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Takaya Hoashi
Goro Matsumiya
Hajime Ichikawa
Masamichi Ono
Yoshiki Sawa
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J Thorac Cardiovasc Surg 2009;138:460-467
© 2009 The American Association for Thoracic Surgery

Evolving Technology/Basic Science

Skeletal myoblast sheet transplantation improves the diastolic function of a pressure-overloaded right heart

Takaya Hoashi, MDa, Goro Matsumiya, MD, PhDa, Shigeru Miyagawa, MD, PhDa, Hajime Ichikawa, MD, PhDa, Takayoshi Ueno, MD, PhDa, Masamichi Ono, MD, PhDa, Atsuhiro Saito, PhDa, Tatsuya Shimizu, MD, PhDb, Teruo Okano, MD, PhDb, Naomasa Kawaguchi, PhDc, Nariaki Matsuura, MD, PhDc, Yoshiki Sawa, MD, PhDa,*

a Department of Cardiovascular Surgery, Osaka University Graduate School of Medicine, Osaka, Japan
b Institute of Advanced Biomedical Engineering and Science, Tokyo Women's Medical University, Tokyo, Japan
c Department of Molecular Pathology, Osaka University Graduate School of Allied Health Science, Osaka, Japan

Received for publication March 17, 2008; revisions received October 1, 2008; accepted for publication February 2, 2009.

* Address for reprints: Yoshiki Sawa, MD, PhD, 2–2 Yamadaoka, Suita, Osaka 565-0871, Japan. (Email: sawa{at}surg1.med.osaka-u.ac.jp).

Objective: The development of right ventricular dysfunction has become a common problem after surgical repair of complex congenital heart disease. A recent study reported that tissue-engineered skeletal myoblast sheet transplantation improves left ventricular function in patients with dilated and ischemic cardiomyopathy. Therefore myoblast sheet transplantation might also improve ventricular performance in a rat model of a pressure-overloaded right ventricle.

Methods: Seven-week-old male Lewis rats underwent pulmonary artery banding. Four weeks after pulmonary artery banding, myoblast sheet transplantation to the right ventricle was performed in the myoblast sheet transplantation group (n = 20), whereas a sham operation was performed in the sham group (n = 20).

Results: Four weeks after performing the procedure, a hemodynamic assessment with a pressure–volume loop showed a compensatory increase in systolic function in both groups. However, only the myoblast sheet transplantation group showed a significant improvement in the diastolic function: end-diastolic pressure (sham vs myoblast sheet transplantation, 10.3 ± 3.1 vs 5.0 ± 3.7 mm Hg; P < .001), time constant of isovolumic relaxation (11.1 ± 2.5 vs 7.6 ± 1.2 ms, P < .001), and end-diastolic pressure–volume relationship (16.1 ± 4.5 vs 7.6 ± 2.4/mL, P < .005). The right ventricular weight and cell size similarly increased in both groups. A histologic assessment demonstrated significantly suppressed ventricular fibrosis and increased capillary density in the myoblast sheet transplantation group in comparison with those in the sham group. Reverse transcription–polymerase chain reaction demonstrated an increased myocardial gene expression of hepatocyte growth factor and vascular endothelial growth factor in the myoblast sheet transplantation group but not in the sham group.

Conclusions: Skeletal myoblast sheet transplantation improved the diastolic dysfunction and suppressed ventricular fibrosis with increased capillary density in a rat model of a pressure-overloaded right ventricle. This method might become a novel strategy for the myocardial regeneration of right ventricular failure in patients with congenital heart disease.

Abbreviations and Acronyms BW = body weight; CFR = coronary flow reserve; EDPVR = end-diastolic pressure–volume relationship; Ees = end-systolic elastance; ESPVR = end-systolic pressure–volume relationship; GAPDH = glyceraldehyde-3-phosphate dehydrogenase; HGF = hepatocyte growth factor; IVS = intraventricular septum; LV = left ventricular; MS = myoblast cell sheet; MST = myoblast sheet transplantation; PA = pulmonary artery; PAB = pulmonary artery banding; PRSW = preload recruitable stroke work; RT-PCR = reverse transcription–polymerase chain reaction; RV = right ventricular; SW = stroke work; VEGF = vascular endothelial growth factor






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