AIM: Endothelial activation and dysfunction may be an important contributor to chronic heart failure (CHF) progression. We sought to investigate whether the calcium sensitizer levosimendan affects beneficially endothelial function and attenuates the deleterious effects of soluble adhesion molecules in patients with advanced CHF. METHODS:Twenty-six advanced CHF patients (mean New York Heart Association class, 2.6+/-0.3; ischemic/dilated, 18/8; mean left ventricular ejection fraction <35%) hospitalized due to syndrome worsening, were randomized (2:1) to receive either a 24-h levosimendan infusion of 0.1 microg/kg/min (n=17) or placebo (n=9). Endothelial function estimated by endothelial-dependent flow-mediated dilatation of the brachial artery (FMD), as well as plasma soluble intercellular adhesion molecule-1 (sICAM-1) and soluble vascular cell adhesion molecule-1 (sVCAM-1), were assessed before and 48 h after therapy. RESULTS: Baseline characteristics and medications were well balanced in the two treatment groups. A significant improvement of FMD (6.4+/-4.4% from 4.8+/-3.0%; p<0.05) with concomitant reduction of plasma concentrations of sICAM-1 (231+/-75 pg/ml from 339+/-157 pg/ml; p<0.05) and sVCAM-1 (1134+/-508 pg/ml from 1386+/-602 pg/ml; p<0.05) were observed only in levosimendan treated patients. CONCLUSION:Levosimendan could be an effective treatment in improving the endothelial function and reducing the detrimental adhesion molecule activation in advanced CHF patients.
RCT Entities:
AIM: Endothelial activation and dysfunction may be an important contributor to chronic heart failure (CHF) progression. We sought to investigate whether the calcium sensitizer levosimendan affects beneficially endothelial function and attenuates the deleterious effects of soluble adhesion molecules in patients with advanced CHF. METHODS: Twenty-six advanced CHFpatients (mean New York Heart Association class, 2.6+/-0.3; ischemic/dilated, 18/8; mean left ventricular ejection fraction <35%) hospitalized due to syndrome worsening, were randomized (2:1) to receive either a 24-h levosimendan infusion of 0.1 microg/kg/min (n=17) or placebo (n=9). Endothelial function estimated by endothelial-dependent flow-mediated dilatation of the brachial artery (FMD), as well as plasma soluble intercellular adhesion molecule-1 (sICAM-1) and soluble vascular cell adhesion molecule-1 (sVCAM-1), were assessed before and 48 h after therapy. RESULTS: Baseline characteristics and medications were well balanced in the two treatment groups. A significant improvement of FMD (6.4+/-4.4% from 4.8+/-3.0%; p<0.05) with concomitant reduction of plasma concentrations of sICAM-1 (231+/-75 pg/ml from 339+/-157 pg/ml; p<0.05) and sVCAM-1 (1134+/-508 pg/ml from 1386+/-602 pg/ml; p<0.05) were observed only in levosimendan treated patients. CONCLUSION:Levosimendan could be an effective treatment in improving the endothelial function and reducing the detrimental adhesion molecule activation in advanced CHFpatients.
Authors: Andrew Sherwood; Christopher M O'Connor; Faye S Routledge; Alan L Hinderliter; Lana L Watkins; Michael A Babyak; Gary G Koch; Kirkwood F Adams; Carla Sueta Dupree; Patricia P Chang; Benson M Hoffman; Julie Johnson; Margaret Bowers; Kristy S Johnson; James A Blumenthal Journal: J Card Fail Date: 2011-01-21 Impact factor: 5.712
Authors: Matti Adam; Sven Meyer; Henning Knors; Anna Klinke; Ulf K Radunski; Tanja K Rudolph; Volker Rudolph; Joshua M Spin; Philip S Tsao; Angelika Costard-Jäckle; Stephan Baldus Journal: Sci Rep Date: 2015-04-13 Impact factor: 4.379
Authors: Matti Kivikko; Mikko Kuoppamäki; Lauri Soinne; Stig Sundberg; Pasi Pohjanjousi; Juha Ellmen; Risto O Roine Journal: Curr Ther Res Clin Exp Date: 2015-01-29