Key result
Levosimendan drives a ~23% increase in TDI-derived systolic mitral annulus velocity at day one versus placebo.
Why the study?
Does a 25-hour infusion of levosimendan improve echocardiographic indices of left ventricular systolic function in patients with acute heart failure following ST-elevation myocardial infarction?
RCT (n=61)
Double-blind
Does a 25-hour infusion of levosimendan improve echocardiographic indices of left ventricular systolic function in patients with acute heart failure following ST-elevation myocardial infarction?
Absolute Event Rate: 23% vs 8%
p-value: p=0.011
TDI-derived systolic mitral annulus velocity is a highly feasible and sensitive echocardiographic index for detecting improvements in left ventricular systolic function during inotropic therapy with levosimendan in acute heart failure post-STEMI.
Supports levosimendan for LV systolic assessment in acute post-STEMI HF; extends mixed evidence on echocardiographic inotropic response.
Background: Echocardiography is recommended for assessment of left ventricular systolic function in patients with acute heart failure but few randomised trials have validated techniques like tissue Doppler (TDI) and speckle tracking (STE) in patients with acute heart failure following ST-elevation myocardial infarction. Methods: This was a substudy from the LEAF (LEvosimendan in Acute heart Failure following myocardial infarction) trial (NCT00324766 ), which randomised 61 patients developing acute heart failure, including cardiogenic shock, within 48 hours after ST-elevation myocardial infarction, double-blind to a 25-hour infusion of levosimendan or placebo. TDI-derived systolic mitral annulus velocity (S′), STE-derived global longitudinal strain (S l ) and strain rate (SR l ) were measured at baseline, day 1, day 5 and after 42 days. Results: Datasets rejected for analyses were 2% (TDI) and 17% (STE). S′ increased by 23% in the levosimendan group versus 8% in the placebo group from baseline to day 1 ( p= 0.011) and by 30% vs. 3% from baseline to day 5 ( p <0.0005). Significant, but less pronounced, improvements in global S l ( p = 0.025 and p = 0.032) and in global SR l ( p = 0.046 and p = 0.001) in favour of levosimendan were also present. Conclusion: S′ by TDI and STE-derived S l and SR l were sensitive indices for changes in left ventricular systolic function related to treatment with levosimendan. However, S′ by TDI was more feasible and sensitive and might be preferred for assessment of changes in left ventricular systolic function in critically ill patients with acute heart failure receiving inotropic therapy.
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Husebye et al. (2017) conducted an RCT in Acute heart failure following ST-elevation myocardial infarction (n=61). Levosimendan vs. Placebo was evaluated on Change in TDI-derived systolic mitral annulus velocity (S') from baseline to day 1 (p=0.011). Levosimendan significantly increased TDI-derived systolic mitral annulus velocity compared to placebo from baseline to day 1 (23% vs 8%, p=0.011) and day 5 (30% vs 3%, p<0.0005).
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