Author + information
- Paul Dorian, MD and
- Kumaraswamy Nanthakumar, MD⁎
- ↵⁎University of Toronto, Cardiology, Toronto General Hospital, 150 Gerrard Street West, PMCC 3-522, Toronto, Ontario M5C 2C4, Canada
We thank Drs. Pippin and Kroll et al. for their interest in our work (1). We disagree with the notion that experimental models are never of any use in understanding and in studying arrhythmias. Most of the work on mechanisms of fibrillation and defibrillation, including studies in cardiac arrest, have been conducted in guinea pigs, rats, pigs, and dogs. Readers of JACC are quite aware of the limitation of experimental models. We do agree that extrapolation to humans has to be done cautiously, as discussed in our study.
The main point of our study was to demonstrate that electrical capture of myocardium, under specific circumstances, can occur after neuromuscular incapacitating device (NID) discharge. Unless the recording system is shielded from electromechanical interference, accurate assessment of cardiac effects of discharges is not possible, and conclusions about the safety of discharges are unreliable. We did not draw conclusions about reports of the possible consequences of NID discharges reported in the media, but we wanted to highlight the potential for myocardial capture and potential risks of high-frequency cardiac stimulation under specific (and likely very uncommon in usual use) circumstances. We agree that it is not possible to directly extrapolate our results to NID use in humans.
The letter by Kroll et al. highlights the same difficulties, with regard to coming to safety conclusions based on the absence of objectively documented arrhythmias predicated on interviews and making surface recordings in humans. This line of argument regarding safety in humans can be misleading; as we have shown in our experiments, immediately before and after the NID discharge there was no observable cardiac stimulation. However, if one is able to “see through” the electrical artifact during the discharge, cardiac stimulation was seen. Until intracardiac recordings can be made in humans with shielding to obliterate the electrical artifact that obscures possible intracardiac events, making safety conclusions in humans is premature. We did not state that NIDs cause ventricular fibrillation in humans, and we agree that we cannot conclude from our study that NID discharges cause arrhythmias in typical use.
We hope that readers agree that our study does suggest the possibility that NIDs may, in some circumstances, cause cardiac capture, and that this possibility should at least be considered in future research in humans. We hope that our work stimulates such research, using similar methods, in this area in humans.
- American College of Cardiology Foundation