Light therapy could offer same benefits as electric shock defibrillation after MI

Doctors at Johns Hopkins University believe they are one step closer to using optogenetic defibrillation on living humans, according to a paper published in the Journal of Clinical Investigation.

The researchers tested the method of using light to manipulate genes on mice and human simulations, finding the light therapy helped terminate heart arrhythmias without some of the negative effects of electrical shock therapy such as pain and the induction other types of heart damage that can be fatal.

This study focused on blue and red light pulses in treating ventricular arrhythmias of the subjects. Blue light pulses had previously only been proven to help pace the heart in humans.

The researchers pointed out, “[T]hese [blue light pacing] results do not imply the feasibility of optogenetic defibrillation, because cardiac pacing entails only a brief depolarization in a few cardiomyocytes with subsequent intrinsic excitation of the whole heart through gap-junctional electrical coupling. In contrast, defibrillation requires the simultaneous depolarization of a large mass of ventricular tissue, and therefore the energy required for a defibrillating shock is dramatically larger than that of a typical pacing stimulus,” meaning a light different to the ones already tested for pacing would be required.

In transgenic channelrhodopsin-2 (ChR2) mice, researchers found that one blue pulse of light on the anteroseptal epicardium successfully terminated ventricular arrhythmia 85 percent of the time. Increasing the therapy to four light pulses showed a 97 percent success rate. The application of the light therapy on certain kinds of wild type mice, though, only had about a 20 percent success rate, which is not much better than the 15 percent rate spontaneous termination of arrhythmia in a control group.

In the transgenic mice that had experienced a heart attack, the researchers found that one light pulse could stop arrhythmia 88 percent of the time, while the control group’s spontaneous arrhythmia termination was only about 27 percent.

In wild type mice that had had the ChR2 gene transferred before therapy (which the researchers pointed out would be necessary for such a method to work in humans), the light pulses worked to correct ventricular arrhythmia in all three of the mice tested.

The human simulation tests were carried out using MRI data from a patient with recurrent ventricular tachycardia and had previously suffered a heart attack. The researchers “transferred” ChR2 genes into the model and treated it with light and the ventricular tachycardia was also terminated.

The study authors wrote that their results fit with previously understood treatments—that optogenetic defibrillation requires a stronger light energy than optogentic cardio pacing, and the gene expression necessary to perform such a treatment is safe for humans. But the researchers called for more information about the practice in living humans before anyone is able to deem optogenetic defibrillation a feasible alternative to electric shock defibrillation.