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New Heart Attack Predictor Identified by Scientists


Scientists have identified a protein fragment called caspase-3 p17 peptide which, when elevated in the bloodstream, could be a warning that a heart attack is imminent.

This finding is the work of cardiologists at the University of Connecticut Health Center.

A heart attack predictor could prompt immediate treatment

Under the direction of Dr. Bruce Liang, director of the Pat and Jim Calhoun Cardiology Center, researchers “discovered a new biomarker for heart attack, and showed that apoptosis, or a particular kind of cell death, is a cause of heart muscle damage,” according to Liang.

In the study, the scientists measured the levels of a cleaved p17 fragment of caspase-3 in 27 patients who had acute ST-segment elevation myocardial infarction (STEMI), the more serious of the two types of heart attack, or acute myocardial infarction (AMI).

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In patients with STEMI, the coronary artery is completely blocked by a blood clot, which means virtually all the heart muscle that receives nourishment from the artery starts to die (cell death, or apoptosis). Caspase-3 is the end effector caspase for apoptosis in patients who have STEMI.

The peak serum p17 level during AMI was nearly four times higher than in a group of 50 healthy subjects used for comparison. When the p17 levels were measured again at an average of 88 days after the initial heart attack, the p17 levels were still higher than in the control group, which is “consistent with persistent apoptosis after AMI.”

Another factor found in the blood that can assess heart attack as well as stroke risk is C-reactive protein. C-reactive protein is an indicator of inflammation, which is an important factor in atherosclerosis, coronary heart disease, and stroke. Research has shown that the higher the C-reactive protein levels, the greater the risk of having a heart attack.

The discovery of a new heart attack predictor and “the ability to see a heart attack coming with a simple blood test,” according to Liang, could lead to the development of new ways to stop apoptosis and enable clinicians “to get a head start on treatment and preserve crucial heart muscle and cardiac function.”

Agosto M et al. Journal of the American College of Cardiology 2011; 57:220-21
American Heart Association
This page is updated on April 18, 2013.