About a teaspoon of muscle may make old hearts new again.
Studies suggest that an injection of muscle cells into hearts flabby and failing from old injuries may reverse a process that leads to death.
Dr. Doris Taylor of Duke University Medical School told a crowd of 200 yesterday that 13 years of work is beginning to pay off in early human trials to treat heart failure. Dr. Taylor spoke at the Medical College of Ohio's 14th annual Cardiovascular Symposium.
Doctors and nurses from throughout the region learned the latest ways to determine who's at risk for a heart attack, new practices to prevent heart disease in vulnerable patients, and a procedure that could offer hope for the nation's 5 million heart-failure patients.
“I believe that cell therapy is a paradigm shift in the treatment of heart disease. I absolutely believe that 15 years from now it's going to be standard treatment,'' Dr. Taylor said. Clinical trials are already under way in the United States and Europe.
In animal studies, Dr. Taylor repaired hearts by injecting them with myoblasts - a cell that develops into a skeletal muscle cell. Not only did the cells take root in the heart, but they seem to act like regular heart cells. Heart contractility improves, and heart walls thicken.
When heart muscle dies, the remaining tissue works harder to compensate for lost squeeze-ability. The result is a bigger, less efficient heart. But when new cells were injected into damaged pig hearts, Dr. Taylor found the hearts shrunk by as much as 25 percent.
Dr. Taylor is also studying the use of bone marrow cells in heart repair, which thus far are nearly as effective as the skeletal muscle cells.
As word about cell implantation spreads, Dr. Taylor is inundated by patients looking for hope as well as doctors in a hurry to put the therapy to work. It's quite a change from the reception her research received as recently as six years ago.
“It was really discouraging for a number of years,'' she said. “It wasn't clear anybody was going to believe us. We were getting lab results, but we were having a very difficult time publishing those results. People would say, `If this works, why hasn't somebody done it before?'''
“My career was essentially doing this'' - she traces a steep slope downward with her palm - “because it looked like I wasn't doing anything. One time, I presented some of these data and one of my colleagues said, `There's no way that can be right.'''
Then, in 1998, Nature Medicine published her research showing functional improvement in cell-injected hearts.
“When that happened, everything changed,'' she said.
Still, the technique faces challenges.
Human trials revealed problems animal studies never showed. Four of nine patients in one Paris study developed a dangerous unstable heart rhythm. Two of five patients in a Rotterdam study died of unknown causes. The unstable rhythms in the Paris clinical trial suggest that the cells may not integrate into the heart's electrical system right away.
While research on this question continues, there's a possibility that patients who receive cell injections experimentally could also have a defibrillator implanted to shock the heart into rhythm while the new cells catch on to the proper beat.
In fact, other research suggests a lot more of us will sport an implanted defibrillator soon. A growing body of work shows that such defibrillators lower the risk for sudden cardiac death in vulnerable patients, said MCO cardiologist Dr. M. Yousuf Kanjawal.
Every year, 450,000 people in the United States die of sudden cardiac death - a constellation of maladies that ranges from a heart-muscle-killing heart attack to a temporary narrowing of the coronary arteries.
Those who survive their first heart attack remain at a higher risk of dying from their next one.
A series of recent studies show that implantable defibrillators - like the one Vice President Dick Chaney received - would prevent many of those deaths.
“Anybody who's had a heart attack should call his doctor at least to find out what his pump is doing,'' said Dr. Kanjawal. Studies show the implantable devices are more effective than drugs in preventing death.
One report in the New England Journal of Medicine this year showed a 38 percent drop in mortality over two years for patients who received the defibrillators compared to patients whose disease was managed with drugs.
Symposium participants also heard from Dr. Paul Ridker of Harvard Medical School about the use of C-Reactive Protein to determine heart attack risk.
In numerous trials, C-Reactive Protein, or CRP, proved more effective than cholesterol in predicting heart attack. This is especially important since half of all heart attack sufferers have normal cholesterol levels. CRP screening is available now, although the Centers for Disease Control will publish guidelines on the test next year.
Dr. Ridker says exercise and weight loss will lower CRP - an indicator of inflammation - as will statin drugs used to lower cholesterol.