• 2018-07
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  • 2018-11
  • 2019-04
  • 2019-05
  • 2019-06
  • 2019-07
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  • 2020-01
  • 2020-02
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  • 2020-04
  • Genomic DNA was isolated from blood after


    Genomic DNA was isolated from blood after obtaining written informed consent. Genetic screening for LQT-1 (KCNQ1), -2 (KCNH2), -3 (SCN5A), -5 (KCNE1), -6 (KCNE2), -7 (KCNJ2), -9 (CAV3), -10 (SCN4B), and -12 (SNTA1) was performed by PCR and direct DNA sequencing. No order monensin was found in these genes.
    Discussion A screening program conducted for all Japanese children (1st, 7th, and 10th grades) revealed that a large number of children had LQTS without a positive family history and with no history of LQTS-related cardiac events at the time of diagnosis [5]. The prevalence of abnormal ECG phenotypes, namely, those of abnormally prolonged QT intervals irrespective of the presence or absence of symptoms and/or family history, is estimated to be 1 in 1164 among 7th graders aged 12 years [6]. The association between the prolonged QTc values and hypokalemia is well known [4]; however, the association between the QT interval and serum potassium concentrations in patients with primary aldosteronism may be controversial. Yang et al. reported that there was no significant correlation (p=0.196) between the longest QT intervals and the serum potassium concentration in 26 patients with primary aldosteronism [7]. On the other hand, Matsumura et al. reported that the QTc order monensin intervals were significantly correlated with serum potassium concentration (p=0.0011) before adrenalectomy and that the prolonged QTc values were normalized after adrenalectomy in 19 patients with primary aldosteronism [8]. In the present case, the QTc interval normalized along with the elevation of the serum potassium concentration, and a significant association was present between the QTc values and the potassium concentration. The findings of Matsumura et al. and the present case may support the notion that hypokalaemia prolongs the QTc interval in patients with primary aldosteronism.
    Conflict of interest
    Introduction Adenosine-sensitive focal atrial tachycardia (AT) can arise from the confined area near the His-bundle. In 1997, Iesaka et al. characterized adenosine-sensitive atrial reentrant tachycardia near the His-bundle as a new disease category [1]. While they have provided several evidences supporting focal reentry as the mechanism of AT, entrainment has not been demonstrated. In fact, few reports published thus far have demonstrated entrainment in this type of AT. In the present report, we describe a case of adenosine-sensitive focal AT, wherein we were able to explain the reentry mechanism through the demonstration of manifest entrainment.
    Case report A 73-year-old woman was admitted for the evaluation of recurrent episodes of palpitation persisting for 16 months. The clinical tachycardia generally appeared on exertion, with sudden onset and cessation. There were no other cardiac symptoms. The patient had been previously diagnosed with hypertension and dyslipidemia. The results of the clinical examination and echocardiographic examination were normal. On admission, the electrocardiogram showed regular sinus rhythm, with the incomplete right bundle-branch block pattern and normal axis. An electrocardiogram recorded during an episode of palpitations showed narrow QRS complex tachycardia of long R–P intervals, with a cycle length of 380ms. P-waves were negative in leads II, III, aVF, and V3–V6; negative/positive, in I; positive/negative, in V1 and V2; and positive, in aVR and aVL (Fig. 1). After receiving informed consent from the patient, we performed an electrophysiologic study without sedation. Antiarrhythmic medication was withdrawn 5 days before the study. Five-French quadripolar and decapolar electrodes were introduced to the high right atrium, His-bundle region (HIS), right ventricular apex (RVA) via the right femoral vein, and into the coronary sinus (CS) via the right internal jugular vein. Pacing at each site was performed at an output of 2 times the diastolic threshold and with a pulse width of 1.0ms, using a programmable cardiac stimulator (BC-05, Fukuda Denshi Co., Ltd., Tokyo, Japan).