Jefferson scientists find anemia drug may help lessen effects of heart attack

October 01, 2003

Researchers at Jefferson Medical College have found that the anemia drug erythropoietin (EPO) may lessen the effects of a heart attack due to ischemia, or lack of oxygen, by protecting heart cells from dying. EPO is a naturally occurring hormone that stimulates the body to produce more red blood cells.

Scientists led by Walter Koch, Ph.D., director of the newly created Center for Translational Medicine of the Department of Medicine at Jefferson Medical College of Thomas Jefferson University in Philadelphia, found that animals that first received a single dose of EPO and then subsequently had the equivalent of an ischemic heart attack had less severe attacks. They also discovered that the reason was because EPO somehow reduced programmed cell death in heart cells.

"As a result, smaller infarcts meant heart function was increased," says Koch, who is W.W. Smith Professor of Cardiology at Jefferson Medical College of Thomas Jefferson University. But Koch isn't convinced that EPO necessarily directly affects heart function. Rather, he says, "there's simply more good muscle left."

"EPO can protect the ischemic heart," Dr. Koch says. "It looks like it is a generalized phenomenon in tissue outside red blood cells." Dr. Koch and his colleagues report their results October 1 in the Journal of Clinical Investigation.

Giving EPO prior to heart attack may be particularly relevant for patients admitted to the hospital with "acute coronary syndrome," where ishemia is present but the patients have not yet had a heart attack, Dr. Koch says. "In these cases, there are opportunities to treat them prophylatically to protect against an ischemic event such as an impending balloon angioplasty procedure. That would be the group to test first."

In some cases, Dr. Koch says, EPO isn't necessarily the best thing for patients with pre-existing heart disease. EPO, in increasing blood cell production, may thicken the blood. That may be dangerous for patients with narrowed arteries. However, according to Dr. Koch, his group's study in rabbits showed that EPO had a direct effect on the heart without increasing the red blood cell count and this benefit would counter any negative benefits.

Dr. Koch had read some published reports that EPO could protect brain cells from ischemia, or a lack of oxygen. He wondered if there was a generalized protection mechanism that might offer some novel protection to the heart.

Koch, who was then at Duke University and his colleagues there first tested the possibility of a generalized protection mechanism in heart cells in the laboratory. They treated such cells with hydrogen peroxide, which mimics cells that have low oxygen content and which suffer oxidative stress. They also exposed the cells to low oxygen conditions. In both cases, fewer cells died when they were treated with EPO. They also discovered that some biochemical signaling pathways were activated after treatment with EPO that appeared to involve the kinase Akt, which plays a role in cell survival, or more specifically, preventing cells from succumbing to programmed cell death.

"This is consistent with EPO stimulating these pro-survival pathways to protect myocytes (a type of heart cell)," he says. They also found an increase in Akt in the animal heart cells after treatment with EPO.

Dr. Koch notes that his lab at Jefferson and his Duke co-workers would like to study other animal models and eventually move to clinical trials. EPO is already used in humans, so safety and toxicity profiles have been established.

Dr. Koch points out the next step prior to clinical trials would be to study the various responses to different doses of EPO. "Maybe we can get by with low doses that won't significantly raise the red blood cell count but will be effective for cardiac protection."

Thomas Jefferson University

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