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Columbia team finds treatment that corrects cellular defect at the root of heart failure

NEW YORK - Researchers at Columbia University have shown for the first time that beta blockers - drugs used to treat cardiovascular disease - can correct a specific defect in failing hearts.

"Up until now we have been treating symptoms but not the cause of heart failure," says Dr. Andrew R. Marks, Clyde and Helen Wu Professor of Molecular Cardiology at Columbia University College of Physicians & Surgeons and principal investigator of the study. "Our research shows that we can treat the cause." Dr. Marks also serves as director of Columbia's Center for Molecular Cardiology and is professor of medicine and pharmacology. The findings will be published in the Dec. 4 issue of the journal Circulation.

Heart failure, the leading cause of death in the developed world, occurs when the heart is too weak to sustain proper circulation. Some patients in heart failure receive left-ventricular assist devices (LVADs), which are implanted in the chest to help pump the blood and give the patient's own heart a rest as he or she waits for a heart transplant. Patients in heart failure may also be given drugs to improve symptoms. But heart transplant is the only way to cure heart failure.

Dr. Marks' research demonstrates that defects in the calcium channel controlling heart muscle function occur in heart failure. The membrane surrounding a cell contains a small calcium channel stimulated by the electrical impulses driving heart rhythm. When stimulated, this calcium channel triggers another, larger calcium channel within the cell, called the ryanodine receptor, to release calcium ions. The rush of calcium ions then signals the heart muscle to contract powerfully. The ryanodine receptor sits at the surface of the sarcoplasmic reticulum, a sac containing calcium ions, and is the major gatekeeper for calcium ion release.

The more calcium released through the ryanodine receptor, the stronger the contraction of the heart. Dr. Marks and his colleagues have
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Contact: Annie Bayne
as862@columbia.edu
Columbia University Medical Center
11-Dec-2001


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