Stem Cells Implicated in Myocyte Formation that Occurs with Cardiac Hypertrophy
NEW YORK (Reuters Health) – Stem cells appear to be responsible for the myocyte formation that accompanies human cardiac hypertrophy, according to a report published in the August 18th early edition of the Proceedings of the National Academy of Sciences.
Traditionally, it was believed that a rise in adult cardiac mass could only come through an increase in myocyte size, not number. Recently, however, this notion was challenged when it was shown that myocytes can, in fact, replicate in acute stress states. Still, exactly how cardiac regeneration occurs has been unclear.
In the new study, Dr. Piero Anversa, from New York Medical College in Valhalla, and colleagues analyzed cardiac tissue from 36 patients with aortic stenosis who were undergoing valve replacement and from 12 control subjects collected within 24 hours postmortem.
The increased cardiac mass that occurs with aortic stenosis results from a combination of myocyte hypertrophy and hyperplasia, the authors note. Delving further into the hyperplasia, they found that the myocyte formation appeared to come from stem cells that were committed to the myocyte lineage.
The putative stem cells were increased 13-fold in hearts with aortic stenosis compared with controls. Moreover, the hypertrophic state seemed to enhance growth and differentiation of these cells.
“The most significant result of this study is that the heart possesses primitive cells, which express surface antigens commonly detected on hemopoietic stem cells,” the investigators note.
“The magnitude of stem cell-dependent myocyte regeneration with aortic stenosis, about 15%, is similar to that observed in cardiac chimerism after transplantation of female hearts into male recipients,” they add.
These findings strengthen previous data on cardiac chimerism, and Dr. Anversa’s group hopes that “they will stimulate more interest in the area of myocardial regeneration.”
Proc Natl Acad Sci USA 2003;August 18th early edition:000-000.
