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  • In summary programmed long AVD

    2019-06-27

    In summary, programmed long AVD, prolonged VA conduction time caused by anti-arrhythmic medication, and the rate of ELT (110bpm, below the upper tracking rate of 120bpm) were the reason ELT continued even in the presence of a programmed ELT termination algorithm. Physicians who manage patients with DDD pacemakers should be aware that ELT does not always occur at the upper tracking rate and recognize the risk of ELT below the upper tracking rate in patients with programmed long AVD to avoid ventricular pacing. The ELT rate, which is determined by retrograde VA conduction time, may be affected by anti-arrhythmic drugs such as amiodarone.
    Conflict of interest
    Introduction Andersen-Tawil syndrome (ATS) is associated with long QT interval and ventricular arrhythmias (VAs), as well as a distinct potassium-sensitive periodic paralysis and dysmorphic features of low-set ears, micrognathia, and clinodactyly. ATS, also known as long QT syndrome (LQTS) type 7, is an autosomal topoisomerase inhibitors or sporadic disorder caused by a KCNJ2 mutation [1–3]. The syndrome is mostly benign; however, lethal cases of ventricular tachyarrhythmia have been reported among ATS patients [4,5]. Because ATS is rare and has been diagnosed only recently, there are few reports about pregnancy complicated with ATS. We describe a case of a woman with ATS whose pregnancy was complicated with frequent premature ventricular contractions (PVCs) and nonsustained ventricular tachycardia (NSVT), which were significantly decreased during the peripartum period.
    Case report When she first visited our hospital, she was at 13 weeks of gestation. She did not complain of any symptoms, including palpitation, syncope, or weakness. Some minor dysmorphic features such as micrognathia and hand clinodactyly were present. An electrocardiogram showed multifocal polymorphic PVCs (Fig. 1A) and NSVT. QT interval could not be measured because of the frequent PVCs. A 24-hour Holter monitor recording demonstrated multifocal PVCs over 48% of the total heartbeat count and a maximum of 29 continuous events of NSVT (Fig. 1B). The echocardiographic result was normal. With regard to her family medical history, her father was frequently found with asymptomatic PVCs at routine health checkups but underwent no further examination. He also had micrognathia but no periodic paralysis. We suspected ATS from her physical and physiological examination results and family medical history. A genetic test was performed after obtaining informed consent, and a missense mutation in KCNJ2 (c.899G>T, p.G300V) was identified. We monitored the patient to maintain her potassium level at higher than 4mmol/L. She continued receiving her medications (120-mg verapamil and 25-mg atenolol daily) throughout her pregnancy. VA was markedly suppressed as her pregnancy progressed (Fig. 2). With maternal beta-blocker use, the fetus grew to an appropriate size according to gestational age. Labor occurred spontaneously at 39 weeks of gestation, and she delivered, under epidural anesthesia, without any complication. The newborn infant weighed 2818g (within the 10th percentile) and showed features of micrognathia and signs of sporadic bigeminy with a QTc of 550ms. There was scarcely any event of ventricular ectopy during labor (Fig. 3). Her QT and QTc intervals were normal (400 and 496ms, respectively), and U wave was observed in leads V2–V4. VA gradually increased during the postpartum period, up to the prepregnancy level. However, she had no complications during puerperium. The patient became pregnant again the following year and took only atenolol (25mg daily) during the pregnancy. VA decreased similarly as in her previous pregnancy, and she also vaginally delivered without any complications at 39 weeks of gestation. The second child had a birth weight of 3056g (mean birth weight for dates) and QTc of 375ms. The mother and her children were doing well a year after the second delivery.