (≤ 5.5%) groups. Cox‐multivariable analysis was used to determine if ePVS was associated with all‐cause mortality within 1 year post‐RHC among transplant‐free patients.Results: Of the 353 patients with LC (median age 59 years, 59% male, 45% Caucasian, and 29% African American), 79% were classified into the high‐ePVS group. Compared to the low‐ePVS group, the high‐ePVS group had significantly higher right atrial pressure (9 vs. 6 mmHg, p = 0.01), pulmonary arterial wedge pressure (14 vs. 11 mmHg, p = 0.014), cardiac output (9.8 vs. 6.4 L/min, p < 0.0001), and cardiac index (5 vs. 3.1 L/min/m², p < 0.0001). Additionally, the high‐ePVS group exhibited a higher prevalence of cirrhosis‐related complications, including ascites, splenomegaly, and varices, and a greater likelihood of receiving orthotopic liver transplantation within 1 year (38% vs. 11%, p < 0.0001). Among transplant‐free patients, ePVS was independently associated with all‐cause mortality at 1 year (HR 1.15, 95% CI: 1.00–1.32, p = 0.048).Conclusion: Our study demonstrated that ePVS was associated with intravascular congestion, hyperdynamic circulation, and cirrhosis complications. Furthermore, ePVS was independently associated with all‐cause mortality among transplant‐free LC patients.

Background/Objectives: Combined pulmonary fibrosis and emphysema (CPFE) is associated with poor outcomes. We investigated the association of antifibrotic therapy on patients with CPFE. Methods: This retrospective study included adult patients, older than 18 years, with a diagnosis of CPFE between 2015 and 2019 using TrinetX database. CPFE was defined as a diagnosis of pulmonary fibrosis (PF) and emphysema or chronic obstructive pulmonary disease. Propensity score matching was performed to compare baseline characteristics for CPFE patients on antifibrotic therapy (nintendanib and pirfenidone) with those not on antifibrotic therapy. The outcomes studied included all-cause mortality, major adverse cardiac event (MACE, [myocardial infarction, unstable angina]), hypoxic and hypercapnic respiratory failure, and stroke. These outcomes were compared at one-, three-, and five-year follow-ups. Results: Patients were divided into two cohorts: those on antifibrotic therapy (cohort 1, n = 861) and those without antifibrotic therapy (cohort 2, n = 861). Although not statistically significant, there was a trend towards increased mortality in cohort 1 at the 5-year follow-up (HR 1.14; CI 0.99–1.33). There was also an increased incidence of MI (HR 1.68; CI 0.88–1.47) and hypoxic respiratory failure (HR 1.17; CI 0.99–1.39). Notably, there was also a trend towards decreased incidence of stroke (HR 0.73; CI 0.51–1.05), and no difference in unstable angina (HR 0.94; CI 0.47–1.86) and hypercapnic respiratory failure (HR 0.99; CI 0.67–1.47). Conclusions: For patients with CFPE, antifibrotic use demonstrated a trend towards increased risk of mortality at 5-year follow-up, raising concerns for “sicker patient” bias. Prospective studies should be designed to include patients with CPFE and evaluate the benefits of antifibrotics.

Background: Glucagon‐like peptide‐1 receptor agonists (GLP‐1 RAs) reduce cardiovascular risk in obesity, but their effect on atrial fibrillation (AF) in heart failure with preserved ejection fraction (HFpEF) remains unclear. Methods: We analyzed TriNetX data comparing obese, non‐diabetic HFpEF patients treated with GLP‐1 RAs ( n = 478) with untreated patients ( n = 6887). Propensity matching yielded 470 patients per cohort. Results: GLP‐1 RA therapy was not associated with reduced AF incidence (HR 0.86; 95% CI, 0.53–1.39; p = 0.543) but was associated with lower mortality (HR 0.42; 95% CI, 0.23–0.75; p = 0.003). Conclusions: GLP‐1 RAs may not reduce AF incidence in obese, HFpEF patients.

Introduction: Patients with rheumatoid arthritis (RA) have higher risk for pneumonia, interstitial lung disease (ILD) and pulmonary fibrosis (PF). However, the association between an ICD-10-coded pneumonia event (CPE) and the incidence of ILD or PF in the RA population remains unclear. Methods: We conducted a retrospective cohort study using the TriNetX database. Patients with ICD-10 for RA aged 50 or older who had a CPE within one year of RA diagnosis (CPE cohort, n = 4553) were matched 1:1 by propensity score for key factors, including demographics, comorbidities (i.e., COPD), and medication use (DMARDs, corticosteroids) to RA patients without a CPE (Control cohort, n = 4553). Cox proportional hazard models assessed the incidence of a composite ILD outcome, PF, and secondary complications over a 4-year follow-up after the index event defined as 1-year after RA diagnosis for both cohorts. Results: The CPE cohort showed an increased risk for all outcomes. Patients with CPE had a 2.48-fold increased risk for PF (HR = 2.48; 95% CI, 1.78–3.45; p < 0.01) and a 2.87-fold increased risk for the composite ILD outcome (HR = 2.87; 95% CI, 2.18–3.80; p < 0.01). The risk of rheumatoid lung disease was 4.15 times higher (HR = 4.15; 95% CI, 2.30–7.50; p < 0.01). Furthermore, the CPE group had a higher risk for all-cause mortality (HR = 1.82; 95% CI, 1.58–2.09; p < 0.01). Conclusions: The CPE within one year of RA diagnosis is associated with an increase in subsequent ILD-coded outcomes. While this retrospective design cannot establish causality, an unspecified pneumonia code in early RA may represent an early clinical manifestation of unrecognized ILD, serving as a high-risk marker that warrants pulmonary surveillance.