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Decoding Heart-Brain Talk to Prevent Sudden Cardiac Deaths

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Deeptankar DeMazundar in a white doctor's coat
Credit: Colleen Kelley/UC Creative + Brand

As a cardiac electrophysiologist, Deeptankar DeMazumder has worked for years with people at risk for sudden cardiac arrest (SCA). Despite the latest medical advances, less than 10 percent of individuals stricken with an SCA will survive this highly dangerous condition in which irregular heart rhythms, or arrhythmias, cause the heart suddenly to stop beating.

In his role as a physician, DeMazumder keeps a tight focus on the electrical activity in their hearts, doing his best to prevent this potentially fatal event. In his other role, as a scientist at the University of Cincinnati College of Medicine, DeMazumder is also driven by a life-saving aspiration: finding ways to identify at-risk individuals with much greater accuracy than currently possible—and to develop better ways of protecting them from SCAs. He recently received a 2020 NIH Director’s New Innovator Award to pursue one of his promising ideas.

SCAs happen without warning and can cause death within minutes. Poor heart function and abnormal heart rhythms are important risk factors, but it’s not possible today to predict reliably who will have an SCA. However, doctors already routinely capture a wealth of information in electrical signals from the heart using electrocardiograms (ECGs). They also frequently use electroencephalograms (EEGs) to capture electrical activity in the brain.

DeMazumder’s innovative leap is to look at these heart and brain signals jointly, as well as in new ways, during sleep. According to the physician-scientist, sleep is a good time to search for SCA signatures in the electrical crosstalk between the heart and the brain because many other aspects of brain activity quiet down. He also thinks it’s important to pay special attention to what happens to the body’s electrical signals during sleep because most sudden cardiac deaths happen early in the waking hours, for reasons that aren’t well understood.

He has promising preliminary evidence from both animal models and humans suggesting that signatures within heart and brain signals are unique predictors of sudden death, even in people who appear healthy [1]. DeMazumder has already begun developing a set of artificial intelligence algorithms for jointly deciphering waveform signals from the heart, brain, and other body signals [2,3]. These new algorithms associate the waveform signals with a wealth of information available in electronic health records to improve upon the algorithm’s ability to predict catastrophic illness.

DeMazumder credits his curiosity about what he calls the “art and science of healing” to his early childhood experiences and his family’s dedication to community service in India. It taught him to appreciate the human condition, and he has integrated this life-long awareness into his Western medical training and his growing interest in computer science.

For centuries, humans have talked about how true flourishing needs both head and heart. In DeMazumder’s view, science is just beginning to understand the central role of heart-brain conversations in our health. As he continues to capture and interpret these conversations through his NIH-supported work, he hopes to find ways to identify individuals who don’t appear to have serious heart disease but may nevertheless be at high risk for SCA. In the meantime, he will continue to do all he can for the patients in his care.


[1] Mitochondrial ROS drive sudden cardiac death and chronic proteome remodeling in heart failure. Dey S, DeMazumder D, Sidor A, Foster DB, O’Rourke B. Circ Res. 2018;123(3):356-371.

[2] Entropy of cardiac repolarization predicts ventricular arrhythmias and mortality in patients receiving an implantable cardioverter-defibrillator for primary prevention of sudden death. DeMazumder D, Limpitikul WB, Dorante M, et al. Europace. 2016;18(12):1818-1828.

[3] Dynamic analysis of cardiac rhythms for discriminating atrial fibrillation from lethal ventricular arrhythmias. DeMazumder D, Lake DE, Cheng A, et al. Circ Arrhythm Electrophysiol. 2013;6(3):555-561.


Sudden Cardiac Arrest (National Heart, Lung, and Blood Institute/NIH)

Deeptankar DeMazumder (University of Cincinnati College of Medicine)

DeMazumder Project Information (NIH RePORTER)

NIH Director’s New Innovator Award (Common Fund)

NIH Support: National Heart, Lung, and Blood Institute; Common Fund

Drug Discovery from A to Z … Arrhythmias to Zebrafish!

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Healthy and mutated zebrafish

Caption: Healthy zebrafish (top) compared to zebrafish with arrhythmia-causing mutation (bottom). Their hearts are shown to the right, with enlargement indicating a weaker heart. The heart’s outflow tract is marked OFT; atrium, a; and ventricle, v.
Credit: Asimaki et al. Science Translational Medicine

Arrhythmia is a condition in which the heart loses its regular rhythm, beating either too rapidly or too slowly. Occasional irregular heartbeats are harmless, but if sustained they can cause dizziness, fainting, and even sudden death. There are a number of drugs available that can prevent arrhythmias, but none are perfect. Implanted devices can help—pacemakers can keep the heart from beating too slowly, and defibrillators can reset the heart’s rhythm with an electrical shock if a dangerously rapid rhythm develops.

But new treatments are needed. Now, an NIH-funded research team has created an animal model that is advancing efforts to find new drugs to prevent arrhythmia.  Led by Jeffrey Saffitz at Beth Israel Deaconess Medical Center, Boston, researchers used genetic engineering techniques to produce zebrafish with genetic mutations identical to those in some people who suffer from a rare inherited disease called arrhythmogenic cardiomyopathy (ACM). In humans, ACM leads to dangerous arrhythmias that can cause sudden cardiac death, usually in people under the age of 35.