Transplanting Cells Into Damaged Hearts Starts 'Self-Repair'
Nov. 12, 2000 (New Orleans) -- The 21st century has arrived in the treatment of heart disease, say experts at a meeting of the American Heart Association (AHA). A handful of very preliminary studies on cell transplantation "point to a whole new era for cardiologists," Lynn Smaha, MD, PhD, immediate past president of the AHA, tells WebMD. New research shows that doctors may now have a chance to actually fix the part of the heart that dies when a patient has a heart attack.
Last June, an elderly Frenchman with a failing heart made history when a team of researchers took cells grown from muscle removed from his thigh and then implanted them into dead muscle in his heart. Five months later, that once-dead muscle is now contracting, says Philippe Menasché, MD, a professor of cardiac surgery at Hopital Bichat in Paris.
He says, however, that although the muscle is contracting, it's not working exactly like the muscle of a healthy heart. What is probably happening, he says, is that these cells are working like the muscle in a thigh, since that's where they were originally. "But that is not a problem," he says, "because we can still achieve the objective -- [improving the contractions of the heart]."
Jeffrey Isner, MD, PhD, professor of medicine and pathology at Tufts University School of Medicine in Boston, is pursuing a different avenue of stem cell research using early forms of the endothelial precursor cells -- the cells that line blood vessels. He gets the cells from the blood and injects them into the damaged areas of hearts.
Thus far, he has used human endothelial precursor cells and transplanted them into rats with damaged hearts similar to those of a person who's had a heart attack. "The cells honed in on the damaged heart muscle, and within two weeks there was evidence of new blood vessel growth," he says.
This area of research is so new, Isner says, that many questions remain unanswered. For example, he says that since the body manufactures endothelial precursor cells, it is unclear why these cells are not automatically dispatched to the site of a heart attack as a normal part of the body's healing response. "But it may be that the attack impairs the endothelial precursor cells' function or that the body is incapable of manufacturing enough cells to repair the [damaged area]," he says. In his animal study, he increased the concentration of the endothelial precursor cells to levels "well beyond normal production in the body," he says. "So this increased dosing, if you will, may be the key factor."