【Background】Heart rate（HR）during atrial fibrillation（AF）varies between individuals. The genetic background of individual HR variation during AF is not well understood.【Objective】We hypothesized that HR-associated single nucleotide polymorphisms（SNPs）reported in genome-wide association studies（GWAS）are related to HR during AF.【Method】Patients with persistent AF（311 for screening and 146 for replication）who underwent AF ablation were genotyped for the 21 HR-associated SNPs reported in GWAS. The patients underwent 24-hour Holter monitoring before AF ablation and electrophysiological study after AF ablation during sinus rhythm. We analyzed relationship among total HR, clinical characteristics, electrophysiological study parameters, and SNP genotypes.【Result】A significant linear correlation was found only between GJA1 SNP（rs1015451, T＞C）and total HR（TT 110,643±17,542 beats/day, TC 116,350±19,060 beats/day, CC 122,163±25,684 beats/day, P=8.5×10⁻⁴）. We confirmed this significant correlation in the replication set. The intra-atrial conduction times were shorter in AF patients with the GJA1 minor allele than in those without it. Multivariable analysis revealed that the presence of the GJA1 SNP rs1015451 additive model, female gender, lower left ventricular ejection fraction, and higher 1 : 1 atrioventricular nodal conduction were independently associated with higher HR during AF.【Conclusion】The GJA1 SNP, a coding gap junction protein（Connexin 43）, may be a new genetic marker of higher HR in patients with AF.

A 65 year-old male with symptomatic persistent atrial fibrillation was referred for radiofrequency catheter ablation. He underwent a box isolation to simultaneously isolate all 4 pulmonary veins （PVs） and the left atrial （LA） posterior wall. During the box isolation with a double lasso catheter positioned in both the left superior and right superior PVs, the atrial fibrillation terminated spontaneously. After the box lesion set was created conduction was still observed between the LA and PVs. After an additional radiofrequency energy delivery to the bottom line of the box lesion, the activation sequence of the PVs became uniform during sinus rhythm and pacing from the coronary sinus （CS）, indicating that only one more conduction pathway was present. The 3-dimensional map revealed that the earliest activation site within the box lesion was located in the anterior aspect of the left superior PV during pacing from the CS, but that of the LA during pacing from the superior right PV within the box was on the postero-lateral LA wall below the left inferior PV. Since the activation in the Marshall vein during pacing from the superior left PV within the box was recorded earlier than that in the CS, we suspected that the LA-PV conduction was occurring via the Marshall bundle. A radiofrequency application at the anterior aspect of the left superior PV just inside the box lesion line isolated all the PVs.