Virtual heart brings hope for rhythm disorder
By Ashley R. Smith
Fluid dynamics plays an integral role in the propulsion of a jet engine. Engineers know how the properties of fluids — density, pressure, temperature and velocity — work in engines to achieve compression, injection and thrust.
Jacques Beaumont, Watson School assistant professor of bioengineering, hopes to one day have that same level of familiarity with biological tissues and systems.
“When we design the engine of an airplane today, the simulation is absolutely phenomenal. It’s reliable to the point where we have eliminated the need for wind-tunnel tests,” Beaumont says.
Creating computer models of the human heart is bringing that kind of progress to medicine as well. “We can simulate blood flow in an aneurism to predict the risk of rupture,” he says. “Or even simulate excitation of the heart.”
Beaumont uses modeling of the heart to develop noninvasive methods for assessing the risk of life-threatening arrhythmias. He notes that one in 2,500 people lives with a gene mutation that causes inherited heart arrhythmia, a life-threatening condition without a simple solution.
A healthy heart has a stable rhythm set in motion by electrical signals. When a mutation causes those electrical impulses to malfunction, the heart can beat irregularly.
Patients are typically diagnosed in their early 20s when they first visit a clinic complaining of weakness, frequent nausea and, in severe cases, syncope or a loss of consciousness. “From that point on, they need to be monitored very closely,” Beaumont says. “If an episode of arrhythmia lasts too long it can cause death.”
The particular mutations are often difficult to diagnose as they can differ from person to person. A certain number of elements are common, but variations in the mutation can cause different triggers of arrhythmias. For some patients, rapid changes in adrenaline — caused by such things as fear, anger or even the surprise of an alarm clock — can short-circuit their heart’s rhythmic beating.
“When the field started in the late 1980s, we had identified three mutations that put an individual at risk. Now we have 200,” Beaumont says.
But current treatment options are unreliable. While there are a number of drugs, Beaumont says their outcomes vary widely. “What works for one patient doesn’t necessarily work for the next.”
Another common treatment is the use of an implantable cardioverterdefibrillator (ICD). This device sends a strong electrical shock to resynchronize the heart’s cells. However, “it has to cover the entire volume of the heart, so the shock has to be strong. When you send a shock like this, you also excite nerves, and that causes pain,” Beaumont says.
“Every single shock produces pain. And when there are a number of false positives — we know it’s at least 20 percent — patients often elect to get their ICD removed despite the risk of cardiac death.”
As time passes, the probability of dying from cardiac arrest increases exponentially. According to Beaumont, by age 40, the probability of death for symptomatic individuals is 80 percent.
Thus, he and PhD student Ashley Raba ’07, MS ’09, are working to develop computer-simulated testing methods that will allow clinicians to assess the cause of a person’s arrhythmia and potentially cure it. If their research proves definitive, current treatments could be rendered unnecessary.
Once you know the mechanism, the cure follows,” Beaumont says, citing another heart condition known as Wolff-Parkinson-White syndrome. Wolff-Parkinson is caused by an extra electrical pathway in the heart that results in severe arrhythmia in young children and teenagers, limiting their ability to exercise. But once the problem was understood, finding a cure was simple. “We now have a protocol to stimulate the heart and, depending on how the heart responds, we locate the zone and apply radio frequency to scar that tissue.” The children are cured.
For their research into inherited arrhythmias, Beaumont and Raba are developing a computer heart model that will reconstruct an individual’s cardiac beat by personalizing the building blocks of the heart. “We know how human cells generate electrical impulse, and we know how they’re transmitted. The template model can then be modified with information collected clinically, including images of the heart through CAT scan and with message RNA through a blood sample,” Beaumont explains.
With this virtual heart, they will be able to run large-scale simulations.
“The model will show where the arrhythmia is initiated, what conditions trigger it, and whether the patient will respond to certain therapies,” Raba explains.
“The modeling aspect of medicine could change everything,” says Ron Miles, Watson School associate dean for research. “It’s an area that is hopeful, but biological tissues are very different, and this kind of research is extremely difficult. But the promise is there.”