Role of endothelin-1 in the development of a special type of cardiomyopathy

Abstract

The role of endothelin-1 (ET-1) in certain pathological states is still unclear. We have investigated the effect of anthracyclines (maximum dose, 450 mg/m(2) of body surface) on left ventricular systolic and diastolic function and how it influences the level of plasma ET-1 in 21 patients (12 female and nine male) with Hodgkin and non-Hodgkin lymphoma. We also studied the association between plasma ET-1 concentration and echocardiographic parameters. Serum ET-1 was measured by ELISA. Left ventricular function was analysed by echocardiography: ejection fraction (EF), velocity-time integral, E- and A-waves, E:A ratio, deceleration time (DT) and Doppler index were all measured. Statistical analysis was made by the Wilcoxon rank test. EF and serum ET-1 level decreased significantly (EF, 56.29+/-5.0% to 48.57+/-5.9%, P<0.0001; ET-1, 6.45+/-4.0 pg/ml to 2.9+/-1.0 pg/ml, P<0.0001). DT increased significantly (179.8+/-47.8 ms to 215.5+/-66.7 ms, P<0.01) after anthracycline therapy. There was no difference in other echocardiographic parameters before and after therapy. The decrease in serum ET-1 concentration might be a result of anthracycline's direct cytotoxic effect and the decreasing level of ET-1 can play a role in the reduction of EF. However, more studies are needed to evaluate the presence and severity of endothelial damage.

Irreversible End‐Stage Cardiomyopathy Following a Single Dose of Cyclophosphamide

“…Endothelin‐1 (ET‐1) is among a number of biomarkers that have been postulated to play a role in predicting the development of cardiomyopathy associated with CPA. In some small studies, a decrease in ET‐1 levels has been shown to correlate well with a decrease in EF after anthracycline administration 10 . This suggests that the reduction in ET‐1 is a result of the direct cytotoxic effect of anthracyclines.…”

“…In some small studies, a decrease in ET-1 levels has been shown to correlate well with a decrease in EF after anthracycline administration. 10 This suggests that the reduction in ET-1 is a result of the direct cytotoxic effect of anthracyclines. If this is indeed the case, CPA may play a similar role in reducing ET-1 levels.…”