OBJECTIVETo investigate the difference of soluble P-selectin levels in different subtype of coronary heart disease and the relationship between soluble P-selectin levels with the severity of coronary artery lesions.

METHODSEnzyme linked immuoserbent assay (ELISA) was used to measure the plasma soluble P-selectin levels in 69 patients with angiocardiography documented coronary heart disease and 19 normal coronary arteries persons without angiocardiography detectable coronary artery disease (control group). The coronary artery lesions score was recorded according to single, double and triple-vessel lesions while the American College of Cardiology and the American Heart Association proposed type A, B, C lesion and Gensini scoring system. The relationships between plasma soluble P-selectin levels and the coronary artery score (the severity of coronary heart disease) were assessed.

RESULTS(1) The level of plasma soluble P-selectin was obviously higher in the coronary heart disease group than in the control group (180.6 +/- 60.5 ng/L vs. 145.3 +/- 21.7 ng/L, P<0.05). (2) The level of plasma soluble P-selectin was significantly higher in the acute coronary syndrome group (191.4 +/- 63.7 ng/L) than in the control group (145.3 +/- 21.7 ng/L, P< 0.01) and in the stable angina pectoris group (141.3 +/- 17.9 ng/L, P<0.01). (3) The level of plasma soluble P-selectin was high in multi-vessel coronary artery lesions group than in single-vessel group (190.1 +/- 64.2 ng/L vs. 157.2 +/- 43.4 ng/L, P < 0.05). The level of plasma soluble P-selectin was positively correlated with the Gensini score (r = 0.391, P = 0.001); the numbers of vessels lesions (rs = 0.349, P = 0.003); Type A, B and C lesions (rs = 0.358, P = 0.002).

CONCLUSIONThe positive correlation between the level of soluble P-selectin and the coronary artery score may indicate that soluble P-selectin levels might reflect the severity of coronary heart disease. The elevated soluble P-selectin level in acute coronary syndrome suggested the possible relation of P-selectin to the pathogenesis of acute coronary syndrome, which may save as a potential marker of plaque unstability.