Abstract 13678: Serum Hepatokine Selenoprotein P is Upregulated by Hepatic Hypoperfusion and Predicts Adverse Prognosis in Heart Failure Patients

Abstract

Introduction: Cardiac and multiple organ network is involved in the pathophysiology of heart failure (HF). Hepatokines, which are produced and secreted from the liver, have regulatory functions in the peripheral tissues. However, the interaction between the heart and liver or clinical relevance of hepakokines in HF remains poorly understood. The present study aimed to elucidate the clinical significance of hepatokine selenoprotein P in HF. Methods and Results: We enrolled 250 participants including 171 hospitalized patients with HF and 79 control subjects. The serum concentration of selenoprotein P was measured by an enzyme-linked immunosorbent assay. We found that the serum selenoprotein P levels in HF patients were significantly higher than those in controls (14.8 ± 7.5 vs. 8.4 ± 4.6 mg/L, P<0.01). Next, the HF patients were categorized into 4 groups based on the hepatic hemodynamics assessed by abdominal-ultrasonography, which determined liver congestion by shear wave elastography (liver-SWE, >1.33 m/s) and liver hypoperfusion by peak systolic velocity of the celiac artery (celiac-PSV, <62.4 cm/s). Selenoprotein P levels were significantly upregulated in patients with liver hypoperfusion compared to patients with liver congestion ( Figure A ). Selenoprotein P was negatively correlated with celiac-PSV (P<0.01), cardiac output (P<0.01), and left ventricular stroke volume (P=0.03), whereas no correlations were observed between selenoprotein P and indices of congestion such as liver-SWE and right atrial pressure. Kaplan-Meier analysis demonstrated that a higher selenoprotein P group showed a lower event-free rate from re-hospitalization due to worsening HF ( Figure B ). Conclusion: Upregulation of liver-derived selenoprotein P was associated with hepatic hypoperfusion, not hepatic congestion, and related to the adverse prognosis in HF. Selenoprotein P may be a novel molecule involved in the cardio-hepatic interaction.