News Release

Circulatory Device -- A Bridge To Recovery For Heart Failure?

Peer-Reviewed Publication

American Heart Association

DALLAS, June 16 -- The dying heart cells of individuals with heart failure were brought back to life with the help of a mechanical circulation device, report researchers in today's Circulation: Journal of the American Heart Association.

"These findings represent the first report of improved function in human heart cells, called myocytes, with any therapy," says the study's lead author Kenneth B. Margulies, M.D., associate professor of medicine and physiology at Temple University Cardiac Transplant Center, in Philadelphia, About 4.9 million Americans suffer from heart failure in which the heart pumps less blood than needed by the body. The result is difficult breathing and fluid retention causing swollen tissues. Heart failure is often progressive with worsening symptoms and gradual deterioration of heart function. Current therapies for heart failure include drugs -- which reduce the heart's workload to slow the progression of the disease -- and heart transplantation. However, heart cells can not regenerate and drugs do little to help injured heart cells recover pumping ability.

For patients with advanced heart failure who do not respond to medications, heart transplantation can be lifesaving. Due to relatively long waiting times for heart transplantation, some people awaiting a transplant can be kept alive only with a mechanical left ventricular assist device (LVAD) which takes over most of the pumping for the failing heart.

The researchers found that LVAD support reduced the workload of the failing left side of the heart (the ventricle) to such an extent that some heart muscle cells recovered their ability to contract and relax.

"Our findings demonstrate that LVAD supports the heart even in the most severely failing hearts and may promote improvement in heart function," says Margulies. "These results clearly demonstrate that failing myocytes can regain some degree of their previously normal function and are not irreversibly damaged." LVAD support may be a means of promoting heart recovery, says Margulies. Further studies are needed to identify the best candidates for LVAD therapy and, most important, whether the improvements in myocytes are lasting or transient. If improvement persist, LVADs may not just be a "bridge to transplantation" but also a "bridge to recovery," he adds.

At the time of transplant, the researchers examined myocyte samples in 22 patients with severe heart failure, six of whom had received LVAD implants an average of 111 days prior to surgery. The measurements of cellular function were compared in 35 myocytes from the LVAD group and 57 myocytes from other transplant recipients.

In failing hearts, the heart cells have a diminished ability to contract, a slowed rate of relaxation and reduced responses to adrenaline-like substances, such as norepinephrine. Responses to norepinephrine usually allow heart function to improve during exercise or other stress. Each of these hallmarks of reduced heart function was significantly improved in the myocytes from LVAD-supported patients. The rates of contraction and relaxation were three times as fast in LVAD-supported myocytes. In addition, myocytes from LVAD supported hearts responded better to increases in heart rate compared with unsupported failing hearts.

"The major finding is that LVAD support of the failing heart improves myocyte function, while other studies from our laboratory indicate improvements in myocyte structure," says Margulies. "In this regard, LVAD support provides a unique opportunity to gain insight into the molecular mechanisms which contribute to defects in contraction, relaxation and cellular structure in the failing heart."

Co-authors are Konstantina Dipla, Ph.D.; Julian A. Mattiello, B.A.; Valluvan Jeevanandam, M.D.; and Steven R. Houser, Ph.D.

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