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Title: Deterioration of the circadian variation of heart rate variability in Brugada syndrome may contribute to the pathogenesis of ventricular fibrillation.
Author: Tokuyama T, Nakano Y, Awazu A, Uchimura-Makita Y, Fujiwra M, Watanabe Y, Sairaku A, Kajihara K, Motoda C, Oda N, Kihara Y.
Journal: J Cardiol; 2014 Aug; 64(2):133-8. PubMed ID: 24495503.
Abstract:
AIMS: Abnormal sympathetic innervation triggers ventricular fibrillation (VF). We examined the circadian variation of autonomic nervous system and its relevance to risk stratification of VF in patients with Brugada syndrome (Brs). METHODS: We enrolled 12 male Brs patients with documented VF (Brs-S; mean age, 42±4 years), 17 without documented VF (Brs-N; mean age 48±4 years), and 16 age- and gender-matched controls. The clinical data, 12-lead electrocardiography (ECG), signal-averaged ECG, electrophysiological study (EPS), and heart rate variability from 24h Holter ECG were compared between the groups. RESULTS: The low frequency components (LF) in Brs-S and Brs-N and high frequency components (HF) in Brs-S patients were significantly lower than in the controls (409.8±128.6ms(2), 329.5±108ms(2) vs. 945.3±111.3ms(2); 135.1±73.8ms(2) vs. 391.8±63.9ms(2), respectively). The circadian variation of the LF and LF/HF decreased in the Brs patients, the standard deviation (SD) of LF/HF (<2.5) and SD of LF (<400ms(2)) had sufficiently high sensitivity (96.6%) and specificity (92.9%) for the diagnosis of Brs. Most of the Brs-S patients (83.3%) were located under the line formed by the SD/mean of HF=SD/mean of LF in the scatter plots. CONCLUSION: Lack of the circadian variation of autonomic function occurs in Brs, and this may contribute to the pathogenesis of VF.

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