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Heart Arrhythmia
Saving Lives from Sudden Cardiac Arrest

Columbia's Center for Molecular Cardiology won widespread attention in the spring of 2004 for developing drugs that can prevent the irregular heartbeats that cause hundreds of thousands of Americans to die every year from sudden cardiac arrest. But this breakthrough required years of preparation—fifteen, to be exact.

In 1989, Dr. Andrew R. Marks, now chair of the Department of Physiology and Cellular Biophysics at Columbia, and his team first singled out a molecule in the muscles that enable the heart to beat. This molecule was a tiny valve that opens to allow calcium into the heart muscle, and then closes to keep the calcium in. The valve, or calcium channel, is vital because calcium is necessary for the regular contractions and relaxation of the heart which pump blood through the body. Without it, normal heartbeats are not possible.

In 2000, Dr. Marks and his team found that defects in this calcium channel were responsible for congestive heart failure, a gradual weakening of the heart that not only debilitates patients, but increases their risk for sudden cardiac arrest. "Developing a drug for a specific molecular target in the heart had never been done before," said Dr. Marks.

By 2004, the team had developed a drug that, in Dr. Marks' words, "makes two molecules want to hold together more tightly" and would stop the leak in the calcium channel. The team tested its drug on mice with defective calcium channels resembling humans with congestive heart failure. Every mouse given the drug thrived.

The team is now working to bring this breakthrough cure to humans, via clinical trials. Perhaps even more importantly, this discovery will encourage researchers to find other secrets in the molecules of our heart.

"Our experiment was a proof of concept for an entirely new approach to treating heart problems," said Dr. Marks. "We plan to continue pushing the envelope and develop new treatments based on these successes."
© 2005 Columbia University