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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.

Author information

1
Department of Cardiac Surgery, Innsbruck Medical University, Austria.
2
Department of Cardiac Surgery, Medical University of Vienna, Austria.
3
Department of Internal Medicine I, Innsbruck Medical University, Austria.
4
Combat Wound Initiative Program, Walter Reed Army Medical Center, Washington, DC, Uniformed Services University of the Health Sciences, Bethesda, MD, USA.
5
Clinic of Anaesthesiology, Intensive Care Medicine and Pain Therapy, Goethe-University Hospital Frankfurt, Frankfurt am Main, Germany.
6
Gender Medicine Unit, Department of Internal Medicine III, Medical University of Vienna, Austria.
7
Department of Internal Medicine II, Medical University of Vienna, Austria.
8
AUVA Trauma Centre Meidling, Vienna, Austria.
9
Laboratory for Cardiovascular Research, Department of Anatomy and Cell Biology, Medical University of Vienna, Austria.

Abstract

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.

KEYWORDS:

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

PMID:
24841341
DOI:
10.1002/term.1890
[Indexed for MEDLINE]

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