Glycoprotein IIIa polymorphism and risk of myocardial infarction

被引:71
作者
Samani, NJ
Lodwick, D
机构
[1] UNIV LEICESTER, DEPT MED, DIV CARDIOL, LEICESTER, LEICS, ENGLAND
[2] UNIV LEICESTER, DEPT MED, DIV MED, LEICESTER, LEICS, ENGLAND
关键词
myocardial infarction; platelets; integrins; glycoprotein IIb/IIIa; human; genetics; DNA polymorphism;
D O I
10.1016/S0008-6363(96)00222-2
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Objectives: To prospectively investigate whether the Pl(A2) variant of the platelet adhesion molecule glycoprotein IIIa influences the risk of myocardial infarction. Background: The platelet glycoprotein IIb/IIIa receptor plays an important role in platelet aggregation. The IIIa polypeptide is polymorphic due to a single base change at position 1565 resulting in either proline Pl(A1) or leucine Pl(A2) at position 33 in the protein. It has recently been reported that the Pl(A2) variant may be strongly associated with the risk of acute coronary syndromes, particularly in younger subjects. Methods: Pl(A) genotypes of 242 prospectively collected cases of first myocardial infarction admitted to our Coronary Care Unit were compared with those of 209 community-based control subjects. Results: We found no difference in either Pl(A) genotype (P = 0.65) or allele (P = 0.64) frequencies between cases and controls. The Pl(A2) allele frequency was 18.2 and 19.4% in cases and controls, respectively. The age- and sex-stratified odds ratio for risk of myocardial infarction associated with the Pl(A2) allele was 0.89 (95% CI 0.58-1.37, P = 0.65) and remained non-significant when the analysis was confined to subjects under the age of 60 (odds ratio 0.77, 95% CI 0.38-1.56, P = 0.44). There was no interaction between Pl(A2) and other coronary risk factors. For cases, the age at myocardial infarction was not different between those carrying the Pl(A2) allele and those not (66.3 +/- 10.8 vs. 65.6 +/- 11.7 years, P = 0.63). Conclusions: We conclude that, in our subjects, the Pl(A2) variant of platelet glycoprotein ma is not an important risk factor for myocardial infarction.
引用
收藏
页码:693 / 697
页数:5
相关论文
共 24 条
  • [1] Adams M, 1996, QJM-MON J ASSOC PHYS, V89, P437
  • [2] COLLABORATIVE OVERVIEW OF RANDOMIZED TRIALS OF ANTIPLATELET THERAPY .1. PREVENTION OF DEATH, MYOCARDIAL-INFARCTION, AND STROKE BY PROLONGED ANTIPLATELET THERAPY IN VARIOUS CATEGORIES OF PATIENTS
    ALTMAN, R
    CARRERAS, L
    DIAZ, R
    FIGUEROA, E
    PAOLASSO, E
    PARODI, JC
    CADE, JF
    DONNAN, G
    EADIE, MJ
    GAVAGHAN, TP
    OSULLIVAN, EF
    PARKIN, D
    RENNY, JTG
    SILAGY, C
    VINAZZER, H
    ZEKERT, F
    ADRIAENSEN, H
    BERTRANDHARDY, JM
    BRAN, M
    DAVID, JL
    DRICOT, J
    LAVENNEPARDONGE, E
    LIMET, R
    LOWENTHAL, A
    MORIAU, M
    SCHAPIRA, S
    SMETS, P
    SYMOENS, J
    VERHAEGHE, R
    VERSTRAETE, M
    ATALLAH, A
    BARNETT, H
    BATISTA, R
    BLAKELY, J
    CAIRNS, JA
    COTE, R
    CROUCH, J
    EVANS, G
    FINDLAY, JM
    GENT, M
    LANGLOIS, Y
    LECLERC, J
    NORRIS, J
    PINEO, GF
    POWERS, PJ
    ROBERTS, R
    SCHWARTZ, L
    SICURELLA, J
    TAYLOR, W
    THEROUX, P
    [J]. BMJ-BRITISH MEDICAL JOURNAL, 1994, 308 (6921): : 81 - 100
  • [3] [Anonymous], 1979, Circulation, V59, P607
  • [4] [Anonymous], 1988, LANCET, V2, P349
  • [5] BRAY PF, 1990, BLOOD, V75, P881
  • [6] A DELETION IN THE GENE FOR GLYCOPROTEIN-IIB ASSOCIATED WITH GLANZMANN THROMBASTHENIA
    BURK, CD
    NEWMAN, PJ
    LYMAN, S
    GILL, J
    COLLER, BS
    PONCZ, M
    [J]. JOURNAL OF CLINICAL INVESTIGATION, 1991, 87 (01) : 270 - 276
  • [7] USE OF A MONOCLONAL-ANTIBODY DIRECTED AGAINST THE PLATELET GLYCOPROTEIN IIB/IIIA RECEPTOR IN HIGH-RISK CORONARY ANGIOPLASTY
    CALIFF, RM
    SHADOFF, N
    VALETT, N
    BATES, E
    GALEANA, A
    KNOPF, W
    SHAFTEL, J
    BENDER, MJ
    AVERSANO, T
    RAQUENO, J
    GURBEL, P
    COWFER, J
    COHEN, M
    CROSS, P
    BITTL, J
    EDDINGS, K
    TAYLOR, M
    DEROSA, K
    HATTEL, L
    COOPER, L
    ESHELMAN, B
    FINTEL, D
    NIEMYSKI, P
    KLEIN, L
    KENNEDY, H
    THORNTON, T
    KEREIAKES, D
    MARTIN, L
    ANDERSON, L
    HIGBY, N
    ELLIS, S
    BREZINA, K
    GEORGE, B
    CHAPEKIS, A
    SMITH, D
    ANWAR, A
    GERBER, TL
    PRITCHARD, GL
    MYLER, R
    SHAW, R
    MURPHY, M
    WARD, K
    MADIGAN, NP
    BLANKENSHIP, J
    HALBERT, M
    FLANAGAN, C
    TANNENBAUM, M
    POLICH, M
    STEVENSON, C
    TCHENG, J
    [J]. NEW ENGLAND JOURNAL OF MEDICINE, 1994, 330 (14) : 956 - 961
  • [8] DELETION POLYMORPHISM IN THE GENE FOR ANGIOTENSIN-CONVERTING ENZYME IS A POTENT RISK FACTOR FOR MYOCARDIAL-INFARCTION
    CAMBIEN, F
    POIRIER, O
    LECERF, L
    EVANS, A
    CAMBOU, JP
    ARVEILER, D
    LUC, G
    BARD, JM
    BARA, L
    RICARD, S
    TIRET, L
    AMOUYEL, P
    ALHENCGELAS, F
    SOUBRIER, F
    [J]. NATURE, 1992, 359 (6396) : 641 - 644
  • [9] MECHANISMS OF DISEASE - THE PATHOGENESIS OF CORONARY-ARTERY DISEASE AND THE ACUTE CORONARY SYNDROMES .1.
    FUSTER, V
    BADIMON, L
    BADIMON, JJ
    CHESEBRO, JH
    [J]. NEW ENGLAND JOURNAL OF MEDICINE, 1992, 326 (04) : 242 - 250
  • [10] APOLIPOPROTEIN B-GENE DNA POLYMORPHISMS ASSOCIATED WITH MYOCARDIAL-INFARCTION
    HEGELE, RA
    HUANG, LS
    HERBERT, PN
    BLUM, CB
    BURING, JE
    HENNEKENS, CH
    BRESLOW, JL
    [J]. NEW ENGLAND JOURNAL OF MEDICINE, 1986, 315 (24) : 1509 - 1515