The presence of infection-related antiphospholipid antibodies in infective endocarditis determines a major risk factor for embolic events

被引:71
作者
Kupferwasser, LI
Hafner, G
Mohr-Kahaly, S
Erbel, R
Meyer, J
Darius, H
机构
[1] Univ Mainz, Med Clin 2, D-6500 Mainz, Germany
[2] Univ Mainz, Inst Clin Chem, D-6500 Mainz, Germany
[3] Essen Univ, Div Cardiol, Essen, Germany
关键词
D O I
10.1016/S0735-1097(99)00024-8
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
OBJECTIVES The impact of infection-associated antiphospholipid antibodies (APA) on endothelial cell activation, blood coagulation and fibrinolysis was evaluated in patients with infective endocarditis with and without major embolic events. BACKGROUND An embolic event is a common and severe complication of infective endocarditis. Despite the fact that APAs are known to be associated with infectious diseases, their pathogenic role in infective endocarditis has not been clearly defined. METHODS The relationship among the occurrence of major embolic events, echocardiographic vegetation size, endothelial cell activation, thrombin generation, fibrinolysis and APA was examined in 91 patients with definite infective endocarditis, including 26 patients with embolic events and 65 control subjects without embolic events. RESULTS Overall, 14.3% of patients exhibited elevated APA levels. Embolic events occurred more frequently in patients with elevated levels of APA than in patients without (61.5% vs. 23.1%; p = 0.008). Patients with elevated levels of APA showed higher levels of prothrombin-fragment F1 + 2 (p = 0.005), plasminogen-activator inhibitor 1 (p = 0.0002), von Willebrand factor (p = 0.002) and lower levels of activated protein C (p = 0.001) than patients with normal levels of APA. Thrombin generation and endothelial cell activation were both positively correlated with levels of APA. The occurrence of elevated APA levels was frequently associated with structural valve abnormalities (p = 0.01) and vegetations >1.3 cm (p = 0.002). CONCLUSIONS Infection-associated elevated APA levels in patients with infective endocarditis are related to endothelial cell activation, thrombin generation and impairment of fibrinolysis. This may contribute to the increased risk for major embolic events in these patients. (C) 1999 by the American College of Cardiology.
引用
收藏
页码:1365 / 1371
页数:7
相关论文
共 52 条
[1]   IMMUNOHEMATOLOGIC CHARACTERISTICS OF INFECTION-ASSOCIATED CEREBRAL INFARCTION [J].
AMERISO, SF ;
WONG, VLY ;
QUISMORIO, FP ;
FISHER, M .
STROKE, 1991, 22 (08) :1004-1009
[2]   CARDIAC INVOLVEMENT IN PATIENTS WITH PRIMARY ANTIPHOSPHOLIPID SYNDROME [J].
BRENNER, B ;
BLUMENFELD, Z ;
MARKIEWICZ, W ;
REISNER, SA .
JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY, 1991, 18 (04) :931-936
[3]   GENERATION IN PLASMA OF A FAST-ACTING INHIBITOR OF PLASMINOGEN-ACTIVATOR IN RESPONSE TO ENDOTOXIN STIMULATION [J].
COLUCCI, M ;
PARAMO, JA ;
COLLEN, D .
JOURNAL OF CLINICAL INVESTIGATION, 1985, 75 (03) :818-824
[4]   Protein C and other cofactors involved in the binding of antiphospholipid antibodies: Relation to the pathogenesis of thrombosis [J].
deGroot, PG ;
Horbach, DA ;
Derksen, RHWM .
LUPUS, 1996, 5 (05) :488-493
[5]  
DELPAPA N, 1992, CLIN EXP RHEUMATOL, V10, P37
[6]  
DESTEFANO V, 1994, THROMB HAEMOSTASIS, V72, P352
[7]   NEW CRITERIA FOR DIAGNOSIS OF INFECTIVE ENDOCARDITIS - UTILIZATION OF SPECIFIC ECHOCARDIOGRAPHIC FINDINGS [J].
DURACK, DT ;
LUKES, AS ;
BRIGHT, DK ;
ALBERTS, MJ ;
BASHORE, TM ;
COREY, GR ;
DOUGLAS, JM ;
GRAY, L ;
HARRELL, FE ;
HARRISON, JK ;
HEINLE, SA ;
MORRIS, A ;
KISSLO, JA ;
NICELY, LM ;
OLDHAM, N ;
PENNING, LM ;
SEXTON, DJ ;
TOWNS, M ;
WAUGH, RA .
AMERICAN JOURNAL OF MEDICINE, 1994, 96 (03) :200-209
[8]  
ERBEL R, 1988, EUR HEART J, V9, P43
[9]   THE PROTEIN-C ANTICOAGULANT PATHWAY [J].
ESMON, CT .
ARTERIOSCLEROSIS AND THROMBOSIS, 1992, 12 (02) :135-145
[10]  
EXNER T, 1991, THROMB HAEMOSTASIS, V65, P320