We know probiotics are good for GI heath. They may also affect mental health. More >
The Human Heart Can Grow New Muscle after a Heart Attack
The human heart has a much greater ability to repair damage than it's credited with.
When a person suffers a heart attack, the heart muscle is often damaged. In what may prove to be a groundbreaking study, 17 heart attack patients who received an infusion of their own stem cells have repaired some of the heart muscle damaged by their attacks. Six months after receiving the stem cells, scarred heart tissue shrank by 50%, apparently replaced by new healthy heart muscle.
Unfortunately, the patients who received the stem cells don't yet show any better blood flow out of the heart than untreated patients, in other words, their hearts don't show an improvement in function. It is still possible that may happen later on. The scarring of the heart after a heart attack has always been thought to be permanent. Until now, no one even knew that new muscle could be regenerated.
Back in 2003, it was discovered that the heart contains stem cells, cells that can give rise to new heart muscle. These are few in number, about one out of every 30 million heart cells. This is sufficient to replace the small number of cells that die during the normal wear and tear on the heart in a person's lifetime, but it is a woefully inadequate supply when dealing with the damage of a heart attack.
Researcher Eduardo Marbán, then at Johns Hopkins University, was able to devise a method to harvest these stem cells, first from animal hearts and later from human ones, and grow them in large numbers in the laboratory. These are not reprogrammed stem cells, they're cells that are naturally found in the body and cultured under conditions that permit more of them to grow than normally would inside of the human body.
Results from reinjection of these cells into pigs that had suffered heart attacks were sufficiently encouraging that Marbán and his team received approval to conduct a Phase I investigative trial in humans.
The trial began recruiting patients in 2009. Twenty-five patients, average age 53, who had suffered a heart attack were recruited. Two to four weeks after their heart attack, all received extensive imaging scans to pinpoint the exact location and severity of the scarring caused by the heart attack.
Seventeen patients underwent biopsies, where small portions of healthy heart tissue--about half the size of a raisin--were removed and used as a source of stem cells to be cultured in the laboratory. After culturing, between 12 and 25 million cells were reintroduced into the coronary artery of each of the 17 patients.
The other eight patients received conventional heart attack after care, including prescription medicine, exercise recommendations and dietary advice.
Six months later, patients who had received the stem cells showed about a 50% reduction in scarring--about 12% of heart as opposed to 24% soon after the heart attack. What once was inert scar tissue now exhibits contractility--is behaving like a muscle. Patients who did not receive the stem cells showed no decrease in scarring.
According to Marbán, the stem cells don't act by reproducing themselves over and over to form new heart tissue. Instead, they seem to be sending some sort of signal to the whole heart to repair itself. How they do so isn't currently known.
Where this all will lead isn't known either. Until recently, it was unthinkable that a damaged human heart could grow new muscle. Just how far the repair process can go remains to be seen.
Marbán sees the study results as saying that half of the injury caused by the heart attack has been repaired. That's not complete recovery, but it's a good start, certainly enough to lead to larger Phase 2 trials, which Marbán hopes will begin soon.
An article on the study was published online by The Lancet.
Eduardo Marbán, MD, PhD is the director of the Cedars-Sinai Heart Institute. Previously, Dr. Marbán spent 26 years at Johns Hopkins University School of Medicine, the last four as director of cardiology.
April 6, 2012