Spontaneous atrioventricular nodal reentrant tachycardia in patients with idiopathic ventricular arrhythmias: the incidence, clinical, and electrophysiologic characteristics.

INTRODUCTION: Spontaneous or inducible atrioventricular nodal reentrant tachycardia (AVNRT) may coexist with idiopathic ventricular arrhythmias (IVAs). The aim of this study was to determine the incidence and the clinical and electrophysiologic characteristics of patients with spontaneous AVNRT among patients with IVAs. METHODS: Nine hundred eighty-seven consecutive patients with IVA (n = 398), patients with clinical and spontaneous AVNRT (n = 327), and patients with preexcitation syndrome (n = 262) were prospectively included in the study. RESULTS: Spontaneous AVNRT was present in 36 (9.0%) of 398 patients with IVA. The most common (97%) mode of presentation was palpitation due to spontaneous AVNRT. Absence of symptoms was frequent among patients with IVA and without spontaneous AVNRT compared to patients with IVA and spontaneous AVNRT (28.9% vs 0%, P = 0.0001). Patients with IVA and spontaneous AVNRT had lower median premature ventricular contraction (PVC) burden (1.9% vs 9.45%, P = 0.0001) and higher left ventricular ejection fraction (LVEF; 64.2 ± 4.9% vs 59.2 ± 9.9%, P = 0.0001) compared to patients with IVA and without spontaneous AVNRT. Relatively high PVC burden (≥10%) was present in 19.4% of patients with spontaneous AVNRT and IVA. The prevalence of IVA was significantly higher in patients with AVNRT compared to patients with preexcitation syndrome (11% vs 0.76%, P < 0.0001). CONCLUSIONS: Spontaneous AVNRT among patients with IVAs was relatively common in our study population. Spontaneous AVNRT in patients with IVAs can be a protective factor for left ventricular function. Greater LVEF in patients with spontaneous AVNRT and IVA compared to patients with IVA alone can be explained by earlier recognition of IVAs due to presence of symptomatic AVNRT and/or lower PVC burden.

Cardiac resynchronization therapy with or without anatomical reverse remodeling does not affect defibrillation threshold.

BACKGROUND: Recent clinical trials have documented beneficial reverse-remodeling effects with cardiac resynchronization therapy (CRT). The aim of this study was to investigate the effect of CRT with or without reverse anatomical remodeling of the left ventricle on defibrillation threshold (DFT) levels in a prospective and consecutive group of patients with class II-IV systolic heart failure. METHODS: Study population consisted of 29 patients (14 women and 15 men; mean age 61±11 years old). All patients underwent baseline (within 24-hours of cardiac resynchronization therapy-defibrillator [CRT-D] implantation) and 6-month follow-up DFT testing. Reverse anatomical remodeling of the left ventricle was defined as ≥15% reduction in left ventricular end-systolic volume at the end of 6 months of follow-up compared to baseline. RESULTS: Baseline, average DFT was 8.8±5.9 J. Left ventricular end-diastolic volume was the only predictor of baseline DFT level (P=0.02) among the baseline demographics. Safety margin of at least 10 J was achieved in all patients. Average DFT at the end of 6 months of biventricular pacing was 9.2±6.9 J. One patient (3.4%) failed to have a safety margin of 10 J. Reverse anatomical remodeling was observed in 14 (48%) patients and did not have any effect on DFT level. There were no complications related to DFT testings. CONCLUSIONS: Baseline average DFT in patients undergoing CRT-D was ≤10 J in our study. CRT-D with or without anatomical reverse remodeling does not affect DFT at the end of 6 months of follow-up. High DFT level at the end of 6 months of follow-up is rare (3.4%) among patients with current CRT-D devices.

Human model simulating right ventricular outflow tract tachycardia by high-frequency stimulation in the left pulmonary artery: autonomics and idiopathic ventricular arrhythmias.

INTRODUCTION: Frequent monomorphic premature ventricular contractions (PVC) and/or ventricular tachycardia (VT) in patients with structurally normal heart usually arise from the right ventricular outflow tract (RVOT). An animal model simulating RVOT tachycardia by high-frequency stimulation (HFS) of the sympathetic input to the proximal pulmonary artery (PA) has been previously described. The aim of this study was to similarly induce RVOT tachycardia in humans. METHODS: In 9 patients with no history of ventricular arrhythmias, a circumferential catheter was placed in the left, main, and proximal PA to contact the endovascular circumference of the PA. A 50-ms train of HFS (200 Hz/0.3 ms pulse duration), coupled to atrial pacing, was applied at each bipolar pair of the circumferential catheter. The coupling interval was adjusted so that the 50-ms train occurred during the ventricular refractory period. RESULTS: In 6 out of 9 patients, HFS in the left PA during dobutamine infusion induced monomorphic PVCs and/or VT with left bundle branch block (LBBB) morphology and inferior axis at an average stimulation level of 12.5 +/- 2.7 V. HFS in the main PA and in the proximal PA did not induce any ventricular arrhythmias with the highest energy of 15 V in baseline state and during dobutamine infusion. HFS in the left PA was associated with hiccough in all patients. CONCLUSION: Stimulation of the sympathetic input to the left PA during dobutamine infusion induces PVCs and/or VT exhibiting LBBB-morphology and inferior axis, closely simulating clinical RVOT tachycardia in humans.

Successful balloon dilatation of the valve of Vieussens for left ventricular lead placement.

Successful balloon dilatation of an obstructive valve of Vieussens for left ventricular lead placement is described in a case with severe left ventricular systolic dysfunction.

High prevalence of concealed Brugada syndrome in patients with atrioventricular nodal reentrant tachycardia.

BACKGROUND: Atrioventricular nodal reentrant tachycardia (AVNRT) may coexist with Brugada syndrome (BrS). OBJECTIVES: The present study was designed to determine the prevalence of drug-induced type 1 Brugada ECG pattern (concealed BrS) in patients presenting with clinical spontaneous AVNRT and to investigate their electrocardiographic, electrophysiological, and genetic characteristics. METHODS: Ninety-six consecutive patients without any sign of BrS on baseline electrocardiogram undergoing electrophysiological study and ablation for symptomatic, drug-resistant AVNRT and 66 control subjects underwent an ajmaline challenge to unmask BrS. Genetic screening was performed in 17 patients displaying both AVNRT and BrS. RESULTS: A concealed BrS electrocardiogram was uncovered in 26 of 96 patients with AVNRT (27.1%) and in 3 of 66 control subjects (4.5%) (P ≤ .001). Patients with concealed BrS were predominantly female patients (n=23 [88.5%] vs n=44 [62.9%], P = .015), had higher prevalence of chest pain (n=10 [38.5%] vs n=13 [18.6%], p=0.042), migraine headaches (n=10 [38.5%] vs n=10 [14.2%], p=0.008), and drug-induced initiation and/or worsening of duration and/or frequency of AVNRT (n=4 [15.4%] vs n=1 [1.4%], p=0.006) as compared to patients with AVNRT without BrS. Genetic screening identified 19 mutations or rare variants in 13 genes in 13 of 17 patients with both AVNRT and BrS (yield = 76.5%). Ten of these 13 genotype-positive patients (76.9%) harbored genetic variants known or suspected to cause a loss of function of cardiac sodium channel current (SCN5A, SCN10A, SCN1B, GPD1L, PKP2, and HEY2). CONCLUSION: Our results suggest that spontaneous AVNRT and concealed BrS co-occur, particularly in female patients, and that genetic variants that reduce sodium channel current may provide a mechanistic link between AVNRT and BrS and predispose to expression of both phenotypes.