Arrhythmogenesis of surgical atrial incisions and lesions in Maze procedure: insights from high-resolution mapping of atrial tachycardias.

BACKGROUND: Atrial tachycardias (ATs) frequently develop after a surgical Maze procedure. We aimed to elucidate the electrophysiologic mechanisms and their arrhythmogenic substrates of these ATs. METHODS AND RESULTS: We retrospectively reviewed 20 patients (14 females, mean age of 55.5 ± 8.6 years) with post-Maze ATs who underwent high-resolution mapping at three institutions. The slow conduction areas, reentry circuits, voltage signals, complex electrograms, and their correlation with the surgical incisions and lesions placed in the surgical Maze procedures were analyzed. Thirty-six ATs with a mean cycle length of 260.0 ± 67.6 ms were mapped in these patients. Among them, 22 (61.1%) were anatomical macro-reentrant ATs (AMAT), 12 (33.3%) non-AMATs (localized ATs), and 2 (5.6%) focal ATs, respectively. Epicardial conduction bridges were observed in 6/20 (30.0%) patients and 7/36 (19.4%) ATs. Different arrhythmogenic substrates were identified in these ATs, including slow conduction regions within the previous lesion areas or between the incisions and anatomical structures, the prolonged activation pathways caused by the short lesions connecting the tricuspid annulus, and the circuits around the long incisions and/or lesions. CONCLUSIONS: Reentry is the main mechanism of the post-Maze ATs. The pro-arrhythmic substrates are most likely caused by surgical incisions and lesions. The slow conduction regions and the protected channels yielded from these areas are the major arrhythmogenic factors.

Inadvertent transseptal puncture into the aortic root: the narrow edge between luck and catastrophe in interventional cardiology.

AIMS: Inadvertent puncture of the aortic root (AR) is a well-known complication of transseptal puncture (TSP). Strategies for handling of this potentially lethal complication have not been identified yet. In this study, we present typical anatomical locations and clinical management of aortic root puncture (ARP) due to TSP. METHODS AND RESULTS: All patients with ARP were retrospectively collected from seven hospitals. Aortic root puncture was identified and classified regarding angiographical and intraoperative findings in cardiac surgery: (i) TSP from the right atrium (RA) to the non-coronary sinus (NCS), (ii) TSP from RA to the non-coronary sinutubular junction (STJ), and (iii) TSP from RA to the ascending aorta (AA). A total of 24 patients with inadvertent ARP were identified. In 19 patients, penetration of the aorta was accomplished by the inner dilator, in 5 patients by the complete sheath. Previous cardiac surgery had been performed in six patients. There were 13 RA-to-NCS punctures, 2 RA-to-STJ punctures, and 9 RA-to-AA punctures. No cardiac tamponade (CT) occurred in patients with RA-to-NCS and RA-to-STJ punctures. In 8 of 9 patients with RA-to-AA puncture, CT occurred immediately requiring urgent pericardiocentesis and surgical repair. Two patients died after surgical repair. In the 16 patients without surgical therapy, no shunt from the AR to the RA was observed 3 months after the procedure. CONCLUSION: Aortic root puncture due to mislead TSP via NCS or STJ is usually not associated with a severe clinical course while ARP into the AA via the epicardial space generally leads to CT requiring surgical repair.

Flutter Wave Morphology of Peri-Mitral Atrial Flutters Is Mainly Determined by Right Atrial Activation: Insights From High-Resolution Mapping.

BACKGROUND: Peri-mitral atrial flutters frequently develop post-atrial fibrillation ablation or postcardiac surgery. The determinants of the flutter wave morphology on surface ECG have been less studied. METHODS: We retrospectively reviewed 24 patients with peri-mitral atrial flutters who underwent biatrial high-resolution mapping at 3 institutions with LUMIPOINT software. We analyzed the overlap between the right atrial (RA) activation time and flutter wave duration and compared the proportion of the endocardial area that was activated in both atria during the flutter wave duration. Biatrial activation patterns and interatrial conductions were also identified. RESULTS: The mean tachycardia cycle length was 264±60 ms, with RA activation time 155±45 ms (60.8±20.6% of the tachycardia cycle length), and the flutter wave duration 107±31 ms (41.6±11.7% of the tachycardia cycle length). The overlap between the RA activation time and the flutter wave duration was 102±29 ms, which takes 68.5±17.2% of the RA activation time and 95.7±9.1% of the flutter wave duration, respectively. Quantitative analysis also showed that during the flutter wave duration, more percentage of the endocardial area was activated in the RA than in the left atrium (73.0±12.7% versus 45.2±13.0%, P<0.001). We consistently observed that the RA anterior wall rightward activation corresponded to the positive component in V1 in both flutter patterns, and the RA downward activation corresponded to the positive component in the counterclockwise group or the upward activation corresponded to the negative component in the clockwise group in the inferior leads. The passive RA activation patterns were varied with spontaneous atrial scarring or previous linear ablation. CONCLUSIONS: ECG flutter wave morphology of peri-mitral atrial flutters is mainly dependent on RA activation patterns.