Sulfatides are associated with neointimal thickening after vascular injury

Abstract

BackgroundSulfatides are known to be a native ligand of P-selectin. Platelet-leukocyte interaction via the cross-talk between P-selectin and Mac-1 (CD11b/CD18) plays an important role in the mechanism of neointimal thickening after vascular injury such as that seen in post-stent restenosis. However, the roles of sulfatides on restenosis have not been elucidated. MethodsSerum sulfatide levels, P-selectin expression on the surface of platelets, and activated Mac-1 on the surface of neutrophils were serially measured using both coronary sinus and peripheral blood samples in 21 patients who underwent coronary stent implantation. ResultsThe trans-cardiac gradient (coronary sinus minus peripheral blood) of the sulfatide levels significantly increased at 15min (−1.47±2.87 to 0.59±1.44nmol/ml, p<0.001), compared to baseline levels. The maximum response of the trans-cardiac gradient of P-selectin expression on the surface of platelets at 15min after stent implantation (R=0.55, p<0.01), and that of activated Mac-1 on the surface of neutrophils at 48h (R=0.59, p<0.01), were both positively correlated with that of serum sulfatide levels at 15min. The angiographic late lumen loss was correlated with the trans-cardiac gradient of sulfatide levels at 15min (R=0.48, p<0.05), platelet P-selectin expression at 15min (R=0.42, p<0.05) and activated neutrophil Mac-1 expression at 48h (R=0.46, p<0.05), but not with values at other sampling points. ConclusionsSulfatides may play a physiological role on inflammation in vascular injury and the development of neointimal thickening.