European Heart Journal Advance Access originally published online on July 7, 2006
European Heart Journal 2006 27(15):1793-1798; doi:10.1093/eurheartj/ehl119
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Endothelin-1 and acute myocardial infarction: a no-reflow mediator after successful percutaneous myocardial revascularization
1 Institute of Cardiology Catholic University of the Sacred Heart L.go A. Gemelli 8, 00168 Rome, Italy
2 Department of Clinical Research, Inselspital, Bern, Switzerland
3 Department of Cardiology, Cardiovascular Center, University Hospital, Zürich, Switzerland
Received 10 February 2006; revised 9 May 2006; accepted 1 June 2006; online publish-ahead-of-print 7 July 2006.
* Corresponding author. Tel: +39 6 3051166; fax: +39 6 3055535. E-mail address: gniccoli73{at}hotmail.it
Aims No-reflow after a primary percutaneous coronary intervention (PCI) is associated with a high incidence of left ventricular (LV) failure and a poor prognosis. Endothelin-1 (ET-1) is a potent endothelium-derived vasoconstrictor peptide and an important modulator of neutrophil function. Elevated systemic ET-1 levels have recently been reported to predict a poor prognosis in patients with acute myocardial infarction (AMI) treated by primary PCI. We aimed to investigate the relationship between systemic ET-1 plasma levels and no-reflow in a group of AMI patients treated by primary PCI.
Methods and results A group of 51 patients (age 59±9.9 years, 44 males) with a first AMI, undergoing successful primary or rescue PCI, were included in the study. Angiographic no-reflow was defined as coronary TIMI flow grade 
2 or TIMI flow 3 with a final myocardial blush grade 2. Blood samples were obtained from all patients on admission for ET-1 levels measurement. No reflow was observed in 31 patients (61%). Variables associated with no-reflow at univariate analysis included culprit lesion of the left anterior coronary descending artery (LAD) (67 vs. 29%, P=0.006) and ET-1 plasma levels (3.95±0.7 vs. 3.3±0.8 pg/mL, P=0.004). At multivariable logistic regression analysis, ET-1 was the only significant predictor of no-reflow (P=0.03) together with LAD as the culprit vessel (P=0.04).
Conclusion ET-1 plasma levels predict angiographic no-reflow after successful primary or rescue PCI. These findings suggest that ET-1 antagonists might be beneficial in the management of no-reflow.
Key Words: Myocardial infarction • Endothelin-1 • Reperfusion • No-reflow • Percutaneous coronary intervention
CiteULike 
Connotea 
Del.icio.us What's this?
This article has been cited by other articles:
|
|
 |
|
  A. Abbate, M. C. Kontos, and G. G.L. Biondi-Zoccai No-reflow: the next challenge in treatment of ST-elevation acute myocardial infarction Eur. Heart J., August 1, 2008; 29(15): 1795 - 1797. [Full Text] [PDF]
|
|
|
|
|
|
G. Niccoli, S. Giubilato, E. Russo, C. Spaziani, A. Leo, I. Porto, A. M. Leone, F. Burzotta, S. Riondino, F. Pulcinelli, et al. Plasma levels of thromboxane A2 on admission are associated with no-reflow after primary percutaneous coronary intervention Eur. Heart J., August 1, 2008; 29(15): 1843 - 1850. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J. Zhao, Y. Yang, W. Pei, Y. Sun, M Zhai, Y. Liu, and R. Gao Carvedilol reduces myocardial no-reflow by decreasing endothelin-1 via activation of the ATP-sensitive K+ channel Perfusion, March 1, 2008; 23(2): 111 - 115. [Abstract] [PDF]
|
|
|
|
 |
|
 F. Bohm and J. Pernow The importance of endothelin-1 for vascular dysfunction in cardiovascular disease Cardiovasc Res, October 1, 2007; 76(1): 8 - 18. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A. M. Leone and F. Crea Stem cells in acute myocardial infarction: the good, the bad, and the ugly Eur. Heart J., December 2, 2006; 27(24): 2911 - 2913. [Full Text] [PDF]
|
|