Download Trygve Husebye 1,2,4, Jan Eritsland 1,2, Harald Arnesen 2,3,4

Peak systolic velocity by tissue Doppler imaging detects changes in myocardial contraction
related to inotropic effects of levosimendan in patients with acute heart failure complicating
myocardial infarction.
Husebye T1,2,4, Eritsland J1,2, Arnesen H2,3,4, Seljeflot I1,2,3,4, Bjørnerheim R1,2 , Andersen GØ1,2,3
1Department
of Cardiology, Oslo University Hospital Ullevål, Norway
for Heart Failure Research, University of Oslo, Norway
3Center for Clinical Heart Research, Oslo University Hospital Ullevål, Norway;
4Faculty of Medicine, University of Oslo, Norway
2Center
Purpose: Peak systolic velocity (PSV) by tissue Doppler imaging (TDI) has been proposed for serial
non-invasive assessment of myocardial contraction in patients receiving inotropic therapy due to its
relative load- and heart rate-independent properties. However, this hypothesis has so far not been
tested in a clinical setting. We therefore examined the ability of PSV by TDI to detect changes in
contraction in a substudy of the LEvosimendan in Acute heart Failure following myocardial infarction
(LEAF) trial (NCT00324766).
Methods: A total of 61 patients developing clinical signs of heart failure within 48 hours after a
primary percutaneous coronary intervention-treated ST-elevation myocardial infarction (including
cardiogenic shock), were randomized double-blind to a 25 hours infusion of levosimendan or placebo.
Levosimendan is an inodilator where the effects, due to active metabolites with very long half-lives,
last for several days after end of the infusion. Echocardiography was performed before infusion
(baseline), on day 1, on day 5 and after 6 weeks. PSV (mean of septal, lateral, anterior and posterior
mitral annular peak systolic velocity) measured by tissue velocity imaging, and global longitudinal
strain (GLS) of the left ventricle measured by speckle tracking were analyzed at all time-points.
Results: There was significantly larger improvement in PSV from baseline to day 1 (P = 0.007) and
day 5 (P <0.001) in the levosimendan group compared to placebo (levosimendan 4.70 cm/s ± 1.34 to
5.74 cm/s ± 1.47 (day 1) and 6.07 cm/s ± 1.47 (day 5) vs. placebo 4.77 cm/s ± 1.02 to 5.08 cm/s ±
1.35 (day 1) and 4.90 cm/s ± 1.26 (day 5)). No significant differences were found in PSV after 6 weeks
or in GLS at any time-point between the treatment groups. We have previously shown that
levosimendan improved left ventricular function measured as changes in wall motion score index
(WMSI) from baseline to day 5 compared to placebo (p = 0.031, primary endpoint of the LEAF trial),
however no significant changes in WMSI were found on day 1 or after 6 weeks between the treatment
groups.
Conclusion: PSV by TDI seems to be a more sensitive echocardiographic method to detect changes
in myocardial contraction during inotropic stimulation with levosimendan than WMSI and GLS. These
results suggest that PSV by TDI can be used for assessment of changes in contraction in patients
hospitalized for acute heart failure receiving inotropic therapy.