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J Tissue Eng Regen Med. 2016 Dec;10(12):1057-1064. doi: 10.1002/term.1890. Epub 2014 May 19.

Epicardial shock-wave therapy improves ventricular function in a porcine model of ischaemic heart disease.

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Department of Cardiac Surgery, Innsbruck Medical University, Austria.
Department of Cardiac Surgery, Medical University of Vienna, Austria.
Department of Internal Medicine I, Innsbruck Medical University, Austria.
Combat Wound Initiative Program, Walter Reed Army Medical Center, Washington, DC, Uniformed Services University of the Health Sciences, Bethesda, MD, USA.
Clinic of Anaesthesiology, Intensive Care Medicine and Pain Therapy, Goethe-University Hospital Frankfurt, Frankfurt am Main, Germany.
Gender Medicine Unit, Department of Internal Medicine III, Medical University of Vienna, Austria.
Department of Internal Medicine II, Medical University of Vienna, Austria.
AUVA Trauma Centre Meidling, Vienna, Austria.
Laboratory for Cardiovascular Research, Department of Anatomy and Cell Biology, Medical University of Vienna, Austria.


Previously we have shown that epicardial shock-wave therapy improves left ventricular ejection fraction (LVEF) in a rat model of myocardial infarction. In the present experiments we aimed to address the safety and efficacy of epicardial shock-wave therapy in a preclinical large animal model and to further evaluate mechanisms of action of this novel therapy. Four weeks after left anterior descending (LAD) artery ligation in pigs, the animals underwent re-thoracotomy with (shock-wave group, n = 6) or without (control group, n = 5) epicardial shock waves (300 impulses at 0.38 mJ/mm2 ) applied to the infarcted anterior wall. Efficacy endpoints were improvement of LVEF and induction of angiogenesis 6 weeks after shock-wave therapy. Safety endpoints were haemodynamic stability during treatment and myocardial damage. Four weeks after LAD ligation, LVEF decreased in both the shock-wave (43 ± 3%, p < 0.001) and control (41 ± 4%, p = 0.012) groups. LVEF markedly improved in shock-wave animals 6 weeks after treatment (62 ± 9%, p = 0.006); no improvement was observed in controls (41 ± 4%, p = 0.36), yielding a significant difference. Quantitative histology revealed significant angiogenesis 6 weeks after treatment (controls 2 ± 0.4 arterioles/high-power field vs treatment group 9 ± 3; p = 0.004). No acute or chronic adverse effects were observed. As a potential mechanism of action in vitro experiments showed stimulation of VEGF receptors after shock-wave treatment in human coronary artery endothelial cells. Epicardial shock-wave treatment in a large animal model of ischaemic heart failure exerted a positive effect on LVEF improvement and did not show any adverse effects. Angiogenesis was induced by stimulation of VEGF receptors.


angiogenesis; endothelial cells; left ventricular ejection fraction; myocardial infarction; shockwave therapy; vascular endothelial growth factor

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