Key result
Eight weeks of levosimendan therapy after LAD occlusion in a pig model significantly decreased myocardial infarct size (12% vs 27% of LV, p=0.03) and reduced left ventricular end-systolic volume.
Why the study?
Does levosimendan reduce myocardial infarct size and improve left ventricular function in an experimental pig model of post-MI heart failure?
Does levosimendan reduce myocardial infarct size and improve left ventricular function in an experimental pig model of post-MI heart failure?
Absolute Event Rate: 12% vs 27%
p-value: p=0.03
In a pig model of post-MI heart failure, 8 weeks of oral levosimendan therapy reduced infarct size and attenuated adverse left ventricular remodeling.
Hypothesis-generating for levosimendan in post-MI remodeling; human trials required before any clinical consideration.
BACKGROUND: Levosimendan is an inotropic agent with cardioprotective and vasodilating properties used for the management of acutely decompensated heart failure. We studied the effects of levosimendan treatment on the size of myocardial infarction (MI) and left ventricular (LV) function in experimental pig model of post MI heart failure. METHODS: After occlusion of the left anterior descending (LAD) coronary artery, animals received levosimendan 5 mg/kg/day orally for 8 weeks (n=7) or no treatment (n=18). One week after stopping treatment, transthoracic echocardiography, CT scan and positron emission tomography were performed to evaluate myocardial function, perfusion and oxidative metabolism. Histology was used to confirm the size of MI and features of LV remodelling. RESULTS: The size of MI was significantly smaller in the levosimendan group than in the controls (12±13% vs 27±15% of the LV, p=0.03). End-diastolic volume (EDV) and end-systolic volume (ESV) were smaller in the levosimendan than in the control group (EDV 161±29 mL vs 245±84 mL, p=0.06; ESV 81±18 mL vs 149±67 mL, p=0.03), whereas ejection fraction tended to be higher in the levosimendan group (50±6% vs 41±8%, p=0.06). CONCLUSIONS: Eight weeks of levosimendan therapy after recent LAD occlusion decreases the size of MI and leads to better preservation of LV function as well as reduced LV remodelling.
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Tarkia et al. (2016) studied Post-myocardial infarction heart failure (experimental pig model) (n=25). Levosimendan vs. No treatment was evaluated on Size of myocardial infarction (% of LV) (p=0.03). Eight weeks of levosimendan therapy after LAD occlusion in a pig model significantly decreased myocardial infarct size (12% vs 27% of LV, p=0.03) and reduced left ventricular end-systolic volume.
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