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Cardiac defibrillation is usually achieved using a single high-energy electric shock of up to 4,000 volts, which can be damaging to the heart tissue. Eberhard Bodenschatz and colleagues show how the disordered electrical dynamics that underlie cardiac fibrillation can be controlled using low-energy electrical pulses. They show, in tests on dogs, that intrinsic homogeneities in the cardiac tissue (such as the vasculature) serve as nucleation sites for the generation of waves of electrical activity that can target the instabilities and bring the tissue dynamics back into synchrony. The new technique, called low-energy antifibrillation pacing or LEAP, delivers five sequential low-energy electrical field pulses to the fibrillating heart — an average energy reduction of 84% compared to standard defibrillation. Controlling the complex spatio-temporal dynamics underlying life-threatening cardiac arrhythmias such as fibrillation is extremely difficult, because of the nonlinear interaction of excitation waves in a heterogeneous anatomical substrate1,2,3,4. In the absence of a better strategy, strong, globally resetting electrical shocks remain the only reliable treatment for cardiac fibrillation5,6,7. Here we establish the relationship between the response of the tissue to an electric field and the spatial distribution of heterogeneities in the scale-free coronary vascular structure. We show that in response to a pulsed electric field, E, these heterogeneities serve as nucleation sites for the generation of intramural electrical waves with a source density ρ(E) and a characteristic time, τ, for tissue depolarization that obeys the power law τ ∝ Eα. These intramural wave sources permit targeting of electrical turbulence near the cores of the vortices of electrical activity that drive complex fibrillatory dynamics. We show in vitro that simultaneous and direct access to multiple vortex cores results in rapid synchronization of cardiac tissue and therefore, efficient termination of fibrillation. Using this control strategy, we demonstrate low-energy termination of fibrillation in vivo. Our results give new insights into the mechanisms and dynamics underlying the control of spatio-temporal chaos in heterogeneous excitable media and provide new research perspectives towards alternative, life-saving low-energy defibrillation techniques.

The RR intervals of sinus and ventricular beats were determined by analysis of a 24-hour ambulatory electrocardiogram in a Boxer before and after treatment with sotalol. These RR intervals were plotted using tachograms, histograms, and Poincaré plots. The tachogram demonstrated a ‘band’ wherein a range of RR intervals was infrequent, the histogram did not take the form of a single Gaussian distribution of RR intervals, and the Poincaré plot showed nonhomogeneous beat to beat variability. This type of patterning was described as a “zone of avoidance” potentially caused by the clustering of beats within specific ranges. Treatment with sotalol enhanced the “zone of avoidance”. Further investigation is needed to understand the mechanism for this observation as well as any clinical implications.

Using 24-hour ambulatory electrocardiography, the RR intervals of all beats were determined in a West Highland white terrier with sick sinus syndrome characterized by sinus arrest, bradycardia, supraventricular tachycardia (SVT) and varying degrees of atrioventricular (AV) heart block and long sinus pauses. Distinctive patterns of bradycardia and 1:1, 2:1, 3:1, 4:1 and 5:1 AV block associated with SVT were evident in the tachogram (RR interval distribution over time) and Poincaré plots (short-term heart rate variability plots of RRn versus RRn + 1). These patterns differed from those of abrupt alteration in cycle length during long sinus pauses or bursts of supraventricular tachycardia. Recognition of such patterns may direct attention to time points for which close attention to the cardiac rhythm should be evaluated in the full-disclosure of the 24-hour ECG recording.