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Ann Thorac Surg 2002;73:343
© 2002 The Society of Thoracic Surgeons
a Department of Cardiovascular Surgery, Hôpital Bichat, 46 rue Henri Huchard, 75877 Paris Cedex 18, France
To the Editor
We thank Drs Gorman and Gorman for their letter, which indeed addresses two distinct issues. The first pertains to the mechanism by which skeletal myoblast transplantation (a term that should be preferred to "cellular myoplasty") improves postinfarct left ventricular function. We totally agree that limitation of remodeling due to the elastic properties of the implanted cells acting as a structural scaffold is likely to play an important role, and this hypothesis is further supported by our most recent experimental data in sheep, which show a significant reduction of end-diastolic left ventricular volumes in the myoblast-transplanted group (manuscript in preparation). However, the limited functional efficacy of fibroblasts compared with smooth muscle cells or fetal cardiomyocytes [1] suggests that the benefits of cell transplantation may also involve an improvement of systolic performance, which is more directly related to the contractile properties of the implanted cells.
The second issue addressed by this letter pertains to the rat model used in our study [2]. It is true that coronary artery ligation may result in infarcts of different sizes. This factor, however, can be easily addressed by increasing the sample size. In our study, the baseline (postinfarct, pretransplant) left ventricular ejection fractions were 32.6 ± 1.8% in controls (n = 23) and 30.3 ± 1.7% in myoblast-injected rats (n = 21), and the close similarity between these two values provides compelling evidence for the appropriate comparability of the initial infarct areas. On the other hand, we agree that regional contractility is difficult to assess echocardiographically in the rat heart. However, such was not the objective of the present study, which was specifically designed to assess to what extent the initial impairment of left ventricular function and the number of injected myoblasts altered the posttransplant functional outcome. "Better experimental models" always exist and we have actually used a sheep model of myocardial infarction to study regional function after myoblast transplantation (manuscript in preparation).
References
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