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Resisting the Impulse
The heart beats rhythmically, with electrical impulses traveling like waves across its surface. However, individuals with cardiovascular diseases, ischemia (lack of oxygen to heart), or heart injury might experience out-of-sync impulses that cause the heart to beat abnormally—also known as an arrhythmia. Cardiac arrhythmia can cause cardiac arrest and, in many cases, death, if not treated immediately. Tandri et al. have addressed this sudden event by stopping the abnormal electrical impulses in their tracks. Using high-frequency alternating current (HFAC) field stimulation, the authors were able to temporarily block wave propagation and terminate deadly reentrant arrhythmias in both cellular and animal models.
First, Tandri and colleagues applied the HFAC field to rat heart cells in vitro in order to not only fine-tune field strength, frequency, and duration, but also to confirm conduction block using a method called optical mapping. Moving into arrhythmic perfused guinea pig and rabbit hearts, they then showed conduction block of sustained ventricular fibrillations (VFs) with application of the optimized electric field. Finally, the authors tested their method in three living rabbits. In the rabbits, VF was induced using a low-voltage electric field. Subsequent application of HFAC resulted in successful termination of VF and survival of all animals. Using computational modeling of the rabbit heart, the authors further showed that their HFAC method works by affecting the opening and closing of the heart cells’ sodium ion channels.
Tandri et al. have demonstrated in multiple models that HFAC-induced conduction block is a viable method to halt erratic electrical impulses. HFAC fields could be applied to the heart using implantable defibrillators, to quickly treat patients in cardiac arrest, without painful side effects. Additionally, this approach could help reduce mortality during persistent VF, where other methods of defibrillation (direct current or biphasic shock) often fail.
Footnotes
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↵* These authors contributed equally to this work.
- Copyright © 2011, American Association for the Advancement of Science
