br Discussion In Brugada syndrome

Discussion In Brugada syndrome (BrS), ICD Imiquimod is recommended for patients experiencing VF. However, up to 48% of such high-risk patients experience frequent ICD shocks [1] that result in significant sequelae such as depression, post-traumatic stress, and difficult VF termination due to a relatively high defibrillation threshold in some patients. Pharmacologic therapy, typically an isoproterenol infusion, can be effective in suppressing VF, and deep sedation has occasionally yielded good results in isolated cases [2]. However, because the patient was relatively stable on admission, suppressing his PVC/VF would have resulted in missing his culprit PVC because trigger PVCs are episodic, appear just before VF, and disappear within a narrow time window. Local ablation of VF-triggering PVCs after ICD implantation has proven effective as adjuvant therapy in a few patients with electrical storm [3]; however, such patients had already been exposed to the ICD discharge sequelae. This is the first case to demonstrate the feasibility of “ablation and implantation” as an alternative approach in suppressing ES during long-term follow-up. Unlike the culprit lesion in myocardial infarction, the culprit PVC of VF in BrS cannot be targeted once the VF subsides, because BrS patients rarely have frequent PVCs that can be mapped or have PVCs during Holter monitoring [4]. For this reason, this case suggests that careful monitoring and possible ablation of VF-triggering PVCs in the acute phase may be clinically significant in selected patients. Because epicardial mapping was not performed in this case, we could not identify whether the LP origin was epicardial or endocardial. However, endocardial ablation could have an epicardial modification effect because of the thin-walled RVOT. While this approach is not first-line therapy for BrS, by taking advantage of reducing the ICD burden in the modern era of new catheter designs and mapping technologies, our approach might be effective in selected cases, especially when the origin of the culprit PVC is easily accessible, such as the RVOT. More invasive epicardial ablation can be reserved for resistant cases after ICD implantation.
Conflict of interest
Introduction The implantable cardioverter defibrillator (ICD) is a universally accepted, evidence-based treatment for the prevention of sudden cardiac death [1]. However, the transvenously implanted endocardial lead still represents the weakest link in the ICD technology, as it is the source of most mechanical complications and is associated with an increased risk of bacteremia and endocarditis infection [2–4]. Recently, a new and totally subcutaneous defibrillator (S-ICD), that leaves the heart and vessels completely “untouched”, has been introduced into clinical practice [5,6]. A recent meta-analysis demonstrated that the most common procedure-related complications for this device were limited to the pocket: infection, hematoma, and skin erosion [7]. One shortcoming of the S-ICD is that the generator size is larger than that of the transvenous ICD (T-ICD), as it requires a larger battery and larger capacitors to deliver a higher energy shock during life-threatening arrhythmias. Today, the standard implanted position of the S-ICD involves a subcutaneous pocket created over the fifth intercostal space between the mid and anterior axillary lines [8].
Materials and methods The procedures were performed in an electrophysiology laboratory under standard sterile conditions and were carried out during general anesthesia. After anesthesia induction, the patient’s head and left arm were positioned to facilitate the surgery and to promote sterility. Abduction of the left arm (60°) improved pocket access and ensured that the generator was seated in the appropriate location. Slight right rotation of the head allowed sterile draping over the manubrium and sternum and facilitated tunneling of the parasternal electrode into its upper location. Before sterile draping, a dummy of the S-ICD and lead were secured on the patient’s chest by adhesive plaster. The positioning of both was guided by anatomical landmarks, as suggested in the manufacturer User’s Manual [8], with the pocket at the fifth intercostal space between the mid and anterior axillary lines and the lead 1–2cm to the left of the sternal midline. The position of the lead and S-ICD relative to the heart silhouette was checked by fluoroscopy. Finally, the lead and S-ICD position were drawn onto the chest with a dermographic marker pen demographic pen, as well as the incision line for the pocket creation along the chest Langer’s lines.