Overdrive pacing mapping: An alternative approach used in scar associated localized atrial tachycardia.

BACKGROUND: Mapping and ablation of localized reentry atrial tachycardia (AT) can be challenging, especially in those with varying cycle length (CL). OBJECTIVE: We attempted to use the traditional maneuver of overdrive pacing to facilitate AT mapping. METHODS: Data were collected from 12 patients with localized ATs. All patients had prior cardiac surgery or prior atrial fibrillation ablation. Overdrive pacing mapping (ODPM) was performed to find independent local activity (ILA) and compared with conventional activation mapping (CAM) during ongoing AT to determine its accuracy and efficacy. Patients with macro-reentry AT around the tricuspid or mitral annulus were excluded. RESULTS: Twelve patients with 14 localized ATs were included. All 14 ATs including 4 (29%) with varying CL successfully completed ODPM and had the ILA, although two ATs terminated during ODP and required repeated mapping. Radiofrequency ablation focused on critical sites with ILA was successful in all 12 patients. Using CAM, however, 6 of 14 ATs (43%) mapping attempts were aborted due to AT termination (2 ATs) or varying CL (4 ATs), and only 5 of 8 (63%) located "critical sites" were ultimately confirmed by entrainment and ablation results. After 25 ± 9 months of follow-up, no patient had AT recurrence. CONCLUSION: Our preliminary results demonstrated that ODPM is superior to CAM in ATs that were poorly sustained or with varying CL and is a useful supplement to CAM.

Accurate localization and catheter ablation of superoparaseptal accessory pathways.

BACKGROUND: There remains some confusion delineating the accurate location and the detailed anatomical relationship between atrioventricular accessory pathways (APs) located in the superoparaseptal region. OBJECTIVE: The purpose of this article was to detail the anatomical relationship and accurate location of APs located in the superoparaseptal region. METHODS: Between May 1, 2009 and November 30, 2016, 11 patients with superoparaseptal APs (SPS-APs) were identified in 129 consecutive patients who underwent catheter ablation for APs in our center. RESULTS: A single SPS-AP was detected in all patients (manifest, n = 5; concealed, n = 6). The location of all 11 APs were precisely identified at the region millimeters superior to the His bundle recording site at the tricuspid annulus (S-HB, n = 6; manifest, n = 4); the area millimeters behind the His bundle recording site, adjacent to the right atrial aspect of the noncoronary aortic cusp (B-HB, n = 2; manifest, n = 1); and the true para-His bundle region (P-HB, n = 3). The electrocardiogram of all 5 manifest APs conformed to the typical "anteroseptal AP" pattern: a positive delta wave in leads I, II, avF, and avL; a narrow positive delta wave in lead V1; and a precordial QRS transition at lead V3. All APs were successfully eliminated by catheter ablation. After 54 ± 26 months of follow-up, all patients were free of arrhythmia. CONCLUSION: Three distinct regions are identified for localization of SPS-APs. Careful mapping and a detailed understanding of the anatomy of this region as well as distinct electrocardiographic characteristics are essential to eliminate such APs safely and effectively.

Optical mapping of V(m) and Ca(i)(2+) in a model of arrhythmias induced by local catecholamine application in patterned cell cultures.

Catecholamines are known to provoke cardiac arrhythmias, but important aspects such as localization of the arrhythmia source in multicellular tissue and exact ionic mechanisms are not well-known. In this work, a multicellular model of arrhythmias caused by local epinephrine application was developed; V (m) and Ca(i)(2+) changes at the arrhythmia source were measured using fluorescent dyes and high-resolution optical mapping. Cultured strands of neonatal rat myocytes (width approximately 0.4 mm) were produced by patterned growth. Epinephrine (1 micromol/l) was applied over an area of 0.3-0.6 mm via two micropipettes, and strands were stimulated by burst pacing. Local epinephrine application caused triggered arrhythmias with cycle lengths of 202-379 ms and duration of >10 s in 9 out of 16 preparations. Optical V(m) mapping demonstrated that in 78% of cases, the source of arrhythmia was located at the boundary of the locally perfused area. Staining with Ca(i)(2+)-sensitive dye Fluo-4 prevented arrhythmia induction in most cases (85%) likely due to Ca(2+) buffering by the dye. Optical Ca(i)(2+) mapping revealed non-propagated Ca(i)(2+) oscillations at the boundary of the locally perfused area in 45% cases. In conclusion, we developed a new model of catecholamine-dependent arrhythmias allowing mapping of V(m) and Ca(i)(2+) at the arrhythmia source with microscopic resolution. The arrhythmias typically originated from the boundary of the epinephrine-perfused area. The location of the arrhythmia source correlated with localized Ca(i)(2+) oscillations suggesting that arrhythmias were caused by Ca(i)(2+) overload at these locations.