Structural relation between the superior vena cava and pulmonary veins in patients with atrial fibrillation.

The superior vena cava (SVC) is a main source of non-pulmonary vein (PV) ectopies that initiate atrial fibrillation (AF). Although the critical role of structural remodeling of the left atrium (LA) in the occurrence of AF was extensively investigated by atrial voltage mapping, that of PVs and the SVC has been less explored. Study subjects comprised 47 patients undergoing catheter ablation of lone AF. During sinus rhythm, PV, SVC, and atrial voltage maps were acquired, and sleeve length of each PV and SVC was determined by an electroanatomical mapping system. The sleeves of the superior PVs were significantly longer than those of the inferior PVs (left superior PV (LSPV): 21 ± 5, left inferior PV: 14 ± 4, right superior PV (RSPV): 19 ± 5, right inferior PV: 15 ± 5, and SVC: 23 ± 10 mm, p < 0.0001). The LSPV sleeve was longer in men than in women (22 ± 6 vs. 19 ± 4 mm, p < 0.05). The sleeve length in the LSPV correlated positively with the body surface area (BSA) (p = 0.003, R = 0.42). Of note, there was a significant correlation in sleeve length between the RSPV and SVC (p < 0.0001, R = 0.64). In conclusion, not right- but left-sided PV sleeves were associated with the BSA of the patients, whereas a structural relation between the right-sided PVs and the SVC was implied based on sleeve mapping. This novel finding may provide mechanistic implications for the development of AF in future studies.

Mechanistic implication of decreased plasma atrial natriuretic peptide level for transient rise in the atrial capture threshold early after ICD or CRT-D implantation.

PURPOSE: Despite the use of steroid-eluting leads, a transient but not persistent rise in the atrial/ventricular capture threshold (TRACT/TRVCT) can occur early after pacemaker implantation in patients with sick sinus syndrome. This study aimed to assess the prevalence, predictors, and mechanisms of TRACT/TRVCT in patients with heart failure undergoing implantable cardioverter defibrillator (ICD) or cardiac resynchronization therapy (CRT) implantation. METHOD: One hundred twenty consecutive patients underwent ICD (N = 70) or CRT (N = 50) implantation. Capture threshold was measured at implantation, 7-day, 1-month, and 6-month post-implantation. TRACT/TRVCT was defined as a threshold rise at 7 days by more than twice the height of the threshold at implantation, with full recovery during follow-up. Atrial and brain natriuretic peptide (ANP and BNP) levels were measured before implantation. RESULTS: TRACT and TRVCT were observed in 13 (11%) and 10 (8%) patients, respectively. Patients with TRACT had lower ANP level (median 72 [42-105] vs. 99 [49-198] pg/mL, P = 0.06), lower ANP/BNP ratio (0.29 [0.20-0.36] vs. 0.50 [0.33-0.70], P < 0.01), lower atrial sensing amplitude (2.0 ± 0.8 vs. 2.7 ± 1.3 mV, P = 0.02), and lower left ventricular ejection fraction (32 ± 12 vs. 40 ± 14%, P = 0.04) than those without TRACT. TRACT recovered within 1 month, whereas TRVCT recovered within 6 months. In multivariable analysis, ANP/BNP ratio was the only independent predictor of TRACT (OR, 0.018; 95% CI, 0.001-0.734; P = 0.034). CONCLUSIONS: Atrial degenerative change characterized by lower ANP/BNP ratio was associated with the occurrence of TRACT in patients with heart failure. TRVCT could also occur, but it required a longer recovery time than TRACT.

Underrecognized entity of the transient rise in the atrial capture threshold early after dual-chamber pacemaker implantation.

BACKGROUND: Steroid-eluting pacemaker leads suppress acute rises in pacing threshold by preventing inflammatory processes. However, we occasionally encounter not persistent but transient rise in the atrial capture threshold (TRACT) early after pacemaker implantation. We believe that this phenomenon is underrecognized in clinical practice and may potentially lead to unnecessary reintervention. We aimed to clarify the prevalence, predictors, and possible mechanisms of TRACT. METHODS AND RESULTS: We reviewed clinical records from 239 consecutive patients who underwent dual-chamber pacemaker implantation for sick sinus syndrome (SSS) (N = 102) or atrioventricular block (AVB) (N = 137). Atrial capture threshold was measured at implantation and 7 days, 2 months, and 8 months postimplantation. TRACT was defined as a rise in the threshold at day 7 to ≥twice that at implantation, with an absolute value ≥1.0 V/0.4 ms, and full recovery by 8 months into follow-up. TRACT was observed in 15 patients (6%), of whom13 (87%) suffered from SSS but not AVB. Patients with TRACT had greater body mass index (BMI) (25 ± 5 kg/m2 vs 23 ± 4 kg/m2 , P = 0.01), larger left atrium (42 ± 5 mm vs 38 ± 7 mm, P = 0.03), and were more likely to suffer from paroxysmal atrial fibrillation (60% vs 31%, P = 0.02) than those without TRACT. In multivariable logistic regression analysis, BMI and SSS were the independent predictors of TRACT (odds ratio [OR], 1.172; 95% confidence interval [CI], 1.019-1.349; P = 0.03 and OR, 11.53; 95% CI, 2.010-66.21; P = 0.006, respectively). CONCLUSIONS: The distinct phenomenon of TRACT was not rare in clinical practice early after dual-chamber pacemaker implantation, and its occurrence was strongly associated with SSS.

Electrophysiological relation between the superior vena cava and right superior pulmonary vein in patients with paroxysmal atrial fibrillation.

INTRODUCTION: The superior vena cava (SVC) is a main source of nonpulmonary vein (PV) ectopies initiating atrial fibrillation (AF). Empiric SVC isolation may improve rhythm outcomes after catheter ablation of AF. Because the SVC passes immediately adjacent to the right superior PV (RSPV), an electrophysiological relation could be present between the two structures. The present study aimed to estimate the interrelation between the SVC and RSPV by evaluating arrhythmogenic activities observed during catheter ablation of AF. METHODS AND RESULTS: Study subjects comprised 121 consecutive patients referred for catheter ablation of paroxysmal AF. Isoproterenol infusion was used to induce ectopies and AF. Patients were divided into two groups depending on the presence of arrhythmogenic SVC: arrhythmogenic-SVC (A-SVC) and nonarrhythmogenic SVC (Non-A-SVC) groups. The prevalence of females was higher and body surface area was smaller in the A-SVC group (N = 22) than Non-A-SVC group (N = 99). Arrhythmogenic activities were observed in 60 (49%) RSPVs, 24 (20%) right inferior PVs, 72 (59%) left superior PVs, and 31 (25%) left inferior PVs. Arrhythmogenic RSPVs were more prevalent in the A-SVC group than Non-A-SVC group (86% vs. 41%, P = 0.0001), whereas these prevalences in the other three PVs were not different between groups (P >0.3). In multivariable analysis, arrhythmogenic RSPV was the only independent predictor of arrhythmogenicity of the SVC (OR, 8.53; 95% CI 2.31-31.46; P = 0.001). CONCLUSIONS: An electrophysiological interrelation may be present between the SVC and RSPV in patients with paroxysmal AF. Semiempiric SVC isolation limited to patients with an arrhythmogenic RSPV may be a more efficient treatment strategy.

Comparison of Pulmonary Venous and Left Atrial Remodeling in Patients With Atrial Fibrillation With Hypertrophic Cardiomyopathy Versus With Hypertensive Heart Disease.

Left ventricular diastolic dysfunction in hypertrophic cardiomyopathy (HC) increases susceptibility to atrial fibrillation. Although phenotypical characteristics of the hypertrophied left ventricle are clear, left atrial (LA) and pulmonary venous (PV) remodeling has rarely been investigated. This study aimed to identify differences in LA and PV remodeling between HC and hypertensive heart disease (HHD) using 3-dimensional computed tomography. Included were 33 consecutive patients with HC, 25 with HHD, and 29 without any co-morbidities who were referred for catheter ablation of atrial fibrillation. Pre-ablation plasma atrial and brain natriuretic peptide levels, post-ablation troponin T level, and LA pressure were measured, and LA and PV diameters were determined 3 dimensionally. LA transverse diameter in the control group was smaller than that in the HHD or HC group (55 ± 6 vs 63 ± 9 vs 65 ± 12 mm, p = 0.0003). PV diameter in all 4 PVs was greatest in the HC group and second greatest in the HHD group (21.0 ± 3.1 vs 23.8 ± 2.8 vs 26.8 ± 4.1 mm, p <0.0001 for left superior PV). Differences in PV size between the HHD and HC groups were enhanced by indexing to the body surface area (12.4 ± 1.9 vs 13.1 ± 1.4 vs 16.1 ± 3.3 mm/m2, p <0.0001). The PV/LA diameter ratio was greater in the HC than in the other groups (0.38 ± 0.06 vs 0.38 ± 0.05 vs 0.42 ± 0.07, p = 0.01). Atrial natriuretic peptide, brain natriuretic peptide, troponin T levels, and LA pressure were highest in the HC group (all p <0.05). In conclusion, the stiff LA caused from atrial hypertrophy may account for higher levels of biomarkers, higher LA pressure, and PV-dominant remodeling in HC.