Patients with hard-to-treat chest pain reported feeling better, and could exercise longer, after doctors injected stem cells taken from their bone marrow into their heart, according to a new study in Circulation Research.
The early-stage research suggests that the cells were able to help heal tiny, damaged blood vessels that are often untouched by procedures like stents and angioplasty, says lead researcher Douglas Losordo of Northwestern University.
Losordo has been searching for more than a decade for ways to repair the heart using a patient’s own stem cells. He is by no means the only scientist on this quest, but Losordo is the only one using a particular stem cell, called CD34+, which is believed to promote blood vessel growth.
Richard Lee, a cardiologist at Brigham and Women’s Hospital in Boston and head of the cardiovascular program at the Harvard Stem Cell Institute, says Losordo’s research is novel because of his use of these cells, and because he is aiming his treatments at a group of people who have not been well helped by medicine so far.
The American Heart Association estimates that 850,000 Americans have lingering bouts of chest pain, a condition called refractory angina, which is not relieved by medication, angioplasty, or stenting. At the beginning of Losordo’s study, the 167 participants had 20 or more episodes of pain a week so severe that they had to stop what they were doing. Six months into the research, patients who received a low dose of the stem cells reported roughly seven attacks a week on average, while those who received a placebo treatment had 11.
The low-dose patients also were able to tolerate exercise for more than two minutes longer at the end of the study compared to the beginning, while those in the placebo arm could last just over a minute longer.
By harvesting a patient’s CD34+ cells from bone marrow, amplifying them, and injecting them directly into the damaged portion of the heart, Losordo says, he is circumventing natural steps that these people’s bodies might not be equipped to perform anymore. In animal studies, he found that the cells were naturally recruited to the heart after an injury to help repair damaged tissue. His research suggests that they secrete growth factors and immune molecules.
“These cells seem to represent one of the natural mechanisms for helping to repair damaged tissue,” he says. “We’re taking a preprogrammed repair mechanism and simply trying to leverage that in patients who have been damaged over the course of many years or decades.”
Lee compliments the thorough nature of Losordo’s work. “I think that this is a promising study, because it was so carefully done and because this patient population can be very incapacitated,” Lee says.
However, he offers three reasons for caution. First, patients in the placebo arm of the study also showed dramatic improvements. Second, although the procedure seemed generally safe, the patients’ hearts released an enzyme that is typically discharged when damage occurs. And third, patients receiving a lower dose of the stem cells fared as well or better than those receiving a higher dose.
“That really implies that we really don’t know what’s going on,” Lee says. “You like to see dose-dependence. If it’s the low-dose [that’s most effective], then you wonder, can we go lower and get the same effect? Have we missed the real benefit?” Other cell therapies for the heart suffer from similar shortcomings, Lee notes.
Losordo expects to start the final phase of clinical trials in a larger group of patients at the end of this year. Trials have already begun using CD34+ cells to help restore blood vessels in people at risk for amputation and in patients with artery blockages in their legs.
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