The validation cohort yielded similar findings.Ĭonclusions: Severe congestion in HF is mainly associated with inflammation, endothelial activation, and mechanical stress. Pathways most prominently involved in congestion were related to inflammation, endothelial activation, and response to mechanical stimulus. KITLG, EGF, and PON3 were the strongest down-regulated proteins (FC <−1.30, FDR P < 0.05). FGF-23, FGF-21, CA-125, soluble ST2, GDF-15, FABP4, IL-6, and BNP were the strongest up-regulated proteins (fold change >1.30, false discovery rate, P < 0.05).
Results: Differential protein expression analysis showed 107/363 up-regulated and 6/363 down-regulated proteins in patients with congestion compared with those without. Results were validated in an independent validation cohort of 1,342 HF patients (436 noncongested and 232 severely congested). Plasma concentrations of 363 unique proteins (Olink Proteomics Multiplex CVD-II, CVD-III, Immune Response and Oncology II panels) were compared between noncongested and severely congested patients. Patients with a score ranking in the bottom or top categories of congestion were deemed noncongested (n = 408) and severely congested (n = 142), respectively. Methods: A congestion score (sum of jugular venous pressure, orthopnea, and peripheral edema) was calculated in 1,245 BIOSTAT-CHF patients with acute or worsening HF. Objectives: Using pathway and differential expression analyses, the authors aim to identify biological processes and biomarkers associated with congestion in HF.
ANKER LIFE NOTE C DRIVER
Background: Congestion is the main driver behind symptoms of heart failure (HF), but pathophysiology related to congestion remains poorly understood.
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