Diabetic patients are at increased risk of death after a heart attack, suggests recent study. The reason why the risk of death is almost doubled in these patients remains unclear.
Diabetes is one of the leading causes of deaths across the world. It is a disease characterized by the presence of excess sugar in urine as well as blood. In 17th century the disease was referred as "pissing evil". Besides heart attack, diabetes is the fastest growing disease affecting millions of people across the world.
AdvertisementA study conducted at the University of Iowa suggests that the over-activation of an important heart enzyme causes the death of pacemaker cells of the heart and results in abnormal heart rhythm and raised chances of sudden death in diabetic mice.
Mark Anderson, M.D., Ph.D., UI professor, chair, and department executive officer of internal medicine, and the senior author of the study published in the Journal of Clinical Investigation, stated, "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."
More than 8 percent of the people of the United States are affected by diabetes. Reactive oxidative stress (ROS) level is raised by diabetes and results in cellular damage.
Anderson's lab in 2008 revealed that oxidation showed CaMKII (calcium/calmodulin-dependent protein kinase II).
CaMKII or Ca2+/calmodulin-dependent protein kinases II or CaM kinases II are serine/threonine-specific protein kinases which are regulated by the Ca2+/calmodulin complex.
Studies have linked oxidative stress occurring due to diabetes to raised chances of death after a heart attack via oxidation-based activation of the CaMKII enzyme.
Min Luo, D.O., Ph.D., a cardiology fellow in the UI Department of Internal Medicine and the lead author, said, "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."
Min Luo and her team assessed the relationship between diabetes and risk of death from heart attack in a mouse model.
The scientists noted a decrease in heart rates in diabetic mice and like human beings, the mice doubled the risk of death occurring after a heart attack.
The facts from the diabetic mice suggested that the deaths occurring as a result of heart attack were due to abnormalities in heart rhythm. This encouraged the researchers to investigate the pacemaker cells controlling the heart rate.
The experts discovered high levels of oxidized CaMKII enzyme in the pacemaker cells of the heart.
When experts inhibited oxidation-based activation of the enzyme less pacemaker cells died and normal heart rates were noted in diabetic mice.
The study suggested that by reducing the activation of the CaMKII enzyme in specific heart cells can lower the risk of death occurring in heart patients with diabetes.
The research was financially supported by grant from the National Heart, Lung and Blood Institute and from the Fondation Leducq.
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