Pediatric Cardiology and Cardiac Surgery
Vol.26 No.5 2010 (384-391)
Mio Noma,1, 3) Kanji Matsuzaki,1, 4) Yuji Hiramatsu,2) and Yuzuru Sakakibara2)
1)Gorman Cardiovascular Research Group, University of Pennsylvania School of Medicine, USA,2)Department of Cardiovascular Surgery, Graduate School of Comprehensive Human Sciences, University of Tsukuba, Tsukuba, Japan,3)Pediatric Cardiac Surgery, Gifu Prefectural General Medical Center, Gifu, Japan,4)Cardiovascular Surgery, Tsukuba Medical Center Hospital, Tsukuba, Japan
Background: The adult response to myocardial infarction results in inflammation, scar formation, left ventricular dilatation, and loss of regional and global function. Regenerative scarless healing has been demonstrated in fetal dermis and tendon and is associated with diminished inflammation. We hypothesized that following fetal myocardial infarction, there would be minimal inflammation, regenerative healing, and preservation of function.
Methods: Anteroapical myocardial infarction of the left ventricle were created in adult and early gestation fetal sheep. The myocardial function was serially assessed using quantitative echocardiography. The infarct architecture was examined histologically for evidence of scar formation. Cellular inflammation, cellular proliferation, and apoptosis were assessed using immunohistochemistry.
Results: In the adult sheep, 4 weeks following myocardial infarction, there was a significant decline in the ejection fraction, and the akinetic myocardial segment had increased in size. In contrast, there was no decline in the fetal ejection fraction and no akinetic fetal myocardial segment 4 weeks post-infarction. The fetal infarcts lacked an inflammatory cell infiltrate and healed with minimal fibrosis compared to the adults. The fetal infarcts also showed proliferating cardiomyocytes within the infarct.
Conclusions: These data demonstrate that the fetal response to myocardial infarction is dramatically different than the adult and is characterized by minimal inflammation, lack of fibrosis, myocardial proliferation, and restoration of cardiac function.