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Altered lipid metabolism, particularly sphingolipid accumulation, has been implicated in heart failure progression. New data presented at the European Society of Cardiology Congress 2025 explored the association between sphingolipid profiles and myocardial recovery in patients supported with left ventricular assist devices.

The study included 85 patients undergoing LVAD implantation, 47 proceeding to heart transplantation, and 13 population-based controls. Patients were classified as responders or non-responders based on structural and functional improvement within one year. Serum and cardiac sphingolipids—including ceramides, sphingosine-1-phosphate, and sphingomyelin—were quantified using targeted liquid chromatography-mass spectrometry.

Responders were more often female, had shorter heart failure duration, and were less likely to be on statin therapy. Non-responders displayed higher myocardial sphingosine-1-phosphate and sphinganine-1-phosphate. Post-LVAD, responders exhibited reductions in circulating sphingosine-1-phosphate and beneficial changes in myocardial sphingolipids.

These findings suggest that sphingolipid signaling is linked to myocardial recovery and could serve as a therapeutic target to optimize LVAD outcomes.
 

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Key highlights
  • Elevated myocardial sphingosine-1-phosphate linked to poor recovery post-Left Ventricular Assist Device.
  • Responders show favorable shifts in cardiac and circulating sphingolipid profiles.
  • Findings highlight potential therapeutic targets to improve mechanical circulatory support outcomes.
Source

Tseliou E, Hamouche R, Tatum S, et al. Sphingolipid pathway alterations in myocardial recovery mediated by left ventricular assist device. Presented at: ESC Congress 2025; August 29-September 1, 2025; London, United Kingdom. https://esc365.escardio.org/presentation/306897 

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Sphingolipid Signaling Linked to Myocardial Recovery After Left Ventricular Assist Device Support
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Serum and cardiac sphingolipids may predict functional improvement in advanced heart failure patients.

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