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  • Introduction Implantable cardioverter defibrillators ICD

    2019-05-15

    Introduction Implantable cardioverter-defibrillators (ICD), cardiac resynchronization therapy defibrillators (CRT-D), and cardiac resynchronization therapy (CRT-P) are useful tools for improving the prognosis and/or sudden cardiac death event rate in patients with heart failure and/or fatal ventricular arrhythmias [ventricular tachycardia (VT) and ventricular fibrillation (VF)] [1–9]. The ICD implantation rate increased significantly worldwide [10–12] following controlled studies of primary and secondary prevention of cardiac death [13–19]. New guidelines for ICD implantation [12] and the progressive technological advances in implantable devices have also contributed to this ongoing increasing trend. In Japan, the first guidelines for ICDs were published by the Japanese Circulation Society (JCS) in 2001 [20], a revised version was reported in its website in 2006 [21], and a further revised version was added in 2011 [22]. CRT-Ds were approved in 2006 and the Japan Cardiac Device Therapy Registry (JCDTR) was started in the same year [23]. Interestingly, it has been reported that the actual implantation rates of these devices in Japan may be different from those of western countries [25]. These differences in device utilization rates might be explained by variable factors such as acceptance of published guidelines, differences in clinical presentation of patients, access to electrophysiologists and other implantation specialists, the overall capacity of the workforce to support ICD implantation, acceptance by policymakers, cost-effectiveness, financial constraints, and capitation [23]. However, little is known regarding the recent conditions associated with implantable defibrillators for the treatment of individual underlying heart diseases. Therefore, we investigated the actual conditions associated with implantable defibrillation therapy over a 5-year period in patients from the JCDTR database.
    Methods
    Discussion The purpose of this study was to determine the current status of defibrillation therapy (ICD/CRT-D) in Japan by using the JCDTR database administrated by the device enrollment and assessment committee of the Japanese Heart Rhythm Society. Specifically, the clinical aspects and trends in the % primary for sudden cardiac death were emphasized, because the effectiveness of defibrillation therapy for secondary prevention has been assessed and confirmed throughout the world [5,9]
    Introduction The early repolarization (ER) pattern, or J wave, is considered to be a benign electrocardiographic phenomenon affecting 2%–5% of the general population, and is most commonly observed in young men [1–3]. However, recent studies have shown a high incidence of the ER pattern confined to the inferolateral leads of patients with idiopathic ventricular fibrillation (VF) [4–6]. These studies, together with previous reports, indicate that ER syndrome may not be as benign as traditionally believed [7]. ER syndrome shares notable cellular and ionic similarities with Brugada syndrome, an autosomal methysergide cost disease with incomplete penetrance characterized by J-point and ST-segment elevation in leads V1–V3 and a high propensity toward sudden cardiac death (SCD) [1,2,8]. Previous studies have examined the prognosis of Brugada syndrome in association with the ER pattern in inferolateral leads, but the results were controversial [9–11]. The retrospective, single center study described herein was carried out to further investigate the prevalence and prognostic significance of the ER pattern in the inferolateral leads of patients with Brugada syndrome.
    Methods
    Results Of the 69 study patients, 66 were males. The mean age of the 69 patients was 50.2±13.9 years (range, 24 to 76 years). Forty-eight patients showed a spontaneous Brugada type 1 ECG pattern, and 21 showed a drug-induced Brugada type 1 ECG pattern. Clinical, genetic, electrocardiographic, and electrophysiological characteristics of the study group are shown in Table 1. Eleven patients were symptomatic (3 with a history of syncope, 2 with presyncope, and 6 with aborted SCD), and 5 patients had a family history of SCD. An SCN5A gene mutation was found in 2 patients (4.5%). The left ventriculogram was normal in all patients, with an ejection fraction of 70.1%±8.2% (range, 55%–89%). The coronary angiogram was also normal. Programmed ventricular stimulation induced VF/polymorphic VT in 49 patients (89.1%). VF/polymorphic VT was induced by 2 extrastimuli from RVA (n=15), RVOT (n=24), and both RVA and RVOT (n=3); VF/polymorphic VT was induced by 3 extrastimuli from RVA (n=1), RVOT (n=5), and both RVA and RVOT (n=1). An ICD was implanted in 19 individuals (27.5%); 11 symptomatic patients and 8 asymptomatic patients with inducible VF who elected to receive an ICD implant. An ER pattern was observed in 7 patients (10.1%) with a spontaneous (n=6) or drug-induced (n=1) Brugada type 1 ECG pattern. No patients associated with ER pattern received Ca2+ antagonists or beta blockers. Notched or slurred J-point elevation was observed in the inferior (n=5, Fig. 1) or both the inferior and lateral leads (n=2, Fig. 2). Three of the 7 patients showed day-to-day changes in the amplitude and shape (slurred or notched) of the J wave, whereas another 4 patients did not show day-to-day changes in J wave morphology. However, none of the 7 patients showed disappearance of the J wave in the consecutive ECG recordings. In 6 patients with spontaneous Brugada type 1 ECG patterns, the J wave and coved-type ST-segment elevation were present in all ECGs; in 1 patient with drug-induced coved-type ST-segment elevation, the presence of J wave and coved-type ST-segment elevation was observed simultaneously only after pilsicainide administration. Late potentials were positive in 3 patients (50.0%) with the ER pattern (n=6) and in 25 patients (45.5%) without the ER pattern (n=55). The root mean square voltage of the terminal 40ms in the filtered QRS complex in patients with and without ER was 40.3±6.9μV and 40.3±10.9μV, respectively (P=0.69), and the duration of the low-amplitude signals <40μV in the terminal filtered R complex with and without ER was 32.0±43.9ms and 19.0±9.5ms, respectively (P=0.80).