Abstract
Context
Management of atrial fibrillation includes either rhythm control that aims at establishing a sinus rhythm or rate control that aims at lowering the ventricular rate, usually with atrioventricular nodal blocking agents. Another potential strategy for ventricular rate control is to induce a negative dromotropic effect by augmenting cardiac vagal activity, which might be possible through noninvasive and nonpharmacologic techniques. Thus, the hypothesis of this study was that occipitoatlantal decompression (OA-D) and transcutaneous auricular vagus nerve stimulation (taVNS) not only increase cardiac parasympathetic tone as assessed by heart rate variability (HRV), but also slow atrioventricular conduction, assessed by the PQ-interval of the electrocardiogram (EKG) in generally healthy study participants without atrial fibrillation.
Objectives
To test whether OA-D and/or transcutaneous taVNS, which have been demonstrated to increase cardiac parasympathetic nervous system activity, would also elicit a negative dromotropic effect and prolong atrioventricular conduction.
Methods
EKGs were recorded in 28 healthy volunteers on three consecutive days during a 30 min baseline recording, a 15 min intervention, and a 30 min recovery period. Participants were randomly assigned to one of three experimental groups that differed in the 15 min intervention. The first group received OA-D for 5 min, followed by 10 min of rest. The second group received 15 min of taVNS. The intervention in the third group that served as a time control group (CTR) consisted of 15 min of rest. The RR- and PQ-intervals were extracted from the EKGs and then used to assess HRV and AV-conduction, respectively.
Results
The OA-D group had nine participants (32.1%), the taVNS group had 10 participants (35.7%), and the CTR group had nine participants (32.1%). The root mean square of successive differences between normal heartbeats (RMSSD), an HRV measure of cardiac parasympathetic modulation, tended to be higher during the recovery period than during the baseline recording in the OA-D group (mean ± standard error of the mean [SEM], 54.6 ± 15.5 vs. 49.8 ± 15.8 ms; p<0.10) and increased significantly in the taVNS group (mean ± SEM, 28.8 ± 5.7 vs. 24.7 ± 4.8 ms; p<0.05), but not in the control group (mean ± SEM, 31.4 ± 4.2 vs. 28.5 ± 3.8 ms; p=0.31). This increase in RMSSD was accompanied by a lengthening of the PQ-interval in the OA-D (mean ± SEM, 170.5 ± 9.6 vs. 166.8 ± 9.7 ms; p<0.05) and taVNS (mean ± SEM, 166.6 ± 6.0 vs. 162.1 ± 5.6 ms; p<0.05) groups, but not in the control group (mean ± SEM, 164.3 ± 9.2 vs. 163.1 ± 9.1 ms; p=0.31). The PQ-intervals during the baseline recordings did not differ on the three study days in any of the three groups, suggesting that the negative dromotropic effect of OA-D and taVNS did not last into the following day.
Conclusions
The lengthening of the PQ-interval in the OA-D and taVNS groups was accompanied by an increase in RMSSD. This implies that the negative dromotropic effects of OA-D and taVNS are mediated through an increase in cardiac parasympathetic tone. Whether these findings suggest their utility in controlling ventricular rates during persistent atrial fibrillation remains to be determined.
Ventricular rate control during atrial fibrillation by cardiac parasympathetic nerve stimulation: a transvenous approach
