Published online 13 July 2011 | Nature | doi:10.1038/news.2011.414

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A kinder, gentler defibrillator

A new technique could lower the intensity of the shock needed to reset electrical instabilities in the heart.

CLEAR!Could dramatic scenes like this be a thing of the past?Corbis Premium RF/Alamy

When electrical rhythms in the heart go haywire, applying a strong electric shock to the chest can set them straight. But the procedure can also damage heart tissue and cause intense pain, prompting a search for a gentler approach. A technique tested in dogs now claims to be just that: it resets heart arrhythmias by applying a series of five small shocks, instead of one large one, slashing the amount of energy needed by about 84%.

Standard defibrillation, used since the 1950s, works by applying about 1,000 volts of electricity to the outside of the chest in medical emergencies such as cardiac arrest. Like a reset button, it depolarizes each cell and returns the whole system to a resting state. Some patients with previous heart problems have surgically implanted defibrillators, which apply about 350 volts, "but even that is very painful," says Flavio Fenton, a physicist at Cornell University in Ithaca, New York, and one of the researchers involved in the work.

Fenton, Stefan Luther, a physicist at the Max Planck Institute of Dynamics and Self-Organization in Göttingen, Germany, and their colleagues, found that the shape of the heart's vasculature determined spatial patterns of electric currents and that it could be used to create 'virtual electrodes' that essentially amplify the voltage applied to the tissue. The results are published today in Nature1.

"It's a really different approach to thinking about the problem," says Richard Gray, a biomedical engineer at the US Food and Drug Administration's Center for Devices and Radiological Health in Silver Spring, Maryland.

Electrical insights

The heart pumps blood using propagating waves of muscle contractions generated by electrical impulses travelling from the atria to the ventricles. The researchers based their work on studies showing that the heterogenous nature of cardiac tissue — which consists of muscle, blood vessels and fatty tissue — can affect the strength and direction of the current when an electric field is applied in the heart2,3.

The researchers induced arrhythmias in isolated pieces of dog atria and ventricles and used optical dyes to trace the electrical waves they generated. They then imaged the tissue's blood vessels and quantified how their structure changed the flow of current. By adjusting the intensity of the electric field they applied, they could affect the number of waves emitted at distinct places in the vasculature.

With the right conformation of virtual electrodes, a series of five small pulses progressively restored order to the electrical chaos caused by the arrhythmias. The technique also worked when in the atria of living dogs, in which the low-power charge was delivered with coiled wire electrodes.

Fenton says that the voltage the technique requires is at or below what researchers believe is the pain threshold for electric shocks, but he thinks it may be possible to further optimize the virtual electrodes to reduce the voltage even more.

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Theoretically, however, there is a limit to how small the voltage can be, says Gray. Also, he says, no one knows whether the approach will work better or worse in a diseased heart, which may have a different geometry.

"The concepts and ideas are very exciting, but this cannot be directly translated into the clinic now," Gray says, adding that the researchers showed the technique worked in vivo in the atria, but only in vitro in the ventricles, where the need is greatest.

Fenton and Luther say that preliminary in vivo experiments in the ventricles showed positive results, and that they are conducting more extensive studies. Although there are still many things to tweak, says Luther, "we don't see any reason why this technique could not be translated to the clinic". 

  • References

    1. Luther, S. et al. Nature 475, 235-239 (2011). | Article |
    2. Fenton, F. H. et al. Circulation 120, 467-476 (2009). | Article | PubMed | ISI |
    3. Sambelashvili, A. T., Nikolski, V. P. & Efimov, I. R. Am. J. Physiol. Heart Circ. Physiol. 286, H2183-H2194 (2004). | Article | PubMed | ISI | ChemPort |

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  • #62341

    I think is indeed impressive. Was surprised that there are quite a few videos of footballers dying/dead of heart attacks on youtube, a bit sad really.

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