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J Thorac Cardiovasc Surg 2007;133:1051-1058
© 2007 The American Association for Thoracic Surgery

Surgery for Acquired Cardiovascular Disease

The reduction of hemodynamic loading assists self-regeneration of the injured heart by increasing cell proliferation, inhibiting cell apoptosis, and inducing stem-cell recruitment

Department of Surgery and Clinical Science, Division of Cardiac Surgery, Yamaguchi University Graduate School of Medicine, Ube, Japan.

Received for publication September 25, 2006; revisions received December 8, 2006; accepted for publication December 13, 2006.

^_* Address for reprints: Tao-Sheng Li, MD, PhD, Department of Surgery and Clinical Science, Division of Cardiac Surgery, Yamaguchi University Graduate School of Medicine, 1-1-1 Minami-Kogushi, Ube, Yamaguchi 755-8505, Japan. (Email: litaoshe{at}yamaguchi-u.ac.jp).

Objectives: Mitotic cardiomyocytes and cardiac stem cells have been identified recently in adult hearts, and both have been found to be increased in acute infarcted myocardium. Although these findings suggest potential self-repair of the heart after injury, obvious self-regeneration of the injured heart has never been observed clinically. We hypothesized that hemodynamic loading impairs myocardial repair.

Methods: Myocardial infarction was induced in C57BL/6 mice by ligating the left anterior descending artery. After 60 minutes, either the infarcted heart was transplanted heterotopically into a healthy recipient C57BL/6 mouse to remove the ventricular hemodynamic loading (unloading group) or it was left as an infarcted heart under normal hemodynamic loading conditions in the same mouse (loading group). The infarcted hearts were dissected for histologic analysis after 3, 7, 14, and 28 days.

Results: Histologic analysis showed that the wall thickness of the infarcted left ventricle was significantly greater and the area of infarction was significantly smaller in the unloading group than in the loading group. Immunostaining analysis revealed significantly more Ki-67-positive cells and significantly fewer apoptotic cells in the infarcted myocardium in the unloading group than in the loading group. There were also significantly more c-kit- and Sca-1-positive stem cells in the infarcted myocardium in the unloading group than in the loading group.

Conclusion: Our findings suggest that hemodynamic unloading assists self-regeneration of the injured heart by increasing cell proliferation, inhibiting cell apoptosis, and inducing stem-cell recruitment.

This article has been cited by other articles:

				T.-S. Li, R. Suzuki, and K. Hamano Reply to the editor. J. Thorac. Cardiovasc. Surg., October 1, 2007; 134(4): 1096 - 1096. [Full Text] [PDF]

				C. Stamm, B. Nasseri, and R. Hetzer Rescue versus regeneration. J. Thorac. Cardiovasc. Surg., October 1, 2007; 134(4): 1095 - 1096. [Full Text] [PDF]