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Researchers Find Reason behind Heart Attack Risk in People with Diabetes

Update Date: Feb 18, 2013 01:52 AM EST
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Researchers have now found why having diabetes type-2 increases a person's risk of dying from sudden heart attack.

The study, conducted by researchers from University of Iowa, has found that the increased risk of heart attack is due to increase in the activation of an enzyme (CaMKII enzyme) in the heart of people with diabetes, which leads to an abnormal heart rhythm.

Diabetes affects roughly 8 percent of the U.S. population and many of these people have an increased risk of dying from heart attack, according to a news release. The number of people being diagnosed with diabetes has tripled from 5.6 million in 1980 to 26.9 million in 2010.

"Many studies have shown that patients with diabetes are at especially high risk for dying from a myocardial infarction (heart attack). Our study provides new evidence that this excess mortality could involve a pathway where oxidized CaMKII enzyme plays a central role," said Mark Anderson, M.D., senior author of the study.

The present study was conducted on mouse models that were genetically tweaked to develop diabetes. Researchers found that the heartbeat rate in these mice slowed down significantly.

Also, pacemaker cells - that control the rhythm of heartbeat - died in large numbers in these mice. These pacemaker cells had high levels of the enzyme. Researchers then blocked the activation of CaMKII enzyme, which led to fewer pacemaker cell deaths over time. These mice then had normal heartbeat and their risk of death from a sudden heart attack was lowered.

"Our findings suggest that oxidized CaMKII may be a 'diabetic factor' that is responsible for the increased risk of death among patients with diabetes following a heart attack," says lead study author Min Luo, a cardiology fellow in the UI Department of Internal Medicine.

Researchers say that targeting the specific enzyme in the pacemaker cells may lower the risk of sudden heart attack in people with diabetes type-2.

The study is published in the Journal of Clinical Investigation.

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