Open AccessGenetic variants of alcohol‐metabolizing enzymes in Brugada syndrome: Insights into syncope after drinking alcohol
Author(s) -
Wu Qi,
Hayashi Hideki,
Hira Daiki,
Sonoda Keiko,
Ueshima Satoshi,
Ohno Seiko,
Makiyama Takeru,
Terada Tomohiro,
Katsura Toshiya,
Miura Katsuyuki,
Horie Minoru
Publication year - 2019
Publication title -
journal of arrhythmia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.463
H-Index - 21
eISSN - 1883-2148
pISSN - 1880-4276
DOI - 10.1002/joa3.12227
Subject(s) - adh1b , aldh2 , medicine , alcohol dehydrogenase , alcohol , odds ratio , asymptomatic , brugada syndrome , alcohol dependence , genotype , aldehyde dehydrogenase , genetics , enzyme , biology , biochemistry , gene , branched chain alpha keto acid dehydrogenase complex , dehydrogenase
Background Patients with Brugada syndrome (BrS) are known to have arrhythmic events after alcohol drinking and are recommended to avoid its excessive intake. Mechanisms underlying the alcohol‐induced cardiac events are however unknown. This study aimed to test the hypothesis whether activity of alcohol‐metabolizing enzymes determines fatal arrhythmic events after drinking alcohol. Methods A total of 198 Japanese patients with BrS were enrolled in this study. These patients were classified into symptomatic (n = 90) and asymptomatic (n = 108) groups. The former was divided into an alcohol‐related group (syncope after alcohol drinking, n = 16) and an alcohol‐unrelated group (n = 74). Polymerase chain reaction was performed to determine genetic variants of genes encoding alcohol dehydrogenase 1B ( ADH1B ) and aldehyde dehydrogenase 2 ( ALDH2 ). Results The genotype distribution for ALDH2 was not significantly different between symptomatic and asymptomatic groups and between alcohol‐related and alcohol‐unrelated groups. The genotype distribution for ADH1B was not significantly different between symptomatic and asymptomatic groups, but the genotype ADH1B His/His was significantly more prevalent in the alcohol‐related group than in the alcohol‐unrelated group (81.3% vs 50%, P = .023). In multivariate logistic regression analysis, the genotype of ADH1B His/His was independently associated with syncope after alcohol drinking (odds ratio, 5.746; 95% confidence interval, 1.580‐28.421; P = .007). Conclusions Arrhythmic events after alcohol drinking was associated with enhanced activity of alcohol‐metabolizing enzyme ADH1B in our cohort of BrS. Therefore, the lifestyle change to avoid the excessive alcohol intake deserves attention.