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Lin et al. conducted across-sectional study to evaluate the relationship between the prevalence of hyperuricaemia (HUA) and non-valvular atrial fibrillation (NVAF) (1). Age, living in urban areas, alcohol consumption, central obesity, elevated fasting plasma glucose level, elevated blood pressure, lower high-density lipoprotein cholesterol level and elevated triglycerides level were significantly associated with increased risk of HUA, and HUA were at higher risk for NVAF. Regarding sex difference, serum uric acid level had a modest predictive value for NVAF in women. I have some concerns about their study.
First, Tu et al. conducted a prospective study to evaluate the risk of gout in patients with alcohol-related diseases and alcohol dependence syndrome (2). Alcohol-related diseases were significantly associated with gout risk, and severe alcohol-dependent patients were significantly associated with an increased risk of gout. The authors recommended that alcohol use assessment and measures to prevent alcohol dependence in patients with gout. I agree with their recommendation, which would partly lead to prevent NVAF.
Second, Yu et al. presented strategies to improve gout/hyperuricemia management for preventing acute arthritis attacks, cardiovascular disease, kidney disease, and other urate-related disorders (3). Alcohol consumption is closely related to gout/hyperuricemia, and psycho-social factors should also be considered for the management.
Third, Kuwabara et al. clarified the role of HUA as an independent risk factor for atrial fibrillation (AF) (4). Adjusted odds ratio (95% confidence interval) of HUA for AF was 3.19 (1.81-5.62). As they used AF as a dependent variable instead of NVAF, sub-analysis is needed to verify the association.
Regarding the mechanism of the association between HUA and NVAF, Liu et al. investigated the relationship between HUA and left atrial (LA) thrombus/spontaneous echo contrast and determined the predictive value of HUA in patients with NVAF (5). They concluded that HUA was closely associated with LA stasis, and it could predict and refine LA stasis risk in patients with NVAF. Maharani et al. investigated the link between HUA and AF with special reference to hyperuricemia-induced atrial remodeling (6). They recommended that uric acid transporters might become a potential strategy to reduce the risk of hyperuricemia-induced AF. Anyway, further studies are needed to accept the mechanism of the association.
1. Lin WD, Deng H, Guo P, et al. High prevalence of hyperuricaemia and its impact on non-valvular atrial fibrillation: the cross-sectional Guangzhou (China) Heart Study. BMJ Open. 2019;9(5):e028007. doi: 10.1136/bmjopen-2018-028007
2. Tu HP, Tung YC, Tsai WC, et al. Alcohol-related diseases and alcohol dependence syndrome is associated with increased gout risk: A nationwide population-based cohort study. Joint Bone Spine. 2017;84(2):189-196. doi: 10.1016/j.jbspin.2016.02.024
3. Yu KH, Chen DY, Chen JH, et al. Management of gout and hyperuricemia: Multidisciplinary consensus in Taiwan. Int J Rheum Dis. 2018;21(4):772-787. doi: 10.1111/1756-185X.13266
4. Kuwabara M, Niwa K, Nishihara S, et al. Hyperuricemia is an independent competing risk factor for atrial fibrillation. Int J Cardiol. 2017;231:137-142. doi: 10.1016/j.ijcard.2016.11.268
5. Liu FZ, Liao HT, Lin WD, et al. Predictive effect of hyperuricemia on left atrial stasis in non-valvular atrial fibrillation patients. Int J Cardiol. 2018;258:103-108. doi: 10.1016/j.ijcard.2018.01.080
6. Maharani N, Kuwabara M, Hisatome I. Hyperuricemia and atrial fibrillation. Int Heart J. 2016;57(4):395-9. doi: 10.1536/ihj.16-192