Background
Pulmonary hypertension (PH) in heart failure with preserved ejection fraction (HFpEF; PH-HFpEF) is a relatively newly recognized condition that poses a leading healthcare burden. The development of PH is the strongest predictor of adverse outcomes in HFpEF patients, with a staggering 60% 5-year mortality rate. Incomplete understanding of pathophysiology, ineffective therapies, and limited non-invasive diagnostic methods contribute to this growing epidemic. HFpEF patients initially develop reversible isolated postcapillary PH (ipc-PH) from passively transmitted backward pressures. If not diagnosed promptly, ipc-PH can transform into pre- and postcapillary PH (cpc-PH), characterized by irreversible pulmonary vascular remodeling. Progression to cpc-PH is not explained by traditional risk factors alone, suggesting the need to examine novel regulatory mechanisms. 
Polyunsaturated Fatty Acid (PUFA) metabolites have emerged as pivotal players in cardiovascular health by regulating balance between anti-inflammatory, pro-inflammatory, and pro-resolutory lipid mediators. Previous research has revealed that an imbalance of these lipids leads to metabolic syndrome, an established risk factor of PH-HFpEF. We aimed to identify PUFA-derived lipid mediators that can predict PH in HFpEF patients.
Methods
A single center prospective cohort study was conducted on 88 enrolled patients with a new diagnosis of HFpEF who were grouped into PH subtypes post-diagnostic right heart catheterization: HFpEF without PH (control, n=40), HFpEF with ipc-PH (ipc-PH-HFpEF, n=30), and HFpEF with cpc-PH (cpc-PH-HFpEF, n=18). Venous samples were collected during catheterization. Levels of 143 PUFA metabolites were analyzed using mass spectroscopy with Multiple Reaction Monitoring. Regression models assessed which PUFA metabolites predicted the PH subtypes. Statistics: p<0.05.
Results
Clinical demographics were similar among all groups. Ipc-PH-HFpEF was characterized by low pro-resolutory 7(S)-Maresin1 (p=0.0003), low anti-inflammatory 11(12)-EpETrE (p=0.02), and low anti-inflammatory 8(S)-HETrE (p=0.02) compared to control. These metabolites collectively predicted ipc-PH-HFpEF with 69% diagnostic accuracy. Cpc-PH-HFpEF was distinguishable from control by low pro-resolutory 7(S)-Maresin1 (p=0.004), high pro-inflammatory 5,6-DiHETrE (p=0.001), and high pro-inflammatory tetranor prostaglandin E2 (p=0.007). Collectively, these metabolites predicted cpc-PH-HFpEF with 83% diagnostic accuracy. High pro-resolutory 12(13)-EpOME (p=0.013) distinguished cpc-PH-HFpEF from ipc-PH-HFpEF, with a 75% predictive value. Interestingly, low pro-resolutory 7(S)-Maresin1 yielded the greatest predictive value of 67% in predicting cpc-PH-HFpEF compared to all groups. 
Conclusion
Our findings demonstrate that distinct PUFA inflammatory mediators are associated with PH pathogenesis in HFpEF. This novel lipidomics framework introduces new non-invasive biomarkers to predict PH and facilitates further experimental study of innovative therapeutic molecular targets.

The Lipid Link: Predicting Pulmonary Hypertension in Heart Failure with Preserved Ejection Fraction

 Cardiology

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The Lipid Link: Predicting Pulmonary Hypertension in Heart Failure with Preserved Ejection Fraction

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