Characterizing the Progression of Pulmonary Edema Severity: Can Pairwise Comparisons in Radiology Reports Help?

Accurately assessing the severity of pulmonary edema is critical for making treatment decisions in congestive heart failure patients. However, the current scale for quantifying pulmonary edema based on chest radiographs does not have well-characterized severity levels, with substantial inter-radiologist disagreement. In this study, we investigate whether comparisons documented in radiology reports can provide accurate characterizations of pulmonary edema progression. We propose a rules-based natural language processing approach to assess the change in a patient's pulmonary edema status (e.g. better, worse, no change) by performing pairwise comparisons of consecutive radiology reports, using regular expressions and heuristics derived from clinical knowledge. Evaluated against ground-truth labels from expert radiologists, our labeler extracts comparisons describing the progression of pulmonary edema with 0.875 precision and 0.891 recall. We also demonstrate the potential utility of comparison labels in providing additional fine-grained information over noisier labels produced by models that directly estimate severity level.

Elevated Serum Fibroblast Growth Factor 21 Is Relevant to Heart Failure Patients with Reduced Ejection Fraction

Objective. The aim of this study was to evaluate the roles of fibroblast growth factor 21 (FGF21) in heart failure patients with reduced ejection fraction and its association with Heart Failure with reduced Ejection Fraction (HFrEF). Methods. The level of FGF21 was measured by enzyme-linked immunosorbent assay (ELISA) in 199 subjects enrolled in this study, including 128 subjects with HFrEF and 71 control subjects. The mean follow-up time was 13.36 months. The left ventricular end-diastolic diameter (LVEDD) and left ventricular ejection fraction (LVEF) percentage were evaluated by the 2D echocardiography. Serum brain natriuretic peptide (BNP) was measured in the routine clinical laboratory. Results. The serum FGF21 level was evidently higher in patients with HFrEF than in the control group ( 228.72 ± 24.04 vs. 171.60 ± 12.98 , p < 0.001 ). After 1 year of follow-up, 61 patients (47.66%) with heart failure were readmitted to the hospital, including 8 deaths (13.11%). The AUC of the receiver operating characteristic (ROC) curve for the predictive value of FGF21 for prognosis was 0.964. Kaplan-Meier analysis results showed that there were significant differences in the 1-year mortality and heart failure readmission events between the grouped subjects. A poor prognosis was correlated with the serum level of FGF21, BNP, LVEDD, and LVEF, which was confirmed by the univariate Cox analysis. Conclusion. FGF21 was independently associated with an increased risk of mortality and readmission HFrEF patients. Therefore, FGF21 has the potential to be a biomarker for the progression of HFrEF in patients.

Skeletal muscle derived Musclin protects the heart during pathological overload

Cachexia is associated with poor prognosis in chronic heart failure patients, but the underlying mechanisms of cachexia triggered disease progression remain poorly understood. Here, we investigate whether the dysregulation of myokine expression from wasting skeletal muscle exaggerates heart failure. RNA sequencing from wasting skeletal muscles of mice with heart failure reveals a reduced expression of Ostn, which encodes the secreted myokine Musclin, previously implicated in the enhancement of natriuretic peptide signaling. By generating skeletal muscle specific Ostn knock-out and overexpressing mice, we demonstrate that reduced skeletal muscle Musclin levels exaggerate, while its overexpression in muscle attenuates cardiac dysfunction and myocardial fibrosis during pressure overload. Mechanistically, Musclin enhances the abundance of C-type natriuretic peptide (CNP), thereby promoting cardiomyocyte contractility through protein kinase A and inhibiting fibroblast activation through protein kinase G signaling. Because we also find reduced OSTN expression in skeletal muscle of heart failure patients, augmentation of Musclin might serve as therapeutic strategy.