« Previous Next » The Journal of Thoracic and Cardiovascular Surgery
Volume 137, Issue 4 , Pages 963-970 , April 2009

Direct epicardial shock wave therapy improves ventricular function and induces angiogenesis in ischemic heart failure

Daniel Zimpfer, MD
- Department of Cardiothoracic Surgery, Medical University of Vienna, Vienna, Austria
- Address for reprints: Daniel Zimpfer, MD, Department of Cardiothoracic Surgery, Medical University of Vienna, Wahringer Guertel 18-20, A-1090 Vienna, Austria.
Seyedhossein Aharinejad, MD, PhD
- Department of Cardiothoracic Surgery, Medical University of Vienna, Vienna, Austria
- Laboratory for Cardiovascular Research, Department of Anatomy and Cell Biology, Medical University of Vienna, Vienna, Austria
Johannes Holfeld, MS
- Department of Cardiothoracic Surgery, Medical University of Vienna, Vienna, Austria
Anita Thomas, MS
- Laboratory for Cardiovascular Research, Department of Anatomy and Cell Biology, Medical University of Vienna, Vienna, Austria
Julia Dumfarth, MD
- Department of Cardiothoracic Surgery, Medical University of Vienna, Vienna, Austria
Raphael Rosenhek, MD
- Department of Internal Medicine, Medical University of Vienna, Vienna, Austria
Martin Czerny, MD
- Department of Cardiothoracic Surgery, Medical University of Vienna, Vienna, Austria
Wolfgang Schaden, MD
- AUVA Trauma Center, Vienna, Austria
Mathias Gmeiner, MD
- Laboratory for Cardiovascular Research, Department of Anatomy and Cell Biology, Medical University of Vienna, Vienna, Austria
Ernst Wolner, MD
- Department of Cardiothoracic Surgery, Medical University of Vienna, Vienna, Austria
Michael Grimm, MD
- Department of Cardiothoracic Surgery, Medical University of Vienna, Vienna, Austria

Received 19 August 2008 ,Revised 20 October 2008 ,Accepted 2 November 2008.

A, Direct epicardial shock wave therapy. B, Technical drawing of the applicator for direct epicardial shock wave therapy.

A, Direct epicardial shock wave therapy. B, Technical drawing of the applicator for direct epicardial shock wave therapy.
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A, Microvascular density and vessel size expressed as the number of vessels per field (± standard deviation) in the treatment and control groups 6 weeks after treatment. ^∗P < .05, treatment versus con

A, Microvascular density and vessel size expressed as the number of vessels per field (± standard deviation) in the treatment and control groups 6 weeks after treatment. ^∗P < .05, treatment versus control groups. B, Microvascular density and vessel size expressed as the number of vessels per field (± standard deviation) in the treatment and control groups 14 weeks after treatment. ^∗P < .05, treatment versus control groups. C, Factor VIII staining of the anterior wall treatment group. D, Factor VIII staining of the anterior wall control group.
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A, Number of endothelial (Factor VIII–positive) cells per field (± standard deviation) 6 and 14 weeks after treatment in the treatment and control groups.Black bar Treatment group; white bar, control

A, Number of endothelial (Factor VIII–positive) cells per field (± standard deviation) 6 and 14 weeks after treatment in the treatment and control groups.Black bar Treatment group; white bar, control group. ^∗P < .05, treatment versus control groups. B, Number of vital cells per field (± standard deviation) in the infarct scar 6 and 14 weeks after treatment in the treatment and control groups. Black bar, myocardial infarction with shock wave therapy; white bar, myocardial infarction without shock wave therapy. ^∗P < .05, treatment versus control groups.
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Development of left ventricular function expressed as left ventricular ejection fraction (LVEF; percentage ± standard deviation) in the treatment and control groups. Solid line, Treatment group; dotte

Development of left ventricular function expressed as left ventricular ejection fraction (LVEF; percentage ± standard deviation) in the treatment and control groups. Solid line, Treatment group; dotted line, control group. ^∗P < .05 compared with before left anterior descending artery (LAD) ligation. †P < .05, treatment versus control groups.
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A, Expression of vascular endothelial growth factor (VEGF) mRNA in the treatment and control groups 24 and 48 hours and 7 days after treatment. Black bar, Treatment group; white bar, control group. ∗P

A, Expression of vascular endothelial growth factor (VEGF) mRNA in the treatment and control groups 24 and 48 hours and 7 days after treatment. Black bar, Treatment group; white bar, control group. ^∗P < .05, treatment versus control groups. B, Expression of Fms-related tyrosine kinase 1 (FLT1) mRNA in the treatment and control groups 24 and 48 hours and 7 days after treatment. Black bar, Treatment group; white bar, control group. ^∗P < .05, treatment versus control groups. C, Expression of placental growth factor (PlGF) mRNA in the treatment and control groups 24 and 48 hours and 7 days after treatment. Black bar, Treatment group; white bar, control group. ^∗P < .05, treatment versus control groups. D, Expression of vascular endothelial growth factor (VEGF) protein in the treatment and control groups 24 and 48 hours and 7 days after treatment. Black bar, Treatment group; white bar, control group. ^∗P < .05, treatment versus control groups.
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Rat brain natriuretic peptide 45 serum levels expressed as picograms per milliliter (± standard deviation) 6 and 14 weeks after treatment in the treatment and control groups. Black bar, Treatment grou

Rat brain natriuretic peptide 45 serum levels expressed as picograms per milliliter (± standard deviation) 6 and 14 weeks after treatment in the treatment and control groups. Black bar, Treatment group; white bar, control group. ^∗P < .05, treatment versus control groups.
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