A 1-standard deviation higher level of 15R-PGF2α was associated with a 1.70-fold increased odds of having heart failure with preserved ejection fraction.
Observational (n=510)
Yes
Specific pro- and anti-inflammatory eicosanoid metabolites are associated with HFpEF status, exercise intolerance, and incident heart failure, highlighting upstream inflammatory pathways in HFpEF pathogenesis.
Effect estimate: OR 1.70 (95% CI 1.30-2.26)
p-value: p=0.0002
Systemic inflammation has been implicated in the pathobiology of heart failure with preserved ejection fraction (HFpEF). Here, we examine the association of upstream mediators of inflammation as ascertained by fatty-acid derived eicosanoid and eicosanoid-related metabolites with HFpEF status and exercise manifestations of HFpEF. Among 510 participants with chronic dyspnea and preserved LVEF who underwent invasive cardiopulmonary exercise testing, we find that 70 of 890 eicosanoid and related metabolites are associated with HFpEF status, including 17 named and 53 putative eicosanoids (FDR q-value < 0.1). Prostaglandin (15R-PGF2α, 11ß-dhk-PGF2α) and linoleic acid derivatives (12,13 EpOME) are associated with greater odds of HFpEF, while epoxides (8(9)-EpETE), docosanoids (13,14-DiHDPA), and oxylipins (12-OPDA) are associated with lower odds of HFpEF. Among 70 metabolites, 18 are associated with future development of heart failure in the community. Pro- and anti-inflammatory eicosanoid and related metabolites may contribute to the pathogenesis of HFpEF and serve as potential targets for intervention.
Lau et al. (Mon,) conducted a observational in Heart failure with preserved ejection fraction (HFpEF) (n=510). Eicosanoid and eicosanoid-related metabolites vs. Individuals without HFpEF was evaluated on HFpEF status (OR 1.70, 95% CI 1.30-2.26, p=0.0002). A 1-standard deviation higher level of 15R-PGF2α was associated with a 1.70-fold increased odds of having heart failure with preserved ejection fraction.