Figure 6. NT-proBNP is significantly elevated in HFrEF and is correlated with levels of 3-HBA in patients with HF but not in the Control group.

A) Bar graphs depicting mean +/− SD of transformed concentration of plasma NT-proBNP in controls, HFpEF, and HFrEF. Asterisks indicate p-value <.05. B) Linear regressions depicting the relationship between the plasma concentration of 3-HBA and the transformed plasma concentration of NT-proBNP within control (top left), HFpEF (top right), and HFrEF (bottom). C) Proposed mechanism by which BNP indirectly acts to increase serum acylcarnitines and ketone bodies. In response to volume overload and increasing wall stress, the failing heart secretes natriuretic peptides, including BNP. BNP is known to act on adipocytes to increase lipolysis, leading to increased serum FFA and triglycerides. Subsequently, the liver oxidizes the FAs generating increased levels of acylcarnitine intermediates and acetyl-CoA, the latter serving as a substrate for ketone synthesis. Created with BioRender.com.