Relationship between abnormal vagus nerve tension and basal ganglia cerebral infarction induced paroxysmal atrial fibrillation
10.1016/j.apjtm.2017.08.019
- Author:
Wen-Bo CHENG
1
;
Qin YANG
1
;
Yue-Mei HOU
1
;
Dong LI
2
Author Information
1. Department of Geriatrics, Shanghai Jiaotong University Affiliated Sixth People's Hospital South Campus
2. Department of Neurology, Zaozhuang Mining Group Hospitals
- Publication Type:Journal Article
- Keywords:
Abnormal vagus nerve tension;
Basal ganglia;
Cerebral infarction;
Paroxysmal atrial fibrillation
- From:
Asian Pacific Journal of Tropical Medicine
2017;10(9):921-924
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the relationship between basal ganglia cerebral infarction and paroxysmal atrial fibrillation (PAF) caused by abnormal vagus nerve tension. Methods A total of 1 483 cases of elder patients with cerebral infarction who received head CT or MRI examination during the period were enrolled, including 830 male and 613 female, with the average age as 78 years. These cases were divided into basal infarction ganglia group (n = 1 045) and non-basal ganglia infarction group (n = 438) according to the anatomic site of cerebral infarction. The differences of the incidence of PAF, left atrial diameter and heart rate variability were compared between the two groups. Results In basal ganglia infarction group, the incidence rate of PAF was significantly higher than that of non-basal ganglia infarction group (P < 0.05). The incidence trend of cerebral infarction in basal ganglia was age-related, in the >79 years basal ganglia cerebral infarction group, the incidence of PAF was significantly higher than that of non-basal ganglia infarction group (P < 0.05). There was no significant difference in the left atrial diameter between the basal ganglia infarction group and non-basal ganglia infarction group. Basal ganglia cerebral infarction patients with high PAF had higher heart rate variability than non-basal ganglia infarction group. Conclusion Elderly patients with basal ganglia infarction have high incidence of PAF. Sympathetic nerve damage in cerebral basal ganglia, increased vagal tension and cardiac vagal tension are the direct causes of PAF. The results indicates that the increased central vagal nerve tension mediated PAF probably is an indication of supplying sympathetic neurotransmitter or cardiac vagal denervation treatment.
