文摘
The aim of this study was to investigate whether mutation in AMP-activated protein kinase (AMPK) subunit genes (PRKAG3-230) is associated with sporadic, isolated Wolff–Parkinson–White (WPW) syndrome.MethodsThis study consisted of 87 patients with symptomatic WPW syndrome and 93 healthy controls. PRKAG3-230 genotypes were determined using real-time polymerase chain reaction assay. Genotype and allele frequencies of PRKAG3-230 between patients with WPW syndrome and healthy controls were ascertained using chi-square test or Fisher exact test when appropriate.ResultsPRKAG3-230 were genotyped in 87 patients (53 men and 34 women; age = 24.4 ± 18.0 years) with WPW syndrome and 93 healthy controls (57 men and 36 women; age = 16.8 ± 4.2 years). There were no significant differences between the two groups in terms of age and sex. The patients with CG and CG+CC genotypes had a significantly increased risk of WPW syndrome compared with those with GG genotype [odds ratio (OR) = 1.99, 95% confidence interval (CI) = 1.01–3.89, p = 0.045; OR = 1.99, 95% CI = 1.04–3.78, p = 0.037, respectively]. The allelic types were not associated with the risk of WPW syndrome. The patients with manifest type with CG and CG+CC genotypes had a significantly increased risk of WPW syndrome compared with those with GG genotype (OR = 2.86, 95% CI = 1.16–7.05, p = 0.022; OR = 2.84, 95% CI = 1.19–6.80, p = 0.019, respectively). The patients with right-side accessory pathways with CG and CG+CC genotypes had a significantly increased risk of WPW syndrome compared with those with GG genotype (OR = 3.07, 95% CI = 1.25–7.51, p = 0.014; OR = 2.84, 95% CI = 1.19–6.80, p = 0.019, respectively). The allelic types were not associated with the risk of WPW types and locations.ConclusionThis study shows that PRKAG3-230 may be associated with sporadic WPW syndrome among a Taiwanese population. Further studies are warranted to elucidate the role of mutations in AMPK subunit genes other than PRKAG3-230 in sporadic WPW syndrome.