"This potentially could become the basis for a new test, used in conjunction with other blood tests, to help diagnose heart attacks," said senior author Sakthivel Sadayappan, PhD. "This is the beginning. A lot of additional studies will be necessary to establish cMyBP-C as a true biomarker for heart attacks."

Sadayappan is an assistant professor in the Department of Cell and Molecular Physiology at Loyola University Chicago Stritch School of Medicine. First author is Suresh Govindan, PhD, a postdoctoral researcher in Sadayappan's lab.

Between 60 and 70 percent of all patients who complain of chest pain do not have heart attacks. Many of these patients are admitted to the hospital, at considerable time and expense, until a heart attack is definitively ruled out.

An electrocardiogram can diagnose major heart attacks, but not minor ones. There also are blood tests for various proteins associated with heart attacks. But most of these proteins are not specific to the heart. Elevated levels could indicate a problem other than a heart attack, such as a muscle injury.

Only one protein now used in blood tests, called cardiac troponin-I, is specific to the heart. But it takes at least four to six hours for this protein to show up in the blood following a heart attack. So the search is on for another heart attack protein that is specific to the heart.

The Loyola study is the first to find that cMyBP-C is associated with heart attacks. The protein is specific to the heart. And it may be readily detectable in a blood test because of its large molecular size and relatively high concentration in the blood.

Researchers evaluated blood samples from heart attack patients. They also evaluated rats that had experienced heart attacks. They found that in both humans and rats, cMyBP-C was elevated significantly following heart attacks.

Sadayappan said cMyBP-C is a large assembly protein that stabilizes heart muscle structure and regulates cardiac function. During a heart attack, a coronary artery is blocked, and heart muscle cells begin to die due to lack of blood flow and oxygen. As heart cells die, cMyPB-C breaks into fragments and is released into the blood.

"Future studies," Sadayappan and colleagues wrote, "would determine the time course of release, peak concentrations and half life in the circulatory system."

Other co-authors are Andrew McElligott, Saminathan Muthusamy, PhD, David Barefield, Jody L. Martin, PhD, and Kyle K. Henderson, PhD, of Loyola's Stritch School of Medicine; Nandini Nair, MD, PhD, and Enrique Gongora of Texas A&M HSC College of Medicine; Kenneth D. Greis, PhD, of the University of Cincinnati College of Medicine, Pradeep K. Luther, PhD, of Imperial College London; and Saul Winegrad, PhD of the University of Pennsylvania.

The study was supported by grants from the National Institutes of Health and American Heart Association.

Sadayappan holds a provisional patent to determine the risk factors associated with cMyBP-C degradation and release into human body fluid.

Note: If no author is given, the source is cited instead.

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