Increased neopterin in patients with chronic and acute coronary syndromes

被引:110
作者
Schumacher, M [1 ]
Halwachs, G [1 ]
Tatzber, F [1 ]
Fruhwald, FM [1 ]
Zweiker, R [1 ]
Watzinger, N [1 ]
Eber, B [1 ]
WildersTruschnig, M [1 ]
Esterbauer, H [1 ]
Klein, W [1 ]
机构
[1] GRAZ UNIV, DEPT BIOCHEM, A-8036 GRAZ, AUSTRIA
基金
奥地利科学基金会;
关键词
D O I
10.1016/S0735-1097(97)00172-1
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Objectives. The aim of our study was to determine neopterin levels in patients with chronic and acute coronary syndromes. Background. In chronic and acute coronary syndromes the release of different cytokines activates cellular defense. Infiltration of neutrophils and monocytes/macrophages is detected in the vessel wall as well as in the myocardium. Neopterin, which is a by-product of the guanosine triphosphate-biopterin pathway, is a marker for those activated macrophages. Methods. We studied 123 subjects: 1) 21 consecutive patients (17 men, 4 women; mean age +/- SD 66 +/- 15 years, range 31 to 87) with acute myocardial infarction (AMI); 2) 62 consecutive patients (50 men, 12 women; mean age 61 +/- 8 years, range 43 to 81) with signs and symptoms of clinically stable coronary artery disease (CAD); and 3) 40 healthy blood donors (28 men, 12 women; mean age 35 +/- 13 years), Neopterin levels were determined with a commercially available enzyme-linked immunosorbent assay method. Results. In patients with AMI before thrombolytic therapy, neopterin levels were significantly higher than levels in patients with CAD and control subjects (13.7 vs. 8.6 and vs. 6.8 nmol/liter, p < 0.0001). Values also differed significantly between patients with CAD and control subjects (p < 0.0001). Neopterin levels in patients with AMI were measured seven times during a 72-h period, Within group comparison showed significant differences over this period (p < 0.00001). The lowest value (11.4 nmol/liter) was observed after 4 h and differed significantly from the initial value and values after 24 and 72 h (p < 0.05). After 72 h, neopterin increased to 14.9 nmol/liter, a value significantly different from all values other than the initial one. There was no correlation between neopterin and creatine kinase (CK); CK, MB isoenzyme; or lactate dehydrogenase as markers for the extent of the myocardial infarction during the observation period. Conclusions. Our data support the hypothesis of an activation of monocytes and macrophages in patients with an acute or chronic coronary syndrome. Neopterin as a marker for macrophage activation is significantly increased in patients with chronic CAD and more pronounced in patients with AMI shortly after the onset of symptoms. (C) 1997 by the American College of Cardiology.
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收藏
页码:703 / 707
页数:5
相关论文
共 25 条
[1]   ACTIVATION OF COMPLEMENT AND KININ SYSTEMS AFTER THROMBOLYTIC THERAPY IN PATIENTS WITH ACUTE MYOCARDIAL-INFARCTION - A COMPARISON BETWEEN STREPTOKINASE AND RECOMBINANT TISSUE-TYPE PLASMINOGEN-ACTIVATOR [J].
AGOSTONI, A ;
GARDINALI, M ;
FRANGI, D ;
CAFARO, C ;
CONCIATO, L ;
SPONZILLI, C ;
SALVIONI, A ;
CUGNO, M ;
CICARDI, M .
CIRCULATION, 1994, 90 (06) :2666-2670
[2]   EARLY CORONARY REPERFUSION BLUNTS THE PROCOAGULANT RESPONSE OF PLASMINOGEN-ACTIVATOR INHIBITOR-1 AND VONWILLEBRAND-FACTOR IN ACUTE MYOCARDIAL-INFARCTION [J].
ANDREOTTI, F ;
RONCAGLIONI, MC ;
HACKETT, DR ;
KHAN, MI ;
REGAN, T ;
HAIDER, AW ;
DAVIES, GJ ;
KLUFT, C ;
MASERI, A .
JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY, 1990, 16 (07) :1553-1560
[3]  
[Anonymous], 1992, NEOPTERIN BIOCH METH
[4]  
ANTMAN EM, 1997, HEART DIS TXB CARDIO, P1184
[5]   EFFECT OF NEOPTERIN AND 7,8-DIHYDRONEOPTERIN ON TUMOR-NECROSIS-FACTOR-ALPHA INDUCED PROGRAMMED CELL-DEATH [J].
BAIERBITTERLICH, G ;
FUCHS, D ;
MURR, C ;
REIBNEGGER, G ;
WERNERFELMAYER, G ;
SGONC, R ;
BOCK, G ;
DIERICH, MP ;
WACHTER, H .
FEBS LETTERS, 1995, 364 (02) :234-238
[6]   ELEVATION OF C-REACTIVE PROTEIN IN ACTIVE CORONARY-ARTERY DISEASE [J].
BERK, BC ;
WEINTRAUB, WS ;
ALEXANDER, RW .
AMERICAN JOURNAL OF CARDIOLOGY, 1990, 65 (03) :168-172
[7]   MINIMALLY MODIFIED LOW-DENSITY-LIPOPROTEIN STIMULATES MONOCYTE ENDOTHELIAL INTERACTIONS [J].
BERLINER, JA ;
TERRITO, MC ;
SEVANIAN, A ;
RAMIN, S ;
KIM, JA ;
BAMSHAD, B ;
ESTERSON, M ;
FOGELMAN, AM .
JOURNAL OF CLINICAL INVESTIGATION, 1990, 85 (04) :1260-1266
[8]   SERUM INTERLEUKIN-6 IN SUSPECTED MYOCARDIAL-INFARCTION [J].
CRUICKSHANK, AM ;
OLDROYD, KG ;
COBBE, SM .
LANCET, 1994, 343 (8903) :974-974
[9]  
DEBEER FC, 1982, BRIT HEART J, V47, P239
[10]   MECHANISMS OF DISEASE - THE PATHOGENESIS OF CORONARY-ARTERY DISEASE AND THE ACUTE CORONARY SYNDROMES .1. [J].
FUSTER, V ;
BADIMON, L ;
BADIMON, JJ ;
CHESEBRO, JH .
NEW ENGLAND JOURNAL OF MEDICINE, 1992, 326 (04) :242-250