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Sustained decrease in plasma sphingosine-1-phosphate concentration and its accumulation in blood cells in acute

Małgorzata Knapp¹, Anna Lisowska, Piotr Zabielski

¹Department of Cardiology, Medical University of Białystok, Skłodowskiej-Curie 24a, 15-276 Białystok, Poland.

Prostaglandins & Other Lipid Mediators

|October 15, 2013

Summary

Myocardial infarction alters sphingolipid metabolism, decreasing cardioprotective Sphingosine-1-phosphate (S1P) in plasma and affecting erythrocyte sphingolipids. These changes persist long-term, potentially reducing S1P

Keywords:

Ceramide Human Red blood cells Sphinganine Sphingosine kinase Thrombocytes

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Area of Science:

Biochemistry
Cardiology
Metabolomics

Background:

Sphingosine-1-phosphate (S1P) is a key cardioprotective sphingolipid.
Its role in blood metabolism following myocardial infarction is not well understood.

Purpose of the Study:

To investigate the dynamic changes in blood sphingolipid concentrations in patients with acute ST-segment elevation myocardial infarction (STEMI).

Main Methods:

Blood samples were collected from STEMI patients (n=32) and healthy controls (n=32) at multiple time points (admission, days 2, 5, 30, and 2 years post-infarction).
Plasma and erythrocyte sphingolipid levels were analyzed.

Main Results:

STEMI patients exhibited reduced plasma S1P and increased erythrocyte sphingoid bases upon admission, persisting for at least 30 days.
Two years post-infarction, plasma S1P partially recovered, while erythrocyte sphingolipids normalized.
Reduced plasma S1P was attributed to decreased release or increased degradation, not altered synthesis by blood cells.

Conclusions:

Acute myocardial infarction causes significant alterations in blood sphingolipid metabolism.
These changes may be linked to the infarction, antiplatelet therapy, or both.
The cardioprotective effects of S1P may be diminished in acute myocardial infarction patients.