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European Heart Journal Advance Access published online on July 7, 2006
European Heart Journal, doi:10.1093/eurheartj/ehl119
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European Heart Journal © The European Society of Cardiology 2006; all rights reserved
Received February 10, 2006
Revised May 9, 2006
Accepted June 1, 2006

Clinical research

Endothelin-1 and acute myocardial infarction: a no-reflow mediator after successful percutaneous myocardial revascularization

Giampaolo Niccoli 1 *, Gaetano Antonio Lanza 1, Sidney Shaw 2, Enrico Romagnoli 1, Domenico Gioia 1, Francesco Burzotta 1, Carlo Trani 1, Mario A. Mazzari 1, Rocco Mongiardo 1, Maria De Vita 1, Antonio G. Rebuzzi 1, Thomas F. Lüscher 3, and Filippo Crea 1

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

* To whom correspondence should be addressed.
Giampaolo Niccoli, E-mail: gniccoli73{at}hotmail.it


  Abstract

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.

Keywords: Myocardial infarction; Endothelin-1; Reperfusion; No-reflow; Percutaneous coronary intervention.
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