Atrial Fibrillation Following Middle Cerebral Artery Infarct.
- Author:
Sa Yoon KANG
1
;
Joung Ho RHA
;
Chung Kun HA
Author Information
1. Department of Neurology, College of Medicine, Inha University.
- Publication Type:Original Article
- Keywords:
MCA infarct;
Insular cortex;
Atrial fibrillation
- MeSH:
Atrial Fibrillation*;
Electrocardiography;
Follow-Up Studies;
Hospitalization;
Humans;
Middle Cerebral Artery*;
Neuroimaging;
Stroke
- From:Journal of the Korean Neurological Association
2000;18(5):551-555
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
BACKGROUND: Atrial fibrillation (AF), commonly considered as a cardiac embolic source, can itself be induced by stroke. We therefore tried to find and analyze this 'stroke-induced' AF. METHODS: From the Inha University Stroke Registry of the past 2 years, 143 middle cerebral artery (MCA) territorial infarct patients who had been admitted within 48 hours after stroke onset were recruited to participate in the study. Electrocardiograms (EKG) on admission and follow-up during hospitalization were analyzed. Also, MCA infarct was subdivided according to insular involvement by brain imaging. RESULTS: Among 143 MCA territorial infarcts, 38 patients had AF on admission (Rt:21; Lt:17). Of those, insular involvements of the MCA infarct was noted in 32 patients. All the patients had a follow-up EKG and AF disappeared in 3 patients (Rt:2; Lt:1). In the remaining 105 patients, 10 patients subsequently developed new AF within 1 week after hospitalization. All those 10 patients had right-sided MCA infarcts and insular involvements were present in 9 patients. In summary, among the 48 MCA infarct associated with AF, 13 AF (Rt:12; Lt:1) were presumed to be the consequence and not the cause of stroke. CONCLUSIONS: Though human insular stimulation and inactivation studies have suggested that AF would be more common in left insular destructive lesions, it was not always supported in clinical series. From our study, presumed 'stroke-induced' AF was highly associated with right insular lesions. The mechanism of arrhythmogenesis by ischemic stroke might be more complicated than previously expected and, not merely the simple inactivation of an anatomical substrate, the insular cortex.
