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Effect of levosimendan therapy on myocardial infarct size and left ventricular function after acute coronary occlusion
  1. Miikka Tarkia1,2,
  2. Christoffer Stark3,
  3. Matti Haavisto1,
  4. Rasmus Kentala3,
  5. Tommi Vähäsilta3,4,
  6. Timo Savunen3,4,
  7. Marjatta Strandberg4,
  8. Virva Saunavaara1,
  9. Tuula Tolvanen1,
  10. Mika Teräs1,
  11. Mikko Pietilä4,
  12. Leena Nyman5,
  13. Emma Duvall6,
  14. Pekka Saukko7,
  15. Jouko Levijoki5,
  16. Anne Roivainen1,8,
  17. Antti Saraste1,4,9,
  18. Juhani Knuuti1
  1. 1Turku PET Centre, University of Turku and Turku University Hospital, Turku, Finland
  2. 2Department of Pharmacology, University of Helsinki, Helsinki, Finland
  3. 3Research Centre of Applied and Preventive Cardiovascular Medicine, University of Turku, Turku, Finland
  4. 4Heart Center, Turku University Hospital and University of Turku, Turku, Finland
  5. 5Orion Corporation Orion Pharma, Espoo, Finland
  6. 6Quotient Bio Analytical Sciences, Fordham, UK
  7. 7Department of Forensic Medicine, University of Turku, Turku, Finland
  8. 8Turku Center for Disease Modeling, University of Turku, Turku, Finland
  9. 9Institute of Clinical Medicine, University of Turku, Turku, Finland
  1. Correspondence to Dr Juhani Knuuti, Turku PET Centre, University of Turku and Turku University Hospital, Kiinamyllynkatu 4-8, Turku FI-20521, Finland; juhani.knuuti{at}


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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