High P-selectin expression and low CD36 occupancy on circulating platelets are strong predictors of restenosis after coronary stenting in patients with coronary artery disease

被引:11
作者
Murasaki, Kagari [1 ]
Kawana, Masatoshi [1 ]
Murasaki, Satoshi [1 ]
Tsurumi, Yukio [1 ]
Tanoue, Kenjiro [1 ]
Hagiwara, Nobuhisa [1 ]
Kasanuki, Hiroshi [1 ]
机构
[1] Tokyo Womens Med Univ, Inst Heart, Dept Cardiol, Shinjuku Ku, Tokyo 1628666, Japan
关键词
platelet; P-selectin; CD36; stent; restenosis; flow cytometry;
D O I
10.1007/s00380-006-0966-5
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Recent studies have shown that circulating platelets play an important role in the development of restenosis early after coronary stent implantation. We investigated P-selectin expression and CD36 blockade on platelets by flow cytometry in 48 consecutive patients who underwent coronary stenting. P-selectin expression was significantly higher 1 day after stenting in patients who had restenosis (n = 15) than in those who had no restenosis (n = 28), and the odds ratio for restenosis in patients with high P-selectin levels (MFI > 6.5) was 11.67 (P < 0.001) as compared with patients who had intermediate and low P-selectin levels. CD36 blockade was assessed with the use of two anti-CD36 antibodies, OKM5 and GS95 (our new anti-CD36 antibody), the binding of which indicates total CD36 amount and free CD36 unoccupied by lipid-related ligands, respectively. Binding of OKM5 to platelets was similar before and after stenting in both groups. CD36 blockade on platelets was seen 1 day after stenting in the non-restenosis group, and the odds ratio for restenosis in patients without CD36 blockade [GS95 binding ratio > 0.8 as compared with binding before stenting] on day 1 was 28.60 (P < 0.001). P-selectin expression and unoccupied CD36 on platelets shortly after stenting may be strong predictors of post-stent restenosis.
引用
收藏
页码:229 / 236
页数:8
相关论文
共 32 条
  • [1] ABUMRAD NA, 1993, J BIOL CHEM, V268, P17665
  • [2] AIKEN ML, 1990, BLOOD, V76, P2501
  • [3] CORONARY ARTERIOGRAPHIC ANALYSIS AND ANGIOGRAPHIC MORPHOLOGY
    AMBROSE, JA
    [J]. JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY, 1989, 13 (07) : 1492 - 1494
  • [4] DIAGNOSING AND MANAGING UNSTABLE ANGINA
    BRAUNWALD, E
    JONES, RH
    MARK, DB
    BROWN, J
    BROWN, L
    CHEITLIN, MD
    CONCANNON, CA
    COWAN, M
    EDWARDS, C
    FUSTER, V
    GOLDMAN, L
    GREEN, LA
    GRINES, CL
    LYTLE, BW
    MCCAULEY, KM
    MUSHLIN, AI
    ROSE, GC
    SMITH, EE
    SWAIN, JA
    TOPOL, EJ
    WILLERSON, JT
    [J]. CIRCULATION, 1994, 90 (01) : 613 - 622
  • [5] BRETON HL, 1996, J AM COLL CARDIOL, V28, P1643
  • [6] Daviet L, 1997, THROMB HAEMOSTASIS, V78, P65
  • [7] ENDEMANN G, 1993, J BIOL CHEM, V268, P11811
  • [8] A novel role for CD36 in VLDL-enhanced platelet activation
    Englyst, NA
    Taube, JM
    Aitman, TJ
    Baglin, TP
    Byrne, CD
    [J]. DIABETES, 2003, 52 (05) : 1248 - 1255
  • [9] Fry ETA, 1998, CURR OPIN CARDIOL, V13, P232
  • [10] Huh HY, 1996, BLOOD, V87, P2020