The relation between endothelin-1 levels and myocardial injury in chronic ischemic heart failure


Yazici M., Demircan S., Durna K., Sahin M.

HEART AND VESSELS, vol.20, no.3, pp.95-99, 2005 (SCI-Expanded) identifier identifier

  • Publication Type: Article / Article
  • Volume: 20 Issue: 3
  • Publication Date: 2005
  • Doi Number: 10.1007/s00380-004-0812-6
  • Journal Name: HEART AND VESSELS
  • Journal Indexes: Science Citation Index Expanded (SCI-EXPANDED), Scopus
  • Page Numbers: pp.95-99
  • Keywords: chronic ischemic heart failure, endothelin-1, myocardial injury, CARDIAC TROPONIN-I, PULMONARY-HYPERTENSION, PLASMA ENDOTHELIN-1
  • Ondokuz Mayıs University Affiliated: No

Abstract

We evaluated whether there was any relation between myocardial injury and endothelin-1 (ET-1) levels, which has been suggested as a contributor to the progression of ischemic heart failure. One hundred and twenty-one patients with chronic ischemic heart failure and 37 healthy individuals were included in the study. Cardiac troponin-I (cTn-I) and ET-1 levels of all subjects were measured on admission. Echocardiographic evaluations were also performed. The positivity of cTn-I increased significantly as the severity changed from New York Heart Association (NHYA) Class I to IV ( P < 0.01). This was also true for quantitative cTn-I levels ( P < 0.05). The ET-1 levels of patients were higher than controls on admission ( P < 0.001). The ET-1 levels increased significantly upon the progression from NHYA Class I to IV ( P < 0.001). Moreover, patients with cTn-I positivity had higher ET-1 levels ( P < 0.05) and a lower ejection fraction ( P < 0.001). A negative correlation was found between ejection fraction and the ET-1 levels ( r = -0.312, P = 0.019). In patients with cTn-I positivity, the cTn-I levels showed a positive correlation with the ET-1 levels ( r = 0.328, P = 0.014) and a negative correlation with ejection fraction ( r = -0.671, P < 0.001). In chronic ischemic heart failure, an increase in ET-1 may exert an influence on the progression of cardiac failure by leading to myocardial injury which may be demonstrated by higher cTn-I levels.