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Ann Thorac Surg 2004;78:14-16
© 2004 The Society of Thoracic Surgeons

Editorial

Video-assisted thoracoscopic transplantation of myoblasts into the heart

Ugo Carraro, MDa*

a Laboratory of Applied Myology, Department of Biomedical Sciences, University of Padua Medical School, Padova, Italy

* Address reprint requests to Dr Carraro, Laboratory of Applied Myology, Department of Biomedical Sciences, University of Padua Medical School, Viale G. Colombo 3, I-35121 Padova, Italy.
e-mail: ugo.carraro@unipd.it

The first 300 words of the full text of this article appear below.

In contrast to what is happening with other cardiac diseases, the incidence of congestive cardiac insufficiency is not decreasing despite significant progress in pharmacologic treatment, and that is likely due to the increased longevity of the population. Cardiac transplantation is the elective therapy, but the limit set by organ donors seems to have been reached all over the world. In the future, xenotransplants could offer a solution to the problem, even though such an approach would still carry the risk of zoonotic viral infections. Mechanical circulatory support has also been studied as a viable option, but many more studies are needed before considering it the final solution.

At present, the more promising alternatives come from biological approaches relying on autologous cell-based or tissue-based treatments (cardiac bioassistance). Although it is difficult to foresee which of the cardiac bioassists will have the highest impact on the existing clinical needs, in the future combined subsets of some of them will provide the long-awaited solutions.

When confronted with the problem of heart damage after infarction, cardiomyocyte replacement is the ideal scenario. In principle, such a goal could be achieved in two ways: by stimulating the proliferation of endogenous mature cardiomyocytes or stem cells, or by implanting exogenous donor cardiomyogenic cells.

See page 303

It should be emphasized that in order to be clinically effective (ie, the patient has to survive an acute insult that disrupts heart function through damage to the individual cardiac myocytes), the enhancement of cardiomyocyte proliferation after damage must be very rapid. In cases in which there is chronic damage to the heart muscle, proliferation would instead have to be sustained, so that it slowly but continuously replaces myocytes as necessary during the course of the disease. Whatever the source of the cells and the use to which they are put, . . . [Full Text of this Article]






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