Abstract
Objective: The relationship between the autonomic nervous system (ANS) modulation of the sinus node and heart rate variability has been extensively investigated. The current study sought to evaluate, in an animal experimental model of pacing-induced tachycardia congestive heart failure (CHF), a possible ANS influence on the P wave duration and PR interval oscillations. Approach: Short-term (5 min) time and frequency domain analysis has been obtained in six dogs for the following electrocardiographic intervals: P wave duration (P), from the onset to peak of P wave (Pp), from the onset of P wave to the q onset (PR) and from the end of P wave to the onset of q wave (PeR). Direct vagal nerve activity (VNA), stellate ganglion nerve activity (SGNA) and electrocardiogram (ECG) intervals have been evaluated contextually by implantation of three bipolar recording leads. Main results: At the baseline, multiple regression analysis pointed out that VNA was strongly positively associated with the standard deviation of PP and PeR intervals (r2:0.997, p < 0.05). The same variable was also positively associated with high-frequency (HF) of P expressed in normalized units, of Pp, and of PeR (b: 0.001) (r2: 0.993; p < 0.05). During CHF, most of the time and frequency domain variability significantly decreased from 20% to 50% in comparison to the baseline values (p < 0.05) and SGNA correlated inversely with the low frequency (LF) obtained from PeR (p < 0.05) and PR (p < 0.05) (r2:0.899, p < 0.05). LF components, expressed in absolute and normalized power, obtained from all studied intervals, were reduced significantly during CHF. Any difference between the RR and PP spectral components was observed. Significance: The data showed a significant relationship between ANS and atrial ECG variables, independent of the cycle duration. In particular, the oscillations were vagal mediated at the baseline, while sympathetic mediated during CHF. Whereas P wave variability might have a clinical utility in CHF management, it needs to be addressed in specific studies.
Highlights
It is well known that acute or chronic increase of left ventricular end-diastolic pressure, induced by several pathological conditions, could fatally induce a change in both atrial structure and function
The major and novel finding of the study was that pacing-induced tachycardia chronic heart failure (CHF) produced a reduction of the temporal variability of the P wave duration and of peak of P wave (Pp), PeR, and PR intervals
Changes in the autonomic nervous system (ANS) modulation of the sinus node autonomic, together with a neuro-humoral and inflammatory activation, are common CHF features possibly related to an increased risk of atrial arrhythmias
Summary
It is well known that acute or chronic increase of left ventricular end-diastolic pressure, induced by several pathological conditions, could fatally induce a change in both atrial structure and function. The autonomic nervous system (ANS) modulates the sinus node activity, leading to the well-known oscillatory behavior of heart rate, due to the opposite and alternating vagal and sympathetic activity. The oscillatory activity of the sinus node constantly and indirectly may provide useful insight into atrial and ventricular functions (Piccirillo et al 2016a, 2016b). The RR interval variability is thought to be an exact surrogate of the PP interval variability, these two electrocardiographic intervals pertain to different cardiac chambers. Both atrial and ventricular damage could affect the supraventricular conduction system and the PP oscillations precede temporally those of the RR intervals (Horner et al 1996). The abovementioned extreme sensitivity of the supraventricular conduction systems to possible structural and functional heart changes raises interest in investigating possible earlier markers of ANS imbalance
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
