Only of ICD implantations are performed in children

Only 1% of ICD implantations are performed in children. As a result, established methods of pediatric ICD implantation are lacking, and long-term outcomes are still unclear. Non-transvenous ICD systems are required in children [1,2], and we chose an epicardial system for our case. The advantage of this system is that the defibrillation threshold is lower than that with a subcutaneous system, and cardiac strangulation caused by the leads is less likely than with a pericardial system [2]. Because the heart was sandwiched between the transverse sinus and the can located in the abdomen, we expected a lower defibrillation threshold. Survival of non-transvenous ICD systems is significantly shorter than that of transvenous systems because of complications [3]. Bryant et al. reported that the shock lead should not cover more than 40% of the surrounding heart to avoid cardiac strangulation [4]. Although cardiac pacing and β-blocker use effectively treated TdP in our patient, a defibrillator was still warranted to prevent lethal cardiac events, considering his long life expectancy.
Conclusion
Conflicts of interest
Case presentation A 90-year-old woman with hypertension and a history of a dual-chamber, rate-modulated (DDDR) pacemaker implantation 9 years previously presented to the hospital with complaints of syncope, moderate shortness of breath, and a headache. She denied any other symptoms. Her vital signs were as follows: blood pressure, 110/80mmHg; pulse, 35beats/min (bpm); and respiratory rate, 18 breaths/min. One month before presentation, she had undergone pacemaker replacement due to battery depletion at another hospital. The electrocardiogram (ECG) on admission is shown in Fig. 1. Pacemaker interrogation showed the following parameters: programmed mode, DDDR with a hexokinase inhibition rate of 60bpm; atrial impedance, 410Ω; ventricular impedance, 540Ω; atrial sensing threshold, 0.5mV; ventricular sensing threshold, 2.0mV; and battery voltage, 2.6V. The paced and sensed atrioventricular intervals (AVIs) were 150 and 120ms, respectively. The pacemaker was switched to AAI mode, and the corresponding ECG is shown in Fig. 2. What is your diagnosis?
Commentary The correct answer is B. In patients with a previously implanted device, pacemaker malfunction is a very rare cause of syncope. On initial evaluation, the pacing spike in our patient only appeared after QRS complexes on the ECG at admission, which is suggestive of undersensing; however, pacemaker interrogation showed normal sensing thresholds and impedances. Undersensing can be due to various factors such as low sensitivity settings, lead insulation defects, event falls within a refractory period (i.e., functional undersensing), too slow of a slew rate, and malfunction of the pacemaker circuitry [1]. The most common causes of noncapture include lead displacement, an insulation defect, wire fracture, electrolyte disturbance, and exit block (a high capture threshold). Atrial noncapture can be detected by the absence of a P-wave and the sudden appearance of a wide complex QRS, whereas during ventricular noncapture, paced output occurs without depolarization of the ventricle, which results in an asystolic pause [1]. Crosstalk is characterized by the inhibition of ventricular output due to the ventricular channel sensing of an atrial pulse. It is seen on the ECG strip as paced atrial P-waves without ventricular output. Crosstalk is rarely seen with current dual-chamber pacemakers because of the ventricular blanking period [2]. In the present case, the pacing spikes were evidently synchronized with the QRS complexes, with a 150-ms interval between two spikes. This pattern only occurs when the leads are switched (Fig. 1). Moreover, the period without pacing only contains F-waves, which strongly suggests that atrial events inhibit output from the ventricular channel of the pacemaker. When the atrial and ventricular leads are switched, the designated sensed event in the ventricular channel is actually an atrial event. Ventricular pacing through the atrial lead can cause atrial fibrillation, hypotension, and clinical heart failure due to 1:1 retrograde atrial activation. Atrial lead dislodgement to the ventricle should be briefly considered; however, since ventricular pacing in such a situation would be inhibited or within the atrioventricular safety window, this diagnosis is incorrect. The diagnosis of switched leads in a permanent pacemaker is usually made within a few hours or days after implantation, but this complication is rarely overlooked in the long-term, as in the present case [2–4].