JACC. Clinical electrophysiology最新文献

Background: Termination of ventricular tachycardia (VT) by a pacing stimulus that does not generate a QRS complex (termination without global propagation [TWGP]) can be a marker for a critical re-entry circuit isthmus. However, the electrophysiologic and anatomic features of these sites and their relation to VT substrate defined by 3-dimensional electroanatomical maps (3D-EAM) remain unknown.

Objectives: This retrospective study aimed to characterize TWGP sites and their relation to VT substrate identified by 3D-EAM.

Methods: A total of 632 consecutive cases of catheter ablation for scar-related VT at 2 University medical centers were reviewed to identify TWGP.

Results: TWGP was observed 12 times at 11 different sites in 10 patients (5 ischemic cardiomyopathy). The TWGP stimulus fell immediately before or synchronous with the QRS in all cases, and evidence of local capture despite absence of a QRS complex was observed 6 times. In 5 sites, pacing after VT termination produced a QRS different than the VT. Four sites were in dense scar areas (<0.1 mV), and 6 in abnormal low voltage zone (0.1-1.5 mV). Additional mapping or ablation that abolished VT were consistent with the TWGP site being in a VT isthmus. A substrate marker for VT of late potentials, evoked delayed potentials, or slow conduction was present at 6 of 11 TWGP sites.

Conclusions: TWGP may be a marker for detecting a re-entry circuit isthmus that has escaped detection based on electrogram or pace mapping-based substrate mapping.

Background: Left bundle branch pacing (LBBP) provides stable pacing parameters and has been suggested as an alternative for right ventricular pacing and cardiac resynchronization therapy.

Objectives: The aim of the study was to assess the incidence and etiology of new-onset left ventricular dysfunction (NOLVD) following LBBP in patients with baseline normal left ventricular (LV) function and cardiomyopathy patients with normalized LV function.

Methods: Patients undergoing successful LBBP for symptomatic bradyarrhythmia or as an alternative to cardiac resynchronization therapy were included. Normalization of LV function was defined as improvement in LV ejection fraction to ≥50%. Patients with baseline normal LV function and those with recovered LV function after LBBP constituted the study group. Loss of conduction system capture (LOCSC) was defined as complete or partial loss of right bundle branch delay pattern along with inability to demonstrate capture transition during threshold assessment.

Results: A total of 426 patients were included; 59% (n = 250) had baseline normal LV function (group I) and 41% (n = 176) had recovered LV function after LBBP (group II). Mean follow-up duration of 28.3 ± 16.7 months. NOLVD was noted in 3.75% (n = 16; group I = 5 and group II = 11) of patients. The etiologies for NOLVD were LOCSC in 62.5% (n = 10), suboptimal atrioventricular (AV) delay in 18.7% (n = 3), atrial fibrillation in 6.3% (n = 1), and idiopathic in 12.5% (n = 2). LOCSC occurred at a mean interval of 9.2 ± 6.4 months after the initial implantation. Reinterventions (n = 6) including lead repositioning, AV delay optimization, and AV junction ablation resulted in renormalization of LV function in all 6 patients.

Conclusions: Periodic assessment in device clinic is required because NOLVD from reversible causes can occur during follow-up in patients after LBBP.

Background: Patients with rare, pathogenic cardiomyopathy (CM) and arrhythmia variants can present with atrial fibrillation (AF). The efficacy of AF ablation in these patients is unknown.

Objective: This study tested the hypotheses that: 1) patients with a pathogenic variant in any CM or arrhythmia gene have increased recurrence following AF ablation; and 2) patients with a pathogenic variant associated with a specific gene group (arrhythmogenic left ventricular CM [ALVC], arrhythmogenic right ventricular CM, dilated CM, hypertrophic CM, or a channelopathy) have increased recurrence.

Methods: We performed a prospective, observational, cohort study of patients who underwent AF catheter ablation and whole exome sequencing. The primary outcome measure was ≥30 seconds of any atrial tachyarrhythmia that occurred after a 90-day blanking period.

Results: Among 1,366 participants, 109 (8.0%) had a pathogenic or likely pathogenic (P/LP) variant in a CM or arrhythmia gene. In multivariable analysis, the presence of a P/LP variant in any gene was not significantly associated with recurrence (HR 1.15; 95% CI 0.84-1.60; P = 0.53). P/LP variants in the ALVC gene group, predominantly LMNA, were associated with increased recurrence (n = 10; HR 3.75; 95% CI 1.84-7.63; P < 0.001), compared with those in the arrhythmogenic right ventricular CM, dilated CM, hypertrophic CM, and channelopathy gene groups. Participants with P/LP TTN variants (n = 46) had no difference in recurrence compared with genotype-negative-controls (HR 0.93; 95% CI 0.54-1.59; P = 0.78).

Conclusions: Our results support the use of AF ablation for most patients with rare pathogenic CM or arrhythmia variants, including TTN. However, patients with ALVC variants, such as LMNA, may be at a significantly higher risk for arrhythmia recurrence.