Pacing and sensing interference by air bubble surrounding the non-extended helix of intact active fixation lead.

BACKGROUND: Active fixation pacing leads with silicon cylinder tips have been used for their safety and flexibility. Measurement of baseline sensing/pacing characteristics before fixation of helix helps to identify the optimal pacing site, but we encountered difficulties in making these measurements despite multiple attempts with the model LPA 1200M lead. To identify the cause and overcome this complication, we compared 4 different retractable active fixation lead models, which enabled baseline sensing/pacing measurements before extension of helix. METHODS AND RESULTS: We immersed 4 different lead tips and rings in a 0.18% saline solution, and measured the lead impedance before and after flushing of air bubble visible inside the lead tip. Before evacuation of the air bubble, the impedance of the model LPA 1200M lead was >4,000 Ω in 8 out of 10 measurements, although that of the other leads was within the measurable range. After evacuation of the air bubble, the lead impedance returned to within the measurable range. There was no prominent change in the impedance of the metal cylinder tip lead. CONCLUSIONS: Air bubbles may interfere with the measurement of baseline sensing/pacing characteristics before active fixation of pacing leads with cylindrical silicon tips. In the case of high impedance beyond the measurable range before extension of helix, the measurement should be repeated after fixation into the myocardium before suspecting lead dysfunction.

Atrial pacing site and atrioventricular conduction in patients paced for sinus node disease.

BACKGROUND: Unnecessary ventricular pacing in sinus node disease (SND) must be avoided. To test the hypothesis that in SND, with or without 1st degree atrioventricular (AV) block, cumulative percent ventricular pacing (cum%VP) can be limited by low right atrial septal (LRAS) instead of right atrial appendage (RAA) pacing. METHODS: We studied 102 dual-chamber pacemaker recipients with SND. The PQ interval on 12-lead electrocardiogram and the atrial paced to ventricular sensed interval (Ap-Vs) during LRAS and RAA pacing were measured and compared at implantation, 3 months and 1 year of follow-up. Group 1 included 62 patients with baseline PQ interval <200 milliseconds during LRAS (n = 28) versus RAA (n = 34) pacing. Group 2 included 40 patients with baseline PQ ≥200 milliseconds during LRAS (n = 20) versus RAA (n = 20) pacing. cum%VP were measured at 3 months and 1 year. RESULTS: The characteristics and AV conduction properties were similar and the Ap-Vs interval was significantly shorter in the LRAS than in the RAA pacing group up to 1 year (193 ± 32 milliseconds vs. 220 ± 27 milliseconds in Group 1; P = 0.003, 222 ± 41 milliseconds vs. 281 ± 30 milliseconds in Group 2; P < 0.001). While cumulative percent atrial pacing was consistently similar, cum%VP was significantly smaller during LRAS than RAA pacing (1 ± 1% vs. 8 ± 18% in Group 1; P = 0.03, 7 ± 10% vs. 48 ± 38% in Group 2; P < 0.001). Similar observations were made with or without left atrial (LA) enlargement. CONCLUSION: Compared with RAA, LRAS pacing showed shorter AV interval in SND patients with or without 1st degree AV block and LA enlargement. This beneficial effect persisted through 1-year follow-up, and decreased cum%VP significantly.

Sodium channelopathy underlying familial sick sinus syndrome with early onset and predominantly male characteristics.

BACKGROUND: Sick sinus syndrome (SSS) is a common arrhythmia often associated with aging or organic heart diseases but may also occur in a familial form with a variable mode of inheritance. Despite the identification of causative genes, including cardiac Na channel (SCN5A), the pathogenesis and molecular epidemiology of familial SSS remain undetermined primarily because of its rarity. METHODS AND RESULTS: We genetically screened 48 members of 15 SSS families for mutations in several candidate genes and determined the functional properties of mutant Na channels using whole-cell patch clamping. We identified 6 SCN5A mutations including a compound heterozygous mutation. Heterologously expressed mutant Na channels showed loss-of-function properties of reduced or no Na current density in conjunction with gating modulations. Among 19 family members with SCN5A mutations, QT prolongation and Brugada syndrome were associated in 4 and 2 individuals, respectively. Age of onset in probands carrying SCN5A mutations was significantly less (mean±SE, 12.4±4.6 years; n=5) than in SCN5A-negative probands (47.0±4.6 years; n=10; P<0.001) or nonfamilial SSS (74.3±0.4 years; n=538; P<0.001). Meta-analysis of SSS probands carrying SCN5A mutations (n=29) indicated profound male predominance (79.3%) resembling Brugada syndrome but with a considerably earlier age of onset (20.9±3.4 years). CONCLUSIONS: The notable pathophysiological overlap between familial SSS and Na channelopathy indicates that familial SSS with SCN5A mutations may represent a subset of cardiac Na channelopathy with strong male predominance and early clinical manifestations.