Skeletal muscle has the limited ability to regenerate following injury, owing to the presence of satellite cells. However, the adult heart has no such reserve capacity. Following injury to the myocardium, as a result of infarct or progressive heart diseases such as cardiomyopathy, cardiac muscle cells are lost resulting in a decline in ventricular function and ultimately failure. Several rather interesting approaches to repair damaged heart muscle have been investigated. Cardiomyoplasty has been used in which a part of the latissimus dorsi muscle, still attached to its nerve and vascular supply, was used, with limited success, to improve hemodynamic function in animals and in patients with dilated or ischemic cardiomyopathy. 1 This muscle has also been used to create an aortic diastolic counterpulsator, a sort of additional or second left ventricle. 2 In a recent study, a line of skeletal muscle myoblasts derived from mouse skeletal muscle satellite cells called C2C12 cells3 were injected into mouse hearts. 4 The C2C12 cells differentiated into myotubes, but apparently formed no functional junctions with the normal ventricular muscle cells, nor was there an apparent affect on cardiac output. Nevertheless, there was an absence of encapsulation or cellular response.

The above studies all employed either skeletal muscle or cells derived from skeletal muscle satellite cells. Over the last few years, transgenic mice were produced in which expression of the SV40 large T antigen was targeted to the cardiac atria. 5 These mice typically exhibit unilateral right atrial tumorigenesis. Transgenic atrial cardiomyocytes isolated from these atria can give rise to transplantable tumor lineages when injected subcutaneously into syngeneic host mice. 6-8 Cardiomyocytes derived from the transplantable tumor lineage, but not from the primary tumor, retain the capacity to proliferate in culture, and express cardiac specific genes. 7, 9 These cardiomyocytes exhibit all the morphological characteristics typi-