Lighting the Heart Back to Normal Rhythm

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Simulation of how optogenetic defibrillation might work in a human heart. [Image: Tobias Brügmann (University of Bonn)/Patrick M. Boyle (Johns Hopkins University)]

Cardiac arrhythmia—a wildly irregular heartbeat—can kill a person in minutes. Implantable defibrillators can provide lifesaving electrical jolts to the hearts of patients with a known risk of arrhythmia, but these shocks can be painful. Research teams in Germany and the United States have developed a potentially gentler method of stimulating a regular heartbeat: a pulse of light (J. Clinical Investigation, doi:10.1172/JCI88950).

Scientists at the University of Bonn, Germany, and Johns Hopkins University, Baltimore, Md., USA, explored the possibility that a light-sensitive channel within cardiac tissue, known as ChR2, could play a role in terminating ventricular fibrillation. Although the researchers experimentally stopped fibrillation only in the hearts of laboratory mice, computer simulations indicate that the optogenetic technique could work for humans too.

The Bonn team experimented on both transgenic mice bred to express ChR2 in all their cardiac muscle cells and wild-type mice that had undergone a ChR2 gene transfer via a virus. Since tiny mouse hearts typically do not sustain arrhythmias for more than a few beats, the scientists had to develop a new protocol for electrically stimulating the heart problem. Then they ended the arrhythmias by illuminating the epicardium (the protective layer of cells on top of the heart’s muscle tissue) with 470-nm blue light for 80 to 100 ms. Notably, the success rate of the light pulse was much lower in wild-type mice that did not have the light-sensitive channel.

Will this technique also work on human hearts? The Johns Hopkins computational cardiology team used a new virtual human-heart model to simulate infarct-related ventricular tachycardia (VT), a rapid heartbeat that can lead to arrhythmia and death. The scientists found that illumination effectively ended a VT episode in simulated diseased human heart tissue that responded to ChR2—although human hearts would require 669-nm red light. They also learned important details of the depolarization mechanism by which the cells of the heart’s myocardium respond to the light signal.

In contrast to today’s implantable devices, optogenetic defibrillators of the future would not require charging a capacitor to generate high-voltage fields. However, the details of an implantable light source for the human heart still must be worked out. Perhaps tiny light sources could be injected into cardiac cells, or perhaps the light emitters could be embedded into a stretchable membrane that could wrap around the heart’s exterior. In the latter case, excess epicardial fat would absorb the light and diminish the device’s effectiveness.

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