4G/5G Polymorphism of the plasminogen activator inhibitor-1 gene and risk of restenosis after coronary artery stenting

被引:22
作者
Böttiger, C
Koch, W
Lahn, C
Mehilli, J
von Beckerath, N
Schömig, A
Kastrati, A
机构
[1] Deutsch Herzzentrum Munich, D-80636 Munich, Germany
[2] Tech Univ Munich, Med Klin Rechts der Isar 1, D-8000 Munich, Germany
关键词
D O I
10.1016/S0002-8703(03)00363-6
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Background Plasminogen activator inhibitor-1 (PAI-1) has been proposed as a candidate risk factor for restenosis after coronary artery stenting. Transcription, level, and activity of PAI-1 are influenced by the 4G/5G polymorphism in the promoter region of PAI-1 gene. The polymorphism may therefore affect wound-healing processes in injured blood vessels and influence restenosis. Methods In 1850 consecutive patients, angiographic measures of restenosis and the clinical outcome at 30 days and 1 year after stent implantation were evaluated. Angiographic restenosis was defined as greater than or equal to50% diameter stenosis determined at follow-up angiography, performed 6 months after stenting. The 4G/5G genotypes were determined with Taq-Man technique. Results Among the patients, the frequency of the 4G allele was 0.55. Follow-up angiography was done in 84% of the patients. We observed restenosis in 32.5% of 4G/4G carriers, 32.2% of 4G/5G carriers, and 35.7% of 5G/5G carriers (P=.52). The occurrence of a major adverse event (death, myocardial infarction, or target vessel revascularization due to restenosis-induced ischemia) was 5.6% in 4G/4G carriers, 5.3% in 4G/5G carriers, and 4.6% in 5G/5G carriers at 30 days (P=.80), and 24.7% in 4G/4G carriers, 23.6% in 4G/5G carriers, and 26.2% in 5G/5G carriers at 1 year (P=.45). Conclusion The 4G/5G polymorphism of the PAI-1 gene is not associated with an increased risk of thrombotic and restenotic events after coronary artery stenting.
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页码:855 / 861
页数:7
相关论文
共 46 条
[1]   Lack of association of a common polymorphism of the plasminogen activator inhibitor-1 gene with coronary artery disease and myocardial infarction [J].
Anderson, JL ;
Muhlestein, JB ;
Habashi, J ;
Carlquist, JF ;
Bair, TL ;
Elmer, SP ;
Davis, BP .
JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY, 1999, 34 (06) :1778-1783
[2]   DIURNAL-VARIATION OF TISSUE-TYPE PLASMINOGEN-ACTIVATOR AND ITS RAPID INHIBITOR (PAI-1) [J].
ANGLETON, P ;
CHANDLER, WL ;
SCHMER, G .
CIRCULATION, 1989, 79 (01) :101-106
[3]  
[Anonymous], 1985, World Health Organ Tech Rep Ser, V727, P1
[4]   Inhibitory role of plasminogen activator inhibitor-1 in arterial wound healing and neointima formation - A gene targeting and gene transfer study in mice [J].
Carmeliet, P ;
Moons, L ;
Lijnen, HR ;
Janssens, S ;
Lupu, F ;
Collen, D ;
Gerard, RD .
CIRCULATION, 1997, 96 (09) :3180-3191
[5]  
Chalmers J, 1999, J HYPERTENS, V17, P151
[6]  
CHANDLER WL, 1990, BLOOD, V76, P930
[7]  
DAWSON SJ, 1993, J BIOL CHEM, V268, P10739
[8]   Plasminogen activator inhibitor type I increases neointima formation in balloon-injured rat carotid arteries [J].
DeYoung, MB ;
Tom, C ;
Dichek, DA .
CIRCULATION, 2001, 104 (16) :1972-1977
[9]   The 4G/5G polymorphism in the plasminogen activator inhibitor-1 gene is not associated with myocardial infarction [J].
Doggen, CJM ;
Bertina, RM ;
Cats, VM ;
Reitsma, PH ;
Rosendaal, FR .
THROMBOSIS AND HAEMOSTASIS, 1999, 82 (01) :115-120
[10]   CORONARY MORPHOLOGICAL AND CLINICAL DETERMINANTS OF PROCEDURAL OUTCOME WITH ANGIOPLASTY FOR MULTIVESSEL CORONARY-DISEASE - IMPLICATIONS FOR PATIENT SELECTION [J].
ELLIS, SG ;
VANDORMAEL, MG ;
COWLEY, MJ ;
DISCIASCIO, G ;
DELIGONUL, U ;
TOPOL, EJ ;
BULLE, TM .
CIRCULATION, 1990, 82 (04) :1193-1202