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Ann Thorac Surg 2002;74:25-30
© 2002 The Society of Thoracic Surgeons

Original article: cardiovascular

Cardiomyocyte transplantation does not reverse cardiac remodeling in rats with chronic myocardial infarction

Yutaka Sakakibara, MDa, Keiichi Tambara, MDa, Fanglin Lu, MDa, Takeshi Nishina, MDa, Noritoshi Nagaya, MDb, Kazunobu Nishimura, MD, PhDa, Masashi Komeda, MD, PhD*a

a Department of Cardiovascular Surgery, Kyoto University, Graduate School of Medicine, Kyoto, Japan
b Department of Internal Medicine, National Cardiovascular Center, Suita, Osaka, Japan

Accepted for publication March 12, 2002.

* Address reprint requests to Dr Komeda, Graduate School of Medicine, Department of Cardiovascular Surgery, Kyoto University, 54 Kawaharacho Shogoin Sakyo-ku, Kyoto, Japan, 606-8507
e-mail: masakom{at}kuhp.kyoto-u.ac.jp

Background. Several reports have documented the potential benefits of cell transplantation as an alternative to cardiac transplantation. This study was designed to investigate whether cardiomyocyte transplantation is effective in rats with chronic myocardial infarction.

Methods. Syngeneic Lewis rats were used in this study. Chronic myocardial infarction was induced in rats by ligating the left anterior descending artery. Four weeks later, after left ventricular (LV) dysfunction with akinetic regions was confirmed by echocardiography, the rats were randomized into two groups: a group that received fetal cardiomyocyte transplantation (TX group; n = 11); and a group that received an intramyocardial injection of culture medium only (control group; n = 12).

Results. Four weeks after treatment, the TX group had smaller end-systolic dimension (LVDs) (7.5 ± 0.9 vs 8.9 ± 0.8 mm, p < 0.01) and better fractional shortening (FS) (26.2 ± 5.9 vs 17.7% ± 5.1%, p < 0.01) than the control group. However, there were no differences in LV end-diastolic dimension, LVDs, and FS between baseline and post-treatment values in the TX group. In addition, plasma levels of atrial natriuretic peptide were not significantly different between the two groups 4 weeks after treatment. In microscopic examination, small amounts of transplanted cardiomyocytes were found only in the periinfarct area, not in the center of scar area, and a thicker ventricular wall in the infract area was detected in the TX group.

Conclusions. Fetal cardiomyocyte transplantation prevented, but did not reverse, cardiac remodeling that was accompanied with heart failure in myocardial infarction rats. Further investigation is warranted for optimal clinical application to the failing heart.




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