Objectives: To determine the association between genetic variants on chromosome 4q25 and atrial fibrillation (AF) in a Taiwanese population. Methods: We enrolled 200 patients with AF (mean age: 67 ± 13 years) and 158 controls (mean age: 63 ± 10 years). The genotypes of five SNPs, RS2634073, RS2200733, RS13143308, RS2220427 and RS10033464, were determined using multiplex single base extension methods. Results: The distribution of the RS2200733 and RS10033464 genotypes did not significantly deviate from the Hardy-Weinberg equilibrium in the control group. The distribution of the RS2200733 genotypes differed significantly between the AF group and the controls (p = 0.03), whereas the distribution of the RS10033464 genotypes did not (p = 0.49). At RS2200733, patients with the CC genotype exhibited a 0.45 times higher risk of developing AF than those with the TT genotype (p = 0.02) and a recessive model was suggested (p = 0.01). After adjusting for various covariates, patients with the CC genotype remained recessively associated with a lower risk of developing AF than those with the TT genotype (odds ratio: 0.27, 95% confidence interval: 0.11–0.65; p < 0.01). Conclusions: In the Taiwanese, there is an association between SNP RS2200733 – but not RS10033464 – and the development of AF. Based on a recessive model of inheritance, individuals with SNP RS2200733 genotype CC are at a lesser risk of developing AF.

Adenosine has a potent negative dromotropic effect. However, comparative effects of adenosine on the three pathways of atrioventricular (AV) nodal reentry remain unclear. In this study, we sought to determine the effects of adenosine on the antegrade fast, antegrade slow, and retrograde fast pathway conduction in patients with AV nodal reentrant tachycardia (AVNRT). Twenty patients with common slow-fast AVNRT (mean cycle length 360 ± 49 ms) were studied. The effects of adenosine on the antegrade slow pathway and on the retrograde fast pathway conduction were determined during sustained AVNRT and constant right ventricular pacing at identical cycle lengths (mean 360 ± 49 ms), respectively. Incremental doses of adenosine were rapidly administered: initial dose of 0.5 mg, followed by stepwise increases of 0.5 or 1.0 mg given at 5-min intervals until termination of AVNRT or second-degree ventriculoatrial block occurred. After the antegrade slow pathway conduction was selectively and completely ablated by radiofrequency catheter ablation, the effect of adenosine on the antegrade fast pathway conduction was evaluated. The dose-response curve of adenosine and the dose of adenosine required to produce AV or ventriculoatrial block among the representative three conduction pathways were compared. The dose-response curve for the effect of adenosine on the antegrade fast pathway lies to the left and upward to that of the effect of adenosine on the antegrade slow pathway which in turn lies to the left and upward to that of the retrograde fast pathway. The mean dose of adenosine required to produce conduction block at antegrade fast, antegrade slow, and retrograde fast pathways were 1.4 ± 0.5, 4.2 ± 1.6, and 8.5 ± 2.6 mg, respectively (p < 0.01). Adenosine has a differential potency to depress antegrade fast, antegrade slow, and retrograde fast pathway conduction in patients with AVNRT. The depressant effect of adenosine on the antegrade fast pathway is more potent than that on the antegrade slow pathway which in turn is more potent than that on the retrograde fast pathway conduction.

The use of ephedrin in complete heart block was first reported by Miller and later by Stecher. But the combined action of ephedrin and atropin on the human heart according to Chen and Schmidt' has never been investigated.A case of complete heart block without Adams-Stokes' attacks was available to study its reaction to ephedrin alone. The patient was kept quiet in bed and undisturbed. Electrocardiograms were taken before and at frequent intervals after the administration by mouth of ephedrin. Blood pressure readings were made at frequent intervals and usually before the electrocardiograms, from which both auricular and ventricular rates were obtained. Results are shown in Table I. It will be seen that after the administration of 150 mg. TABLE I. Effect of Ephedrin on Complete Heart BIock. (Ephedrin 0.09 gm. at 10:30 a.m., and 0.06 gm. at 10:SO am., a total of 0.15 gm. in 2 0 minutes.) Time. Vent. rate Aur. ra!e B. P. a.m. per min. per min. mm. Hg. 10: 28 38 91 110/70 10:40 38 82 1 l0/70 11:oo 38 80 llolrs 11:20 37 80 11s/rs 11:so 38 '19 115/75 12:lO 38 78 115/7J--* of ephedrin in 20 minutes, there was no increase in ventricular or auricular rate, but an increase of 5 mrn. Hg. in systolic and diastolic blood pressure. Different explanations have been offered for the negligible pressor effect occasionally encountered as, in this case. Chen and Schmidt attributed the depressant effect of large doses of ephedrin either to direct depression of heart muscle, or to a'difference in the quantity of "receptors" present in the individual. Kreitmair explained the difference on the basis that small doses of ephedrin stimulate the sympathetic nerve endings, while large doses stimulate the para-1

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