Abstract

Background: Increasing evidence suggests that N-terminal probrain natriuretic peptide (NT-proBNP) may be a more discerning marker for the detection and evluation of heart failure than BNP. However, fundamental mechanisms that contribute to the heart failure in aortic stenosis (AS) and ischemic heart disease (IHD) via NT-proBNP remain unclear. Objectives: The purpose of this study was to investigate whether NT-proBNP represents autocrine/paracrine factors and are accumulated in pericardial fluid (PF) in patients with AS and IHD. Methods: With an electrochemiluminescent immunoassay, we measured the concentrations of NT-proBNP in serum and pericardial fluid simultaneously in 48 patients undergoing aortic valve replacement and 101 patients undergoing coronary artery bypass grafting. We investigated the correlation of NT-proBNP levels in serum or PF with hemodynamic variables. Results: In patients with AS, the PF levels of NT-proBNP were markedly elevated compared with serum levels (10747±17619 pg/ml vs. 2828±7787 pg/ml, p=0.0054). In patients with IHD, the PF levels of NT-proBNP were markedly elevated compared with serum levels (7224±16345 pg/ml vs. 764±1199 pg/ml, p=0.0001). In AS, NT-proBNP levels in PF but not in serum had closer relations with left ventricular (LV) end-diastolic (r=0.338, p=0.0463) and systolic volume indexes (r=0.551, p=0.0005). In AS, NT-proBNP levels in PF but not in serum inversely correlated with LV ejection fraction (EF) (r=-0.510, p=0.0002). In IHD, NT-proBNP levels in PF but not in serum had closer relations with left ventricular (LV) end-diastolic (r=0.493, p<0.0001) and systolic volume indexes (r=0.582, p<0.0001). NT-proBNP levels in PF but not in serum inversely correlated with LV ejection fraction (EF) (r=-0.406, p<0.0001). NT-proBNP levels in serum and PF is higher in AS due to pressure overload than in IHD due to volume overload. Conclusion: Increased PF concentrations of NT-proBNP reflects the direct actions as a local mediator against cardiac pressure overload in AS patients and cardiac voume overload in IHD patients with left ventricular systolic dysfunction.

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