Angiogenesis in myocardial infarction - An acute or chronic process?

被引:37
作者
Chung, NAY [1 ]
Lydakis, C [1 ]
Belgore, F [1 ]
Blann, AD [1 ]
Lip, GYH [1 ]
机构
[1] City Hosp, Univ Dept Med, Haemostasis Thrombosis & Vasc Biol Unit, Birmingham B18 7QH, W Midlands, England
关键词
angiogenesis; vascular endothelial growth (VEGF); soluble Flt-1; myocardial infarction (MI);
D O I
10.1053/euhj.2002.3312
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Background In the acute phase of myocardial infarction (acute MI) marked endothelial damage occurs within the first 24 h following thrombolysis with streptokinase. We investigated whether this is associated with a change in levels of vascular endothelial growth factor (VEGF, possibly marking angiogenesis) in the first 24 h post thrombolysis compared to chronic MI patients (defined as MI > 3 months previously). Methods We recruited 15 patients (nine male, mean age 59 +/- SD 10 years) with first-presentation acute MI, who were given 1.5 million U streptokinase over 1 h and aspirin 300 mg orally as standard treatment. Plasma samples were taken prior to the start of thrombolysis, followed every 15 min for 1 h, at 3 h and finally at 24 h post-thrombolysis. Baseline levels of measured indices in the acute MI patients were compared to two control groups: (i) 26 chronic MI patients (18 male, mean age 59.9 +/- 7.0 years); and (ii) 26 apparently healthy controls (17 male, mean age 59.6 +/- 14.1 years). Plasma VEGF and the soluble form of its receptor Flt-1 (sFlt-1) were measured by ELISA. Results Plasma levels of VEGF were significantly higher in patients with a history of chronic MI compared to patients with acute MI (P=0.007) and healthy controls (P=0.002) with similar levels between acute MI patients and healthy controls (P=0.755). Levels of sFlt-1 in the acute (P=0.013) and chronic (P<0.001) MI groups were lower compared to healthy controls. In the first 24 h post-thrombolysis in the acute MI group, levels of sFlt-1 changed significantly (P=0.039), but there was no change in levels of VEGF (P=0.207). Conclusion In the first 24 h of acute MI, significant changes in levels of VEGF receptor sFlt-1, but not VEGF, are seen. Plasma VEGF and sFlt-1 levels are markedly changed in chronic MI patients, suggesting that the activation of angiogenesis in MI patients may be a delayed response.
引用
收藏
页码:1604 / 1608
页数:5
相关论文
共 29 条
[1]   UP-REGULATION OF VASCULAR ENDOTHELIAL GROWTH-FACTOR EXPRESSION INDUCED BY MYOCARDIAL-ISCHEMIA - IMPLICATIONS FOR CORONARY ANGIOGENESIS [J].
BANAI, S ;
SHWEIKI, D ;
PINSON, A ;
CHANDRA, M ;
LAZAROVICI, G ;
KESHET, E .
CARDIOVASCULAR RESEARCH, 1994, 28 (08) :1176-1179
[2]   HYPOTHESIS - VASA VASORUM AND NEOVASCULARIZATION OF HUMAN CORONARY-ARTERIES - A POSSIBLE ROLE IN THE PATHO-PHYSIOLOGY OF ATHEROSCLEROSIS [J].
BARGER, AC ;
BEEUWKES, R ;
LAINEY, LL ;
SILVERMAN, KJ .
NEW ENGLAND JOURNAL OF MEDICINE, 1984, 310 (03) :175-177
[3]  
BATTEGAY EJ, 1995, J MOL MED, V73, P333
[4]   Measurement of free and complexed soluble vascular endothelial growth factor receptor, Flt-I, in fluid samples: development and application of two new immunoassays [J].
Belgore, FM ;
Blann, AD ;
Lip, GY .
CLINICAL SCIENCE, 2001, 100 (05) :567-575
[5]   Von Willebrand factor and soluble E-selectin in hypertension: Influence of treatment and value in predicting the progression of atherosclerosis [J].
Blann, AD ;
Waite, MA .
CORONARY ARTERY DISEASE, 1996, 7 (02) :143-147
[6]   von Willebrand factor and soluble thrombomodulin as predictors of adverse events among subjects with peripheral or coronary atherosclerosis [J].
Blann, AD ;
McCollum, CN .
BLOOD COAGULATION & FIBRINOLYSIS, 1999, 10 (06) :375-380
[7]  
BLANN AD, CLIN SCI, P101
[8]   INDIRECT ANGIOGENIC CYTOKINES UP-REGULATE VEGF AND BFGF GENE-EXPRESSION IN VASCULAR SMOOTH-MUSCLE CELLS, WHEREAS HYPOXIA UP-REGULATES VEGF EXPRESSION ONLY [J].
BROGI, E ;
WU, TG ;
NAMIKI, A ;
ISNER, JM .
CIRCULATION, 1994, 90 (02) :649-652
[9]   Immunohistochemical expression of vascular endothelial growth factor vascular permeability factor in atherosclerotic intimas of human coronary arteries [J].
Chen, YX ;
Nakashima, Y ;
Tanaka, K ;
Shiraishi, S ;
Nakagawa, K ;
Sueishi, K .
ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY, 1999, 19 (01) :131-139
[10]  
DE L, 1915, AM J CARDIOL, V88, P353