A case of cardiac sarcoidosis with successful heart transplantation after COVID-19 infection.

Arrhythmogenic right ventricular cardiomyopathy and cardiac sarcoidosis can both present with ventricular tachycardia. We report a case of a patient whose histological diagnosis was not only confirmed by the transplanted heart but who also underwent successful transplantation after overcoming COVID-19. .

Management of peri-device leak following left atrial appendage closure: A systematic review.

OBJECTIVE: This study aimed to examine the cumulative experience of peri-device leak (PDL) closure following left atrial appendage (LAA) closure. BACKGROUND: The management of PDL following LAA closure remains controversial. While PDL closure has been proposed, procedural features and clinical outcomes have not been well established. METHODS: A systematic review of all published cases of PDL closure with available anatomical, procedural, and clinical outcomes was performed. RESULTS: We identified 18 indexed publications and 110 cases between April 2013 and March 2020. 71 patients (mean age 72 ± 8 yrs), met study criteria and were included. PDL closure was most common in males, bilobar LAA morphology, and after Watchman procedures. The mean PDL size was 7.6 ± 5.8 mm (range 2-26 mm). Leaks were classified according to size: small (<5 mm; 45%), moderate (≥5-9 mm; 25%), and large (≥10 mm; 30%). Endovascular coils and endovascular plugs were used to close both small and moderate sized leaks, and second LAA closure devices were exclusively used for large PDLs. Successful PDL closure occurred in 90%, and was similar between PDL sizes and types of occluder used. Procedural complication rates were uncommon (2.8%). No strokes were reported following PDL closure at 6 months. CONCLUSIONS: In patients with PDL for whom discontinuation of OAC may be considered unsafe, percutaneous closure using a tailored approach with either endovascular coils, plugs, or second occluder represents a safe, and feasible alternative associated with favorable clinical outcomes.

Ethanol infusion in the vein of Marshall leads to parasympathetic denervation of the human left atrium: implications for atrial fibrillation.

OBJECTIVES: This study sought to determine whether ethanol infusion in the vein of Marshall (VOM) can ablate intrinsic cardiac nerves (ICN). BACKGROUND: ICN cluster around the left atrial epicardium and are implicated in the genesis of atrial fibrillation (AF). METHODS: Patients undergoing catheter AF ablation underwent adjunctive ethanol injection in the VOM. A multipolar catheter was introduced in the VOM and used for high-frequency stimulation (HFS), either as HFS with P-wave synchronized (SynchHFS), 30 pulses, 100 Hz (n = 8) or as HFS with 3 to 10 s bursts (BurstHFS), 33 Hz (n = 72) at 25 mA for 1-ms duration. Atrioventricular (AV) nodal conduction slowing (asystole >2 s or R-R interval prolongation >50%) and AF inducibility were assessed before and after VOM ethanol infusion. Up to 4 1-ml infusions of 98% ethanol were delivered via an angioplasty balloon in the VOM. RESULTS: SynchHFS induced AF in 8 of 8 patients. In 4 of 8 AF initiated spontaneously without VOM capture. No parasympathetic responses were elicited by SynchHFS. BurstHFS was performed in 32 patients undergoing de novo AF ablation (Group 1) and 40 patients undergoing repeat ablation (Group 2). Parasympathetic responses were found in all 32 Group 1 patients and in 75% of Group 2 patients. After VOM ethanol infusion, parasympathetic responses were abolished in all patients (both groups). There were no acute complications related to VOM ethanol infusion. CONCLUSIONS: The VOM contains ICN that connect with the AV node and can trigger AF. Retrograde ethanol infusion in the VOM reliably eliminates local ICN responses. The VOM is a vascular route for ICN-targeting therapies.

Ethanol infusion in the vein of Marshall facilitates mitral isthmus ablation.

BACKGROUND: Treatment of perimitral flutter (PMF) requires bidirectional mitral isthmus (MI) block, which can be difficult with radiofrequency ablation (RFA). The vein of Marshall (VOM) is located within the MI. OBJECTIVE: To test whether VOM ethanol infusion could help achieve MI block. METHODS: Perimitral conduction was studied in patients undergoing ablation of atrial fibrillation. Group 1 included 50 patients with a previous atrial fibrillation ablation undergoing repeat ablation, 30 of whom had had MI ablation. Spontaneous (8 of 50) or inducible PMF (21 of 50) was confirmed by activation mapping. Group 2 included 21 patients undergoing de novo VOM ethanol infusion. The VOM was cannulated with a quadripolar catheter for pacing and with an angioplasty balloon to deliver up to four 1-mL infusions of 98% ethanol. Voltage maps were created before and after VOM ethanol infusion. Bidirectional MI block was verified by differential pacing. RFA times required to achieve it were assessed. RESULTS: In group 1, VOM ethanol infusion acutely terminated PMF in 5 of 29 patients. RFA needed to achieve bidirectional MI block was 2.2 ± 1.6 minutes. Presence of PMF or previous MI ablation did not affect RFA times. In group 2, RFA needed to achieve bidirectional MI block was 2.0 ± 1.6 minutes (P = NS). Five patients had bidirectional MI block achieved solely by VOM ethanol infusion without RFA. In both groups, ablation after VOM ethanol infusion was required in the annular aspect of the MI. There were no acute complications. CONCLUSION: VOM ethanol infusion is useful in the treatment of PMF and assists in reliably achieving bidirectional MI block.

Role of the vein of Marshall in atrial fibrillation recurrences after catheter ablation: therapeutic effect of ethanol infusion.

UNLABELLED: Vein of Marshall Ethanol in Recurrent AF. INTRODUCTION: Atrial fibrillation (AF) or flutter can recur after pulmonary vein (PV) antral isolation (PVAI). The vein of Marshall (VOM) has been linked to the genesis of AF. We hypothesized that the VOM may play a role in AF recurrences and that VOM ethanol infusion may have therapeutic value in this setting. METHODS AND RESULTS: Sixty-one patients with recurrent AF or flutter after PVAI were studied. The VOM was successfully cannulated in 54; VOM and PV electrograms were recorded, and differential PV-VOM pacing was performed. VOM signals were present in all patients; however, VOM triggers of AF could not be demonstrated. VOM tachycardia was present in 1 patient. Left inferior (LIPV) and left superior (LSPV) reconnection was present in 32 and 30 patients, respectively. Differential pacing in VOM and LIPV showed VOM-mediated LIPV reconnection in 5/32 patients. In others, VOM and PV connected indirectly via left atrial tissues. Up to four 1 cc infusions of 98% ethanol were delivered in the VOM. Regardless of the reconnection pattern, ethanol infusion eliminated LIPV and LSPV reconnection in 23/32 and 13/30 patients, respectively. Ethanol terminated VOM and LIPV tachycardias in 2 patients. There were no acute procedural complications. CONCLUSIONS: VOM signals are consistently present in recurrent AF. VOM may rarely play a role in PV reconnection. However, VOM ethanol infusion can be useful in patients with recurrent AF after PVAI, assisting in achieving redisconnection of reconnected left PVs.

Ranolazine safely decreases ventricular and atrial fibrillation in Timothy syndrome (LQT8).

Long QT eight (LQT8), otherwise known as Timothy syndrome (TS), is a genetic disorder causing hyper-activation of the L-type calcium channel Cav 1.2. This calcium load and the resultant increase in the QT interval provide the substrate for ventricular arrhythmias. We previously presented a case in a patient with TS who had a profound decrease in his burden of ventricular arrhythmias after institution of an L-type calcium channel blocker. Although this patient's arrhythmia burden had decreased, he displayed an increasing burden of atrial fibrillation and still had bouts of ventricular fibrillation requiring defibrillator therapy. Basic research has recently shown that ranolazine, a multipotent ion-channel blocker, may be of benefit in patients with LQT8 syndrome. This case report details the decrease of atrial fibrillation and ventricular fibrillation events in our LQT8 patient with the addition of ranolazine.

Robotic catheter ablation of left ventricular tachycardia: initial experience.

BACKGROUND: Catheter ablation of ventricular tachycardia (VT) can be technically challenging due to difficulty with catheter positioning in the left ventricle (LV) and achieving stable contact. The Hansen Sensei Robotic system (HRS) has been used in atrial fibrillation but its utility in VT is unclear. OBJECTIVE: The purpose of this study was to test the technical feasibility of robotic catheter ablation of LV ventricular tachycardia (VT) using the HRS. METHODS: Twenty-three patients underwent LV VT mapping and ablation with the HRS via a transseptal, transmitral valve approach. Nineteen patients underwent substrate mapping and ablation (18 had ischemic cardiomyopathy, 1 had an apical variant of hypertrophic cardiomyopathy). Four patients had focal VT requiring LV VT mapping and ablation. Procedural endpoints included substrate modification by endocardial scar border ablation and elimination of late potentials, or elimination of inducible focal VT. RESULTS: Mapping and ablation were entirely robotic without requiring manual catheter manipulation in all patients and reaching all LV regions with stable contact. Fluoroscopy time of the LV procedure was 22.2 ± 11.2 minutes. Radiofrequency time was 33 ± 21 minutes. Total procedural times were 231 ± 76 minutes. Complications included a left groin hematoma (opposite to the HRS sheath), 1 pericardial effusion without tamponade that was drained successfully, and transient right ventricular failure in a patient with previous left ventricular assist device. At 13.4 ± 6.7 months of follow-up (range 1-19 months), recurrence of VT occurred in 3 of 23 patients. CONCLUSION: Our initial experience suggests that the HRS allows successful mapping and ablation of LV VT.

Late potential at the high ventricular septal level in a patient with Brugada: possible mechanisms and clinical implications.

The Brugada syndrome (BS) accounts for approximately 20% of cases of sudden cardiac death in patients with structurally normal hearts. The electrophysiologic basis for ST-segment elevation in the precordial electrocardiogram (ECG) leads that characterize the Brugada phenotype and its strong linkage to ventricular tachycardia (VT)/ventricular fibrillation is still a subject of controversy. Electrocardiographic manifestations of the syndrome have been attributed to one of two basic mechanisms: (1) conduction delay in the right ventricular (RV) epicardial-free wall in the region of the outflow tract or (2) premature repolarization of the RV epicardial action potential secondary to loss of the action potential dome. Signal-averaged ECG recordings have demonstrated late potentials that extend beyond the QRS complex in patients with the BS, especially in the anterior wall of the RV outflow tract. The basis for these epicardial late potentials remains a subject of interest among basic and clinical electrophysiologists. Endocardial late potentials in BS are even less well understood. We present a case of a patient with Brugada syndrome with a distinct endocardial late potential in the high ventricular septum coinciding with the ST-segment elevation. We discuss the possible mechanisms for this intracardiac finding and its clinical significance. We also review the effect of isoproterenol infusion on both the late potential and the surface ECG.