Common anemia drug may protect hearts of infants undergoing surgical repair of congenital defects

Medical College of Wisconsin researchers may have promising news for the many infants who are born with a congenital heart defect serious enough to require surgery before their first birthday. Congenital heart defects occur in one out of every 125 newborn children. One-third of these infants will require a major surgical procedure within their first year to prevent premature death.

The team, led by John E. Baker, Ph.D., professor of pediatric surgery at the Medical College of Wisconsin, found that infant rabbit hearts receiving a single, pre-surgical treatment of erythropoietin, a drug commonly used to treat anemia, recovered better than hearts that did not.

Their study, funded in part by the National Institutes of Health, and reported in the April 21 issue of Basic Research in Cardiology, indicates that erythropoietin may be a practical way to increase protection of the heart from damage due to temporary interruptions of blood flow during surgery.

“Protecting a child’s heart during surgical repair of birth defects remains a challenge for the cardiac surgeon,” says Dr. Baker. “We are encouraged by the results of this study because currently, there are no medical therapies available to protect the heart against the damaging effects of surgery.”

Dr. Baker’s team found that, when measured by improved heart function, erythropoietin appears to substantially and immediately decrease injury to the rabbit heart in a setting simulating surgical repair.

Children undergoing heart surgery suffer varying degrees of oxygen deprivation or cyanosis when the heart is chronically perfused with inadequately oxygenated blood. Dr. Baker and colleagues sought to unravel the natural mechanisms by which hearts protect themselves against chronic hypoxia.

In earlier studies, the team showed that infant human and rabbit hearts adapted to chronic hypoxia by activating specific signaling pathways and increasing nitric oxide production. They also found that the method by which hearts adapt to chronic hypoxia from birth results in a process called erythropoiesis, which is an increase in hemoglobin and hematocrit. These blood components are key to increasing the transport of oxygen to the heart. This process is moderated by the protein erythropoietin, of which a human recombinant version, sold as Procrit or Epogen, is currently used to treat anemia.

In a classic example of translational, bench-to-bedside, research the authors are planning to seek approval to conduct a clinical trial at Children’s Hospital of Wisconsin to evaluate the ability of erythropoietin to protect the infant human heart during surgical repair of congenital heart defects. Children’s Hospital is a major teaching affiliate of the Medical College.

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