Possible involvement of minor lysophospholipids in the pathogenesis of acute coronary syndrome

Abstract

Lysophosphatidic acids (LPA) have important roles in the field of vascular biology and are derived mainly from lysophosphatidylcholine (LPC) via autotaxin. In our previous study, however, only the plasma LPA levels, and not the serum autotaxin levels, increased in patients with acute coronary syndrome (ACS). We measured the plasma glycero-lysophospholipids (glycero-LPLs) species in 141 consecutive patients undergoing coronary angiography using a liquid chromatography-tandem mass spectrometry analysis to elucidate the pathway by which LPA increased in subjects with ACS. Among the ACS subjects, notable increases in the 22:6 LPA, 18:2 LPA, and 20:4 LPA levels were observed. Minor glycero-LPLs other than LPA were also elevated in ACS subjects and were well correlated with the corresponding LPA species, including 22:6 LPA. A multiple regression analysis also revealed that lysophosphatidylinositol, LPC, and lysophosphatidylethanolamine were independent explanatory variables for several LPA species. Therefore, minor glycero-LPLs might be involved in the generation of LPA in ACS. Moreover, a specific and significant association was observed only between the plasma serotonin and the plasma lysophosphatidylserine levels. In conclusion, minor glycero-LPLs might be involved in the generation of LPA, especially 22:6 LPA. Minor glycero-LPLs in themselves might be also involved in the pathogenesis of ACS.