Archives

  • 2018-07
  • 2018-10
  • 2018-11
  • 2019-04
  • 2019-05
  • 2019-06
  • 2019-07
  • 2019-08
  • 2019-09
  • BLU9931 manufacturer Introduction Radiofrequency catheter ab

    2019-06-11

    Introduction Radiofrequency catheter ablation (RFCA) has been established as an effective and safe non-pharmacological therapy for arrhythmias [1]. Idiopathic left ventricular outflow tract ventricular arrhythmias (LVOT-VAs) arising from the LVOT are rare compared with VAs arising from the right ventricular outflow tract (RVOT) [2]. Idiopathic repetitive monomorphic ventricular tachycardia (RMVT) and symptomatic monomorphic ventricular premature contractions (VPCs) are known to originate from the RVOT, and RFCA has been widely accepted as a curative therapy for RVOT-VAs due to the high success rate [3,4]. However, the success rate for LVOT-VAs has not been as high [3,5–8]. The ability to safely perform RFCA for LVOT-VAs is important because of their critically important anatomical origin. Four types of LVOT-VAs origins are known to exist within very close anatomical proximity. These are the aorto-mitral continuity (AMC) [9,10], the anterior sites around the mitral annulus (MA) [11,12], the aortic sinus cusps (ASC) [13,14], and the epicardium [15,16]. Differentiating among LVOT-VAs originating from these various sites has been difficult since they all exhibit a similar QRS morphology, including a right bundle branch block (RBBB) morphology in lead V1 or atypical left bundle branch block (LBBB) morphology associated with an early precordial transition in lead V2 [17]. Predicting the origin of the LVOT-VA by analyzing ECG characteristics is essential for evaluating the possibility of safely performing RFCA.
    Conclusions
    Conflict of interest
    Background Tetralogy of Fallot (ToF), which is characterized by (1) a large ventricular septal defect (VSD), (2) obstruction or narrowing of the right ventricular outflow tract (RVOT), (3) overriding of the aorta, and (4) right ventricular (RV) hypertrophy, is the most common form of cyanotic congenital BLU9931 manufacturer disease, accounting for approximately 10% of congenital heart defects [1]. Because of advances in surgical treatment for congenital heart diseases, long-term prognosis of patients with ToF has improved. However, ventricular tachycardia (VT), which may develop late after corrective surgery, is a major cause of sudden cardiac death in these patients [2,3]. A previous study showed that the incidence of VT in these patients is approximately 12%, with an 8.3% risk of sudden death (based on 35 years of follow-up) [4]. The ideal therapeutic strategy for VT in patients after corrective surgery for ToF has not yet been established, and few data are available on the results of long-term management of VT. VT, which develops in these patients, is usually caused by a macroreentrant mechanism supported by a circuit around an anatomical and/or surgical RV obstacle [5,6], although other mechanisms (microreentrant and nonreentrant mechanisms) are also involved. Descriptions of successful catheter ablation for VT in ToF patients first appeared in the early 1990s [7,8]. These began as isolated case reports and have grown to small clinical series. Owing to advances in electrophysiological knowledge and medical technology, the acute success rate of radiofrequency (RF) catheter ablation in VT currently approaches 90%, although recurrence of VT is observed in approximately 20% of the patients [5,6,9–12]. This is probably because the characteristics of arrhythmogenic myocardium and the location, size, and length of the critical part of the reentry circuit vary among patients.
    Mapping procedures Macroreentrant VT, which is supported by anatomical obstacles and surgically related nonexcitable regions (surgical scars or patches), is a unique form of VT and is believed to be the most common mechanism of VT in patients after corrective surgery for ToF [5,6,9–12]. VT due to other mechanisms (microreentrant and/or nonreentrant mechanisms) also occurs in these patients, but mapping and ablation procedures for non-macroreentrant VT are similar to those for other VTs that develop in patients with various other structural heart diseases. Accordingly, in this paper, we focus on the mapping and ablation procedures for macroreentrant VT in patients after ToF repair.