Author + information
- Saila Vikman, MD and
- Heikki Huikuri, MD, FACC⁎ ()
- ↵⁎Division of Cardiology, Department of Medicine, Oulu University Hospital, Kajaanintie 50, 90220 Oulu, Finland
We are very pleased to get an intellectual input from Wichterle and Malik related to the mechanisms of heart rate (HR) turbulence after atrial premature beats (APBs). The major observation of our study (1) was that “paradoxical” increase of R-R intervals after APBs, resulting in a positive turbulence onset (TO), precedes the spontaneous onset of atrial fibrillation (AF) episodes. Our interpretation was that enhanced vagal responses to APBs might be the major factor behind this phenomenon.
Wichterle and Malik propose another potential mechanism, discussed also in our report, that resetting of sinus node activity after APBs might be the possible mechanism behind the paradoxical TO. The resetting phenomenon might then reflect the change in the origin or prematurity of APBs in the vicinity of AF episodes. For example, the APBs originating from the pulmonary veins might result in a different resetting of the sinus node.
As commented on by Wichterle and Malik, the TO after APBs has actually no relationship with other markers of autonomic tone measured from 24-h electrocardiograph recordings. This observation is consistent with our previous study (2). However, it should be noted that tonic autonomic regulation may be completely different from reflex regulation in response to acute hemodynamic fluctuation. Therefore, the lack of this correlation does not exclude the potential contribution of vagal reflexes in response to APBs, and it is evident that we do not seem to have enough data at the moment to precisely define the mechanisms of HR behavior after APBs. New study designs are needed to clarify this issue—for example, studies where APBs are delivered from various sites of atria, including pulmonary veins, with and without autonomic blockade.
- American College of Cardiology Foundation