Drug May Save Lives of Heart Failure Patients

Corrects molecular problem in heart cells that cause arrhythmia

THURSDAY, April 8, 2004 (HealthDayNews) -- Researchers say they have found a medication to correct a cellular flaw that can lead to the death of many people with heart failure.

The discovery is based on 15 years of research into the molecular mechanism of heart failure, said Dr. Andrew R. Marks, chairman of physiology and cellular biophysics at Columbia University Medical Center in New York City, and leader of the group reporting the finding in the April 9 issue of Science.

Heart failure, which affects an estimated 4.6 million Americans and contributes to 300,000 deaths a year, is a progressive loss of the heart's ability to pump blood. It now is treated with a number of drugs aimed at improving heart function in one way or another. Drugs can help many patients, but the ultimate treatment involves such drastic measures as implanted defibrillators and heart transplants.

"We hope to develop a pill that millions of people could take at a cost that is relatively low compared to such measures," Marks said.

Columbia University, which holds the patent on the new treatment, already is talking to "a couple of large pharmaceutical companies" about development of such a pill. It is not the medication described in the Science report, Marks said, but one discovered after that report was written and is "200 times more potent."

About half of the deaths related to heart failure are caused by arrhythmia, a fast and erratic heartbeat. The Columbia researchers discovered the cause of that problem more than three years ago, Marks said. It is a leakiness of the cellular channels through which calcium flows to control the regular beating of the heart. That leakage can result in a fatal arrhythmia.

Calcium channel problems are known to be involved in heart disease, and a class of drugs called calcium channel blockers are used against a variety of cardiac problems. But they are not effective in heart failure, and the new drug works in an entirely different way than calcium channel blockers, Marks said.

The drug described in the journal report, designated JTV519, makes a protein that attaches itself to the leaky calcium channels, closing them to stop the leakage. In laboratory tests, the drug prevented arrhythmias in 10 mice with the same molecular defect found in human heart failure, while eight of nine mice with the same defect who did not get the drug developed fatal arrhythmias.

That drug was discovered "by trial and error," Marks said. The newer drug, developed by working with variants of the original molecule, is even more effective, he said.

"The next step is to optimize the drug and to test it in an animal model in preparation for a clinical trial," he said. "We would hope that we could move into patients, at least on an experimental basis, in a year or two."

More information

You can learn about current treatment options for heart failure, including lifestyle changes, from the American Heart Association, which also describes arrhythmias.

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