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Maths, not medicine, could prevent fatal heart attacks

August 12, 2017

About 200 Australians aged 25 to 34 years die each year from heart attacks caused by cardiac arrhythmia. Most are apparently healthy young men who die within five minutes of the initial symptoms -- a suddenly irregular or fast heartbeat.

But the challenge of designing a pacemaker capable of correcting a potentially fatal arrhythmia is mathematical, not medical, according to University of New South Wales researcher, Dr Adelle Coster.

"The goal is to make an implantable artificial pacemaker that can arrest an abnormal heart rhythm before it becomes fatal," she says. "The mathematical challenge is to describe the complex patterns of electrical, chemical and neurological signals that trigger a potentially fatal heart attack.

"An arrhythmia is like a short circuit to the heart's electrical system," says Dr Coster, who has a three-year Australian Research Council grant to untangle the problem. "It interrupts the heart's rhythmic contraction and relaxation so it doesn't pump the way it's supposed to."

This abnormal rhythm can occur when electrical signals in the heart trigger rapid (tachycardia), slow (bradycardia) or chaotic beating (ventricular fibrillation).

"Normally, the heart's four chambers contract in a coordinated way, with the signal beginning in the sinoatrial node, which is the heart's natural pacemaker," she says. "The signal then travels through a series of heart chambers and nodes but problems can happen anywhere on this pathway.

"Understanding how these signals get passed from cell to cell is a non-linear dynamical problem we can treat mathematically by solving numerous simultaneous equations."

science.unsw.au

Dr Adelle Coster - (bh) 02-9385 7048 (ah) 0411 156 015

Dan Gaffney - UNSW Science Media - 0411 156 015

"We found there are very specific differences in the way these two systems respond to changes in the cell," Dr. Hilgemann said. "For example, the one in the kidney is involved in reabsorbing sodium, but it is not regulated at all by changes in cell volume."

Dr. Hilgemann and his colleagues improved upon an existing experimental technique in order to study the NHE transporters and how acidity changes within a cell. The existing method involves skewering a single cell on a tiny, hollow needle called a pipette. Dr. Hilgemann's group made their pipette larger to make a larger hole in the cell, which allowed them better control over what was inside and outside of the cell.

They also optimized the use of tiny sensors that can measure exactly the movement of protons across the cell membrane. "This tells us how the acidity is changing," Dr. Hilgemann said. "Our advancements allow us to better show and study how these systems are working."

Other UT Southwestern researchers who contributed to the study are Dr. Daniel Fuster, a postdoctoral researcher in internal medicine, and Dr. Orson Moe, director of the Charles and Jane Pak Center for Mineral Metabolism and Clinical Research.

The research was funded by the National Institutes of Health and the Department of Veterans Affairs Research Service.

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