Ting-Wei Ernie Liao1,2, Li-Wei Lo1,2,3, Yenn-Jiang Lin1,2,3, Shih-Lin Chang1,2,3, Yu-Feng Hu1,2,3, Cheng-I Wu1,2,3, Fa-Po Chung1,2,3, Tze-Fan Chao1,2,3, Jo-Nan Liao1,2,3, Shih-Ann Chen1,2,3. 1. Faculty of Medicine, School of Medicine, National Yang-Ming University, Taipei, Taiwan. 2. Division of Cardiology, Department of Medicine, Taipei Veterans General Hospital, Taipei, Taiwan. 3. Institute of Clinical Medicine, Cardiovascular Research Institute, National Yang-Ming University, Taipei, Taiwan.
Abstract
BACKGROUND: The autonomic activity plays a critical role in generating paroxysmal atrial fibrillation (PAF). This study aimed to evaluate the changes in the autonomic nerve activity before and after PAF events in patients with and without ischemic heart disease (IHD). METHODS: The study included 49 patients (71.43 ± 12.24 years old, 26 males) with PAF events lasting more than 30 s during 24-hr ambulatory Holter monitoring. The 20-min intervals before and after PAF events were divided into eight segments of 5 min each. Heart rate variability (HRV) analyses of the time and frequency domains were applied to each time segment. RESULTS: Patients with IHD had significant increases in the root mean square successive differences (r-MSSD, p = .008) and HF component (p = .04), followed by a significant increase in the LF/HF ratio (p = .02) preceding the onset of PAF. Patients without IHD had only a significant increase in the r-MSSD (p = .045) preceding the onset of PAF. During the termination of PAF events, patients in both the IHD and control groups had a significantly decreased r-MSSD and HF, respectively. CONCLUSION: Ischemic heart disease causes a sympathovagal imbalance in the initiation of PAF. Decreased parasympathetic activity regulated the termination of PAF in both the IHD and control groups. The modification of the autonomic nervous system (ANS) activity should be individualized due to the autonomic complexity in AF arrhythmogenesis and termination.
BACKGROUND: The autonomic activity plays a critical role in generating paroxysmal atrial fibrillation (PAF). This study aimed to evaluate the changes in the autonomic nerve activity before and after PAF events in patients with and without ischemic heart disease (IHD). METHODS: The study included 49 patients (71.43 ± 12.24 years old, 26 males) with PAF events lasting more than 30 s during 24-hr ambulatory Holter monitoring. The 20-min intervals before and after PAF events were divided into eight segments of 5 min each. Heart rate variability (HRV) analyses of the time and frequency domains were applied to each time segment. RESULTS: Patients with IHD had significant increases in the root mean square successive differences (r-MSSD, p = .008) and HF component (p = .04), followed by a significant increase in the LF/HF ratio (p = .02) preceding the onset of PAF. Patients without IHD had only a significant increase in the r-MSSD (p = .045) preceding the onset of PAF. During the termination of PAF events, patients in both the IHD and control groups had a significantly decreased r-MSSD and HF, respectively. CONCLUSION: Ischemic heart disease causes a sympathovagal imbalance in the initiation of PAF. Decreased parasympathetic activity regulated the termination of PAF in both the IHD and control groups. The modification of the autonomic nervous system (ANS) activity should be individualized due to the autonomic complexity in AF arrhythmogenesis and termination.
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