Prolonged fractionation of paced right atrial electrograms in patients with atrial flutter and fibrillation

OBJECTIVES: This study investigated the extent of fractionation of paced right atrial electrograms in patients with and without paroxysmal atrial flutter (AFL) or atrial fibrillation (AF). BACKGROUND: Slow conduction through nonuniform anisotropic atrial muscles, represented by fractionated electrograms, may favor the generation of atrial tachyarrhythmias. METHODS: This study included 10 control patients (Group 1), 8 patients with documented paroxysmal AFL (Group 2) and 10 patients with documented paroxysmal AF (Group 3). Five electrode catheters were placed in the different sites of the right atrium and one catheter was positioned at the coronary sinus ostium. Atrial pacing from one site was done by a constant drive train with an extrastimulus inserted every fourth beat while recording at the other five sites was performed. The delay of each fractionated potential in the high-pass filtered atrial electrogram in response to extrastimulation was determined and used to construct conduction curves of delay versus the S1S2 interval. RESULTS: The mean increase in electrogram duration between a coupling interval of 350 ms and 10 ms above atrial refractoriness was significantly greater in Groups 2 and 3 compared with that in Group 1 (8.5 +/- 2.5 vs. 11.0 +/- 2.7 vs. 5.9 +/- 2.3 ms, respectively, p < 0.001). The mean S1S2 interval at which delay increased suddenly was also longer in Groups 2 and 3 compared with Group 1 (326 +/- 9 vs. 343 +/- 12 vs. 307 +/- 17 ms, respectively, p < 0.001). CONCLUSIONS: Increased delays in the individual potential of the fractionated atrial electrograms may be related to the development of AFL and AF.     

成功消融右房峡部依赖型心房扑动的径线位置及临床特点

目的总结成功治疗右房峡部依赖型心房扑动(简称房扑)的消融线位置及临床特点。方法收集2009年至2014年间成功消融的右房峡部依赖型房扑患者的临床资料,分析总结成功消融的消融线位置及特点。结果共274例患者入选,年龄[54.1±13.8(14~84)]岁,65例(23.7%)为心脏外科术后患者。术中266例(97.1%)在6点钟位置消融成功,8例(2.9%)在7-8点钟位置消融成功。后者心脏外科术后的比例及再次/多次消融的患者比例明显高于前者。结论对于绝大部分右房峡部依赖型房扑患者,于6点钟位置消融即可,极少数患者需于偏游离壁位置(7-8点钟)方可消融成功,特别是对于心脏外科术后患者及曾消融失败的患者。     

Mechanism of conversion of atypical right atrial flutter to atrial fibrillation

The purpose of this study was to explore the mechanisms of conversion from atypical atrial flutter (AFL) to atrial fibrillation (AF), and the long-term results of cavotricuspid isthmus ablation in these patients. We retrospectively reviewed the records of 221 patients with typical AFL referred to our hospital for ablation. A total of 25 patients had atypical AFL, and cavotricuspid isthmus ablation was performed in 23 with isthmus-dependent atypical AFL, as well as in 180 patients with typical counterclockwise and/or clockwise AFL. In all, 13 spontaneous transitions from atypical AFL to AF were documented in 11 of 17 patients. Before AF, a pattern of lower loop reentry was observed in 11 of 13 patients (85%) and upper loop reentry in 3 (1 had both). Multiple early breaks along the tricuspid annulus during AFL were noted in 6 of 13 patients (46%). Among the 13 transitions, discrete atrial premature complexes before AF were found in 5 patients with lower loop reentry and in 1 with upper loop reentry (46%). In the remaining patients, a more rapid atrial rhythm was involved in the development of AF with a pulmonary venous focus in 2. In some cases, additional "breaks" in the functional line of block occurred before the development of AF. There was a significant increased incidence of AF (68%) in those with atypical AFL compared with those with typical AFL (38%) (p = 0.004). After a mean follow-up of 28 +/- 9 months for the atypical group and 18 +/- 11 months for the typical group, the AF recurrence rate was similar (57% vs 48%, p = 0.4). Discrete atrial premature complexes or atrial tachycardia may initiate AF either directly or by producing further breaks in lines of functional block. Bidirectional cavotricuspid isthmus block is associated with cure or control of AF in approximately 50% of patients with AFL.     

Electrophysiological evaluation and ablation of atypical right atrial flutter

Right atrial reentry which does not critically depend upon activation through the cavotricuspid isthmus is considered to be a subtype of atypical flutter. Diagnosis is dependent upon demonstrating the nonparticipation of the cavotricuspid isthmus. Right atrial free wall atriotomy incisions, the superior vena cava, the inferior vena cava, electrically silent or mute areas, incomplete variants of the posterior intercaval crista terminalis line of block and other functional/anisotropic lines of block form the central barriers around which macroreentry occurs. The length, location and orientation of fixed lines of block such as atriotomy incisions are important determinants of their arrhythmogenicity. Successful catheter ablation depends upon delineating the circuit in order to choose the optimal isthmus for ablation and producing complete block across it.     

Substrate mapping to detect abnormal atrial endocardium with slow conduction in patients with atypical right atrial flutter.

OBJECTIVES: The purpose of this study was to investigate the relationship between the abnormal substrate and peak negative voltage (PNV) in the right atrium (RA) with atypical flutter. BACKGROUND: The impact of a local abnormally low voltage electrogram on the local activation pattern and velocity of atrial flutter (AFL) remains unclear. METHODS: Twelve patients with clinically documented AFL were included to undergo noncontact mapping of the RA. The atrial substrate was characterized by the: 1) activation mapping; 2) high-density voltage mapping; and 3) conduction velocity along the flutter re-entrant circuit. The normalized PNV (i.e., the relative ratio to the maximal PNV) in each virtual electrode recording was used to produce the voltage maps of the entire chamber. The protected isthmus was bordered by low voltage zones. RESULTS: Atypical AFL of the RA was induced by atrial pacing in 12 patients, including 10 upper loop re-entry and 2 RA free wall re-entry flutter. These protected isthmuses were located near the crista terminalis. The mean width of the protected isthmus was 1.7 +/- 0.3 cm and mean voltage at the isthmus was -0.91 +/- 0.39 mV. The conduction velocities within these paths were significantly slower than outside the path (0.30 +/- 0.18 m/s vs. 1.14 +/- 0.41 m/s, respectively; p = 0.004). The ratiometric PNV of 37.6% of the maximal PNV had the best cut-off value to predict slow conduction, with a high sensitivity (92.3%) and specificity (85.7%). CONCLUSIONS: Characterization of the RA substrate in terms of the unipolar PNV is an effective predictor of the slow conduction path within the critical isthmus of the re-entrant circuit.     

Progressive action potential duration shortening and the conversion from atrial flutter to atrial fibrillation in the isolated canine right atrium.

OBJECTIVES: We sought to evaluate the effects of progressive shortening of the action potential duration (APD) on atrial wave front stability. BACKGROUND: The mechanisms of conversion from atrial flutter to atrial fibrillation (AF) are unclear. METHODS: Isolated canine right atria were perfused with 1 to 5 micromol/l of acetylcholine (ACh). We mapped the endocardium by using 477 bipolar electrodes and simultaneously recorded transmembrane potentials from the epicardium. The APD(90) was measured during regular pacing (S(1)) with cycle lengths of 300 ms. Atrial arrhythmia was induced by a premature stimulus (S(2)). RESULTS: At baseline, only short runs of repetitive beats (<10 cycles) were induced. After shortening the APD(90) from 124 +/- 15 ms to 72 +/- 9 ms (p < 0.01) with 1 to 2.5 micromol/l of ACh, S(2) pacing induced single, stable and stationary re-entrant wave fronts (307 +/- 277 cycles). They either anchored to pectinate muscles (5 tissues) or used pectinate muscles as part of the re-entry (4 tissues). When ACh was raised to 2.5 to 5 micromol/l, the APD(90) was further shortened to 40 +/- 12 ms (p < 0.01); S(2) pacing induced in vitro AF by two different mechanisms. In most episodes (n = 13), AF was characterized by rapid, nonstationary re-entry and multiple wave breaks. In three episodes with APD(90) <30 ms, AF was characterized by rapid, multiple, asynchronous, but stationary wave fronts. CONCLUSIONS: Progressive APD shortening modulates atrial wave front stability and converts atrial flutter to AF by two mechanisms: 1) detachment of stationary re-entry from the pectinate muscle and the generation of multiple wave breaks; and 2) formation of multiple, isolated, stationary wave fronts with different activation cycle lengths.     

碎裂电位消融对心房颤动患者自主神经功能和预后的影响

在经典的环肺静脉隔离术(PVI)的基础上配合心房碎裂电位(CFAE)消融可明显提高消融治疗的成功率,降低心房颤动(房颤)的复发.本研究利用无创手段--心率变异性分析(HRV)探索单纯PVI和PVI结合CFAE消融两种术式对自主神经活性的影响.     

Activation patterns in experimental canine atrial flutter produced by right atrial crush injury.

OBJECTIVES. This study was designed to localize and characterize the atrial flutter reentrant circuit and the electrophysiologic effects of right atrial crush injury in a new canine model. BACKGROUND. In previous studies sustained atrial flutter was induced in the canine heart by rapid atrial pacing after a linear crush injury was placed in the right atrial free wall. METHODS. Eight dogs (group 1) with three electrode plaques on the right and left atria and Bachmann's bundle and seven dogs (group 2) with a single high density electrode plaque on the right atrium were studied with use of a 64-channel computerized mapping system. RESULTS. At baseline, during sinus rhythm and right and left atrial pacing, activation spread uniformly without areas of slow conduction. Crush injury produced marked conduction delay or complete block during sinus rhythm, increasing the mean difference in activation times across the injury compared with control values (group 1, 31 +/- 4 vs. 14 +/- 5 ms, p less than 0.01; group 2, 28 +/- 10 vs. 7 +/- 2 ms, p less than 0.01). Rapid atrial pacing (S1S1 200 ms) above and below the crush injury revealed a line of complete block across which adjacent electrodes recorded markedly different activation times (33 +/- 5 and 38 +/- 12 ms difference, respectively) and around which activation wave fronts proceeded, colliding opposite the stimulating electrodes. The mean atrial flutter cycle length of 11 episodes induced in group 1 and 14 episodes in group 2 was 157 +/- 16 and 140 +/- 16 ms, respectively (p = NS). Activation mapping revealed a reentrant circuit in the right atrium around the crush injury in all episodes. Although the reentrant circuit did not contain a discrete area of slow conduction, activation time below was longer than that above the crush injury (92 +/- 14 vs. 66 +/- 8 ms and 82 +/- 12 vs. 59 +/- 9 ms in groups 1 and 2, respectively, p less than 0.01 for both). Rapid atrial pacing or premature stimuli produced progressive conduction delay and unidirectional block between the crush injury and the tricuspid anulus, inducing atrial flutter directly in 9 of 25 episodes. In 16 episodes, atrial flutter developed after transient induction of atrial fibrillation. CONCLUSIONS. 1) Atrial flutter in this model is due to reentry in the right atrium; 2) the crush injury functions as an anatomic obstacle around which reentry may occur; and 3) the reentrant circuit does not contain a discrete area of slow conduction but, rather, generally slower conduction below the crush injury.