Rapid atrial pacing induced a significant increase in rMSSD (p<0.001), reflecting transient parasympathetic activation that was completely abolished following atropine administration (p<0.001).
Observational (n=37)
Does rapid atrial pacing induce measurable changes in rMSSD reflecting parasympathetic tone before and after atropine administration in patients undergoing electrophysiological study?
Assessment of the parasympathetic response to rapid atrial pacing using rMSSD may serve as a simple, repeatable intraoperative method to verify the effectiveness of parasympathetic neuromodulation.
p-value: p=<0.001
Abstract Introduction The widespread use of cardioneuroablation (CNA) as an effective therapeutic tool in the treatment of both cardiodepressive vasovagal syncope and functional disorders of the sinus and atrioventricular nodes necessitates the development of diagnostic methods enabling rapid, reliable, and repeatable assessment of CNA, intraprocedural endpoints. Methods used to date for assessing the intraoperative efficacy of CNA have either required general anesthesia and extracardiac vagal stimulation or have not allowed for repeatable assessment, such as the atropine test.A method without these limitations would represent an important step forward, both in the optimization of therapies targeting parasympathetic neuromodulation, or unintentionally during procedures like pulmonary vein isolation. Intraoperative assessment of short-term heart rate variability (HRV) parameters may fulfill these criteria; however, such an approach requires validation against established and physiologically proven methods. Aims To evaluate short-term changes in HRV in response to rapid atrial pacing (AP) based on variations in rMSSD measured before and after ap, both prior to and following intravenous atropine administration. Methods This prospective observational study included 37 patients (44 28-68 years) without structural heart disease who were referred for electrophysiological study. Short-term HRV was assessed using rMSSD calculated from four consecutive p-p intervals in four predefined periods: immediately before rapid AP (period A), directly after 30 seconds of pacing at 100 bpm (period B), before pacing following intravenous atropine administration (period C), and after pacing under atropine blockade (period D). All measurements after atropine were performed 10 minutes after intravenous atropine at a dose of 0.04 mg/kg. Results Rapid ap performed before atropine administration produced a significant increase in rMSSD (A→B, p0.001), indicating a transient parasympathetic activation. After intravenous atropine, the same pacing maneuver no longer modified rMSSD (C→D, p=0.71), confirming effective muscarinic blockade. Post-pacing rmssd values were significantly lower after atropine compared with the pre-atropine state (B→D, p0.001), demonstrating complete abolition of the vagally mediated HRV response while simultaneously excluding respiratory-related variability as a contributor to the A→B effect (Figure 1.). Conclusions Rapid AP induces an increase in rMSSD, reflecting transient enhancement of parasympathetic tone - an effect that is absent following atropine administration. Assessment of the parasympathetic response to rapid AP using rmssd may serve as a simple, repeatable method to verify the effectiveness of parasympathetic neuromodulation of the sinus node, although further validation is required.Figure 1.Median rMSSD values
Skoczynski et al. (Mon,) conducted a observational in Referred for electrophysiological study without structural heart disease (n=37). Rapid atrial pacing before and after atropine administration vs. Baseline (pre-pacing and pre-atropine states) was evaluated on Short-term changes in HRV (rMSSD) (p=<0.001). Rapid atrial pacing induced a significant increase in rMSSD (p<0.001), reflecting transient parasympathetic activation that was completely abolished following atropine administration (p<0.001).