Proinflammatory cytokines and myocardial viability in patients after acute myocardial infarction

被引:30
作者
Kosmala, W [1 ]
Przewlocka-Kosmala, M [1 ]
Mazurek, W [1 ]
机构
[1] Med Univ, Dept Cardiol, Wroclaw, Poland
关键词
tumor necrosis factor-alpha; interleukin-6; myocardial viability; dobutamine stress echocardiography; acute myocardial infarction;
D O I
10.1016/j.ijcard.2004.03.067
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Background: Proinflammatory cytokines such as tumor necrosis factor-alpha (TNF-alpha) and interleukin-6 (IL-6) can potentiate heart muscle damage during acute myocardial infarction (AMI). Whether changes in their plasma levels after AMI are dependent on the presence of myocardial viability is unclear. The aim of the study was to estimate the relation of time course of plasma TNF-a and IL-6 and the presence of reversible and irreversible myocardial dysfunction in patients early after AMI treated thrombolytically. Material and methods: Patients (54; mean age 60.4 +/- 11.7 years) with AMI plasma TNF-alpha and IL-6 were evaluated on the 2nd, 10th and 30th day after thrombolysis. Based on the response of dysfunctional segments of myocardium during dobutamine stress echocardiography performed on the 10th day, patients were divided into four groups: A, sustained improvement in contractility; B, biphasic (improvement followed by worsening); C, only worsening; D, no change. Twenty-two healthy persons served as controls. Results: On the 2nd day, all four groups of patients demonstrated increased levels of TNF-alpha and IL-6 and did not differ among one another regarding both cytokines. On the 10th day, plasma TNF-alpha and IL-6 decreased in each group and were the lowest in group A, intermediate in group B and the highest in groups C and D. On the 30th day, both cytokines were not different among all studied groups. Conclusion: Elevated plasma TNF-alpha and IL-6 early after AMI decreased more quickly in patients with dysfunctional myocardium comprising not only necrotic but also viable segments. This decline is attenuated by the presence of residual ischemia. (c) 2004 Elsevier Ireland Ltd. All rights reserved.
引用
收藏
页码:449 / 456
页数:8
相关论文
共 37 条
[1]   Stress echocardiography: Recommendations for performance and interpretation of stress echocardiography [J].
Armstrong, WF ;
Pellikka, PA ;
Ryan, T ;
Crouse, L ;
Zoghbi, WA .
JOURNAL OF THE AMERICAN SOCIETY OF ECHOCARDIOGRAPHY, 1998, 11 (01) :97-104
[2]   Circulating interleukin-1 beta, interleukin-6, tumor necrosis factor-alpha, and soluble ICAM-1 in patients with chronic stable angina and myocardial infarction [J].
Balbay, Y ;
Tikiz, H ;
Baptiste, RJ ;
Ayaz, S ;
Sasmaz, H ;
Korkmaz, S .
ANGIOLOGY, 2001, 52 (02) :109-114
[3]   Influence of HMG-CoA reductase inhibitors on markers of coagulation, systemic inflammation and soluble cell adhesion [J].
Bickel, C ;
Rupprecht, HJ ;
Blankenberg, S ;
Espinola-Klein, C ;
Rippin, G ;
Hafner, G ;
Lotz, J ;
Prellwitz, W ;
Meyer, J .
INTERNATIONAL JOURNAL OF CARDIOLOGY, 2002, 82 (01) :25-31
[4]   Cardiac cytokine expression is upregulated in the acute phase after myocardial infarction. Experimental studies in rats [J].
Deten, A ;
Volz, HC ;
Briest, W ;
Zimmer, HG .
CARDIOVASCULAR RESEARCH, 2002, 55 (02) :329-340
[5]   Effect of propranolol on cardiac cytokine expression after myocardial infarction in rats [J].
Deten, A ;
Volz, HC ;
Holzl, A ;
Briest, W ;
Zimmer, HG .
MOLECULAR AND CELLULAR BIOCHEMISTRY, 2003, 251 (1-2) :127-137
[6]   Differential cytokine expression in myocytes and non-myocytes after myocardial infarction in rats [J].
Deten, A ;
Volz, HC ;
Briest, W ;
Zimmer, HG .
MOLECULAR AND CELLULAR BIOCHEMISTRY, 2003, 242 (1-2) :47-55
[7]   INTERLEUKIN-6 (IL-6) AS A MEDIATOR OF STUNNED MYOCARDIUM [J].
FINKEL, MS ;
HOFFMAN, RA ;
SHEN, L ;
ODDIS, CV ;
SIMMONS, RL ;
HATTLER, BG .
AMERICAN JOURNAL OF CARDIOLOGY, 1993, 71 (13) :1231-1232
[8]   NEGATIVE INOTROPIC EFFECTS OF CYTOKINES ON THE HEART MEDIATED BY NITRIC-OXIDE [J].
FINKEL, MS ;
ODDIS, CV ;
JACOB, TD ;
WATKINS, SC ;
HATTLER, BG ;
SIMMONS, RL .
SCIENCE, 1992, 257 (5068) :387-389
[9]   Tumor necrosis factor-alpha is released from the isolated heart undergoing ischemia and reperfusion [J].
Gurevitch, J ;
Frolkis, I ;
Yuhas, Y ;
Paz, Y ;
Matsa, M ;
Mohr, R ;
Yakirevich, V .
JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY, 1996, 28 (01) :247-252
[10]   Cardiac myocytes produce interleukin-6 in culture and in viable border zone of reperfused infarctions [J].
Gwechenberger, M ;
Mendoza, LH ;
Youker, KA ;
Frangogiannis, NG ;
Smith, CW ;
Michael, LH ;
Entman, ML .
CIRCULATION, 1999, 99 (04) :546-551