医源性房性心动过速的三维标测及其机制研究
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摘要
第一部分经右房切口外科术后峡部依赖性心房扑动与普通典型心房扑动峡部传导时间的对比研究
目的通过比较经右房切口外科术后峡部依赖性心房扑动(右房切口术后房扑)与普通典型心房扑动(典型房扑)患者下腔静脉-三尖瓣环峡部(CTI)传导时间和速度,探讨两类心动过速发生的不同电生理机制及其相应的消融策略。
方法2006年2月至2008年1月之间共有17例三尖瓣峡部依赖性房扑患者采用非接触三维标测系统(EnSite-array)指导下进行标测和射频消融治疗。其中9例心脏外科手术后房扑患者,男6例,女3例,年龄47.2±16.9岁;典型房扑患者8例,男7例,女1例,年龄52.0±19.1岁。应用非接触标测系统构建右房三维模型,标测心动过速的折返激动顺序及其关键峡部。在心动过速下,分别测量两组患者房扑的周长、CTI传导时间和长度、游离壁传导时间和长度及间隔部传导时间和长度。分别计算两组患者CTI传导时间和游离壁传导时间及间隔部传导时间占心动过速周期的比值和传导速度,并对其传导时间和速度进行比较。CTI传导时间定义为三尖瓣环7点至冠状静脉窦口上缘之间的传导时间,CTI传导速度为该部位长度与时间之比。游离壁传导时间定义为三尖瓣环12点至7点之间的传导时间,传导速度为该部位长度与时间的比值。间隔部传导时间定义为三尖瓣环12点至冠状静脉窦口上缘之间的传导时间,传导速度为该部位长度与时间的比值。在导航系统指导下行关键峡部线性消融,并验证双向阻滞。
结果右房切口术后房扑组与普通典型房扑组房扑周长分别为254.3±50.7 ms与219.8±18.9 ms;CTI传导时间为50.5±13.0 ms与76.6±11.6 ms,CTI传导时间占心动周期比值分别为20.2±4.7%与35.3±6.9%,峡部传导速度分别为0.84±0.15 m/s与0.53±0.15 m/s;游离壁传导时间分别为148.4±36.4 ms与82.1±28.4 ms,游离壁传导时间占心动周期比值分别为58.1±5.6%与36.8±10.5%,游离壁传导速度分别为0.42±0.14 m/s与0.76±0.25 m/s;间隔部传导时间分别为55.3±18.5 ms与61.1±19.9 ms,间隔部传导时间占心动周期比值分别为21.6±5.1%与27.7±9.3%,间隔部传导速度分别为0.94±0.29 m/s与0.81±0.23 m/s。两组患者的CTI及游离壁传导时间和传导速度存在明显差别。典型房扑组CTI传导时间明显长于右房切口术后房扑组(P＜0.05),而其传导速度较后者明显缓慢(P＜0.05)。右房切口术后房扑组游离壁传导时间明显较典型房扑组延长(P＜0.05),其传导速度明显缓慢(P＜0.05)。两组患者间隔部传导时间及传导速度无显著性差异(P＞0.05)。所有患者射频消融均取得成功。随访10.1±6.6个月,1例右房切口术后房扑患者复发,再次消融CTI后房扑终止,随访12个月无复发。
结论典型房扑CTI传导时间较右房切口术后房扑明显延长,CTI是其缓慢传导区。右房切口术后房扑CTI参与折返环的形成,是此类房扑折返的解剖峡部,但不是关键的电生理区域,消融CTI仍能治愈此类心动过速。另外,非接触标测还可以指导合并其他房性心动过速的标测与消融。
第二部分心房颤动消融术后二尖瓣峡部房性心动过速的机制及消融策略
目的探讨心房颤动(房颤)患者环肺静脉左房线性消融术后发生的二尖瓣峡部房性心动过速(房速)的机制及其消融策略。
方法2006年6月至2007年6月之间122例房颤患者采用EnSite-NavX和环状电极行环肺静脉左房线性消融,术后32例复发房颤或房速患者,接受再次射频消融治疗。8例患者经EnSite-NavX激动标测及拖带标测证实存在二尖瓣峡部房速,其中男6例,女2例,年龄54.9±8.6岁。在三维导航下于左下肺静脉口部下缘至二尖瓣环之间行线性消融,能量设置为35～40 W,温度为43～45℃,冷盐水灌注流量为17～25 ml/min。对不能成功阻断二尖瓣峡部传导者予以冠状静脉窦内消融,能量设置为20～25 W,温度为43℃,冷盐水灌注流量为17 ml/min。术中同时探查双侧肺静脉电位,如传导恢复予以再次隔离。
结果8例二尖瓣峡部房速,2例临床上呈无休止性发作,6例为阵发性,可被程序刺激诱发。房速的周长217.5±20.6 ms,其中顺钟向折返5例,逆钟向折返3例。二尖瓣峡部线性消融至完全性双向传导阻滞5例,3例心内膜途径失败者经冠状静脉窦内消融,其中1例获得成功。术后随访5.5±4.3个月,6例无房颤及房速发作,1例仍有阵发性房速发作。另1例术后房速呈无休止发作,予以胺碘酮及美托洛尔控制心室率治疗。
结论环肺静脉线性消融术后发生的二尖瓣峡部房速与左房线性消融治疗房颤的致心律失常作用有关,其主要的机制是消融线和缝隙相关的大折返性心动过速。于左下肺静脉口部下缘至二尖瓣环之间行线性消融可阻断二尖瓣峡部传导。但部分患者需经冠状静脉窦内消融,有时虽经心内膜及冠状静脉窦内联合消融仍不能完全阻断峡部传导。
Objective The purpose of this study was to evaluate the electrophysiological mechanism of atrial flutter after surgical repair procedure (SAFL) and typical atrial flutter (TAFL) by analysis of the cavo-tricuspid isthmus conduction time (CTI-CT) and the conduction velocity of the two groups.
Methods Nine patients (47.2±16.9 years, 6 males) with SAFL and eight patients (age 52.0±19.1 years, 7 males) with TAFL received catheter ablation from February 2006 to January 2008 under the guidance of the noncontact mapping system. Three-dimensional geometry of right atrium was reconstructed and the special anatomical landmarks were tagged on the map. After geometry making, the isopotential maps of each tachycardia was created to analyze its activation sequence, reentrant circuit, critical isthmus. Then the tachycardia cycle length (TCL), conduction time and conduction velocity in the cavo-tricuspid isthmus (CTI), the right atrium free wall (RAFW) and atrial septum (AS) of the two groups were measured and compared with each other. The CTI-CT was defined as the conduction time between the seven o'clock of the tricuspid annulus (TV7) and the upper margin of the coronary sinus ostium (CSO). The conduction time of RAFW was defined as the conduction time between TV12 and TV7. The conduction time of AS was defined as the conduction time between CSO and TV12. Conduction velocities in CTI, RAFW and AS were measured by the ratio of the length and the conduction time in each part. Linear ablation was performed in the critical isthmus guided by three dimensional mapping systems to the endpoint of bidirectional block.
Results The mean cycle length was 254.3±50.7 ms in SAFL and 219.8±18.9 ms in TAFL. CTI-CT in SAFL was significantly shorter than TAFL (50.5±13.0 ms vs 76.6±11.6 ms) (P < 0.05) while conduction velocity was faster than the latter (0.84±0.15 m/s vs 0.53±0.15 m/s) (P < 0.05 ) . The conduction time was significantly longer (148.4±36.4 ms vs 82.1±28.4 ms) with the conduction velocity slower (0.42±0.14 m/s vs 0.76±0.25 m/s) in RAFW in SAFL group than those in TAFL group (P < 0.05 ) . There was no significant difference in conduction time (55.3±18.5 ms vs 61.1±19.9 ms) and the conduction velocity (0.94±0.29 m/s vs 0.81±0.23 m/s) of AS between the two groups (P > 0.05 ). All the tachycardia was successfully eliminated by catheter ablation guided by noncontact mapping system. After a mean follow up of 10.1±6.6 months,one tachycardia in SAFL group recurred and received a second ablation.
Conclusions The slow conduction in the CTI is the basic electrophysiological substrate for TAFL, but in SAFL, CTI is more a critical anatomical isthmus than an electrophysiological isthmus. The slow conduction area of SAFL was located in the RAFW.
Objective The purpose of this study is to demonstrate the mechanisms of mitral isthmus dependent atrial tachycardia (MI-AT) after circumferential pulmonary vein isolation (CPVI) for the treatment of atrial fibrillation (AF) and to discuss its ablation strategy.
Methods One hundred and twenty-two consecutive patients with AF were treated with CPVI guided by EnSite-NavX and circular mapping catheter, thirty-two of which received a repeat ablation procedure because of recurrent AF or AT. MI- AT was found in eight patients( male 6, mean age 54.9±8.6years) which was confirmed by electrophysiological study and EnSite-NavX three-dimension mapping system. Linear lesion was performed between the ostium of left inferior pulmonary vein and the mitral annulus ( power 35～40 W, temperature 43～45℃, irrigation rate 17～25 ml/ min ). If the complete bidirectional conduction block of mitral isthmus could not be achieved, further ablation would be attempted within the coronary sinus ( power 20～25 W , temperature 43℃, irrigation rate 17ml/ min). Reisolation is necessary when reconduction between pulmonary vein and left atrium was found.
Results Three-dimension mapping showed clockwise activation going around mitral ring in five patients while counterclockwise activation in three patients. The mean cycle length of MI-AT was 217.5±20.6 ms. Bidirectional block of mitral isthmus was obtained in five patients after endocardial linear lesions. The left three patients which were failed by endocardial approach had coronary sinus attempt with only one success. After a mean follow up of 5.5±4.3 months, six patients were free of AT or AF attack, one patient still had paroxysmal AT, another patient developed incessant AT and had the medication of Amiodarone and Metoprolol to control the heart rate.
Conclusions MI-AT can be developed because of the proarrhythmia effect of CPVI for the treatment of AF and also be due to macro-reentrant induced by incomplete lines or recovery conduction. Bidirectional block of the mitral isthmus can be achieved by liner ablation between the ostium of left inferior pulmonary vein and the mitral annulus. In some patients, additional ablation should be attempted within coronary sinus. But this endpoint could not be always obtained even after the joint ablation approach both endocardially and epicardially.
目的通过比较经右房切口外科术后峡部依赖性心房扑动(右房切口术后房扑)与普通典型心房扑动(典型房扑)患者下腔静脉-三尖瓣环峡部(CTI)传导时间和速度,探讨两类心动过速发生的不同电生理机制及其相应的消融策略。
方法2006年2月至2008年1月之间共有17例三尖瓣峡部依赖性房扑患者采用非接触三维标测系统(EnSite-array)指导下进行标测和射频消融治疗。其中9例心脏外科手术后房扑患者,男6例,女3例,年龄47.2±16.9岁;典型房扑患者8例,男7例,女1例,年龄52.0±19.1岁。应用非接触标测系统构建右房三维模型,标测心动过速的折返激动顺序及其关键峡部。在心动过速下,分别测量两组患者房扑的周长、CTI传导时间和长度、游离壁传导时间和长度及间隔部传导时间和长度。分别计算两组患者CTI传导时间和游离壁传导时间及间隔部传导时间占心动过速周期的比值和传导速度,并对其传导时间和速度进行比较。CTI传导时间定义为三尖瓣环7点至冠状静脉窦口上缘之间的传导时间,CTI传导速度为该部位长度与时间之比。游离壁传导时间定义为三尖瓣环12点至7点之间的传导时间,传导速度为该部位长度与时间的比值。间隔部传导时间定义为三尖瓣环12点至冠状静脉窦口上缘之间的传导时间,传导速度为该部位长度与时间的比值。在导航系统指导下行关键峡部线性消融,并验证双向阻滞。
结果右房切口术后房扑组与普通典型房扑组房扑周长分别为254.3±50.7 ms与219.8±18.9 ms;CTI传导时间为50.5±13.0 ms与76.6±11.6 ms,CTI传导时间占心动周期比值分别为20.2±4.7%与35.3±6.9%,峡部传导速度分别为0.84±0.15 m/s与0.53±0.15 m/s;游离壁传导时间分别为148.4±36.4 ms与82.1±28.4 ms,游离壁传导时间占心动周期比值分别为58.1±5.6%与36.8±10.5%,游离壁传导速度分别为0.42±0.14 m/s与0.76±0.25 m/s;间隔部传导时间分别为55.3±18.5 ms与61.1±19.9 ms,间隔部传导时间占心动周期比值分别为21.6±5.1%与27.7±9.3%,间隔部传导速度分别为0.94±0.29 m/s与0.81±0.23 m/s。两组患者的CTI及游离壁传导时间和传导速度存在明显差别。典型房扑组CTI传导时间明显长于右房切口术后房扑组(P＜0.05),而其传导速度较后者明显缓慢(P＜0.05)。右房切口术后房扑组游离壁传导时间明显较典型房扑组延长(P＜0.05),其传导速度明显缓慢(P＜0.05)。两组患者间隔部传导时间及传导速度无显著性差异(P＞0.05)。所有患者射频消融均取得成功。随访10.1±6.6个月,1例右房切口术后房扑患者复发,再次消融CTI后房扑终止,随访12个月无复发。
结论典型房扑CTI传导时间较右房切口术后房扑明显延长,CTI是其缓慢传导区。右房切口术后房扑CTI参与折返环的形成,是此类房扑折返的解剖峡部,但不是关键的电生理区域,消融CTI仍能治愈此类心动过速。另外,非接触标测还可以指导合并其他房性心动过速的标测与消融。
第二部分心房颤动消融术后二尖瓣峡部房性心动过速的机制及消融策略
目的探讨心房颤动(房颤)患者环肺静脉左房线性消融术后发生的二尖瓣峡部房性心动过速(房速)的机制及其消融策略。
方法2006年6月至2007年6月之间122例房颤患者采用EnSite-NavX和环状电极行环肺静脉左房线性消融,术后32例复发房颤或房速患者,接受再次射频消融治疗。8例患者经EnSite-NavX激动标测及拖带标测证实存在二尖瓣峡部房速,其中男6例,女2例,年龄54.9±8.6岁。在三维导航下于左下肺静脉口部下缘至二尖瓣环之间行线性消融,能量设置为35～40 W,温度为43～45℃,冷盐水灌注流量为17～25 ml/min。对不能成功阻断二尖瓣峡部传导者予以冠状静脉窦内消融,能量设置为20～25 W,温度为43℃,冷盐水灌注流量为17 ml/min。术中同时探查双侧肺静脉电位,如传导恢复予以再次隔离。
结果8例二尖瓣峡部房速,2例临床上呈无休止性发作,6例为阵发性,可被程序刺激诱发。房速的周长217.5±20.6 ms,其中顺钟向折返5例,逆钟向折返3例。二尖瓣峡部线性消融至完全性双向传导阻滞5例,3例心内膜途径失败者经冠状静脉窦内消融,其中1例获得成功。术后随访5.5±4.3个月,6例无房颤及房速发作,1例仍有阵发性房速发作。另1例术后房速呈无休止发作,予以胺碘酮及美托洛尔控制心室率治疗。
结论环肺静脉线性消融术后发生的二尖瓣峡部房速与左房线性消融治疗房颤的致心律失常作用有关,其主要的机制是消融线和缝隙相关的大折返性心动过速。于左下肺静脉口部下缘至二尖瓣环之间行线性消融可阻断二尖瓣峡部传导。但部分患者需经冠状静脉窦内消融,有时虽经心内膜及冠状静脉窦内联合消融仍不能完全阻断峡部传导。
Objective The purpose of this study was to evaluate the electrophysiological mechanism of atrial flutter after surgical repair procedure (SAFL) and typical atrial flutter (TAFL) by analysis of the cavo-tricuspid isthmus conduction time (CTI-CT) and the conduction velocity of the two groups.
Methods Nine patients (47.2±16.9 years, 6 males) with SAFL and eight patients (age 52.0±19.1 years, 7 males) with TAFL received catheter ablation from February 2006 to January 2008 under the guidance of the noncontact mapping system. Three-dimensional geometry of right atrium was reconstructed and the special anatomical landmarks were tagged on the map. After geometry making, the isopotential maps of each tachycardia was created to analyze its activation sequence, reentrant circuit, critical isthmus. Then the tachycardia cycle length (TCL), conduction time and conduction velocity in the cavo-tricuspid isthmus (CTI), the right atrium free wall (RAFW) and atrial septum (AS) of the two groups were measured and compared with each other. The CTI-CT was defined as the conduction time between the seven o'clock of the tricuspid annulus (TV7) and the upper margin of the coronary sinus ostium (CSO). The conduction time of RAFW was defined as the conduction time between TV12 and TV7. The conduction time of AS was defined as the conduction time between CSO and TV12. Conduction velocities in CTI, RAFW and AS were measured by the ratio of the length and the conduction time in each part. Linear ablation was performed in the critical isthmus guided by three dimensional mapping systems to the endpoint of bidirectional block.
Results The mean cycle length was 254.3±50.7 ms in SAFL and 219.8±18.9 ms in TAFL. CTI-CT in SAFL was significantly shorter than TAFL (50.5±13.0 ms vs 76.6±11.6 ms) (P < 0.05) while conduction velocity was faster than the latter (0.84±0.15 m/s vs 0.53±0.15 m/s) (P < 0.05 ) . The conduction time was significantly longer (148.4±36.4 ms vs 82.1±28.4 ms) with the conduction velocity slower (0.42±0.14 m/s vs 0.76±0.25 m/s) in RAFW in SAFL group than those in TAFL group (P < 0.05 ) . There was no significant difference in conduction time (55.3±18.5 ms vs 61.1±19.9 ms) and the conduction velocity (0.94±0.29 m/s vs 0.81±0.23 m/s) of AS between the two groups (P > 0.05 ). All the tachycardia was successfully eliminated by catheter ablation guided by noncontact mapping system. After a mean follow up of 10.1±6.6 months,one tachycardia in SAFL group recurred and received a second ablation.
Conclusions The slow conduction in the CTI is the basic electrophysiological substrate for TAFL, but in SAFL, CTI is more a critical anatomical isthmus than an electrophysiological isthmus. The slow conduction area of SAFL was located in the RAFW.
Objective The purpose of this study is to demonstrate the mechanisms of mitral isthmus dependent atrial tachycardia (MI-AT) after circumferential pulmonary vein isolation (CPVI) for the treatment of atrial fibrillation (AF) and to discuss its ablation strategy.
Methods One hundred and twenty-two consecutive patients with AF were treated with CPVI guided by EnSite-NavX and circular mapping catheter, thirty-two of which received a repeat ablation procedure because of recurrent AF or AT. MI- AT was found in eight patients( male 6, mean age 54.9±8.6years) which was confirmed by electrophysiological study and EnSite-NavX three-dimension mapping system. Linear lesion was performed between the ostium of left inferior pulmonary vein and the mitral annulus ( power 35～40 W, temperature 43～45℃, irrigation rate 17～25 ml/ min ). If the complete bidirectional conduction block of mitral isthmus could not be achieved, further ablation would be attempted within the coronary sinus ( power 20～25 W , temperature 43℃, irrigation rate 17ml/ min). Reisolation is necessary when reconduction between pulmonary vein and left atrium was found.
Results Three-dimension mapping showed clockwise activation going around mitral ring in five patients while counterclockwise activation in three patients. The mean cycle length of MI-AT was 217.5±20.6 ms. Bidirectional block of mitral isthmus was obtained in five patients after endocardial linear lesions. The left three patients which were failed by endocardial approach had coronary sinus attempt with only one success. After a mean follow up of 5.5±4.3 months, six patients were free of AT or AF attack, one patient still had paroxysmal AT, another patient developed incessant AT and had the medication of Amiodarone and Metoprolol to control the heart rate.
Conclusions MI-AT can be developed because of the proarrhythmia effect of CPVI for the treatment of AF and also be due to macro-reentrant induced by incomplete lines or recovery conduction. Bidirectional block of the mitral isthmus can be achieved by liner ablation between the ostium of left inferior pulmonary vein and the mitral annulus. In some patients, additional ablation should be attempted within coronary sinus. But this endpoint could not be always obtained even after the joint ablation approach both endocardially and epicardially.
引文
1. Granada J, Uribe W, Chyou PH, et al. Incidence and predictors of atrial flutter in the general population. J Am Coll Cardiol 2000; 36: 2242-2246.
2. Cosio FG, Lopez GM, Goicolea A, et al. Electrophysiologic studies in atrial flutter. Clin Cardiol 1992; 15: 667-673.
3. Olshansky B, Okumura K, Hess PG, et al. Demonstration of an area of slow conduction in human atrial flutter. J Am Coll Cardioal 1990; 16: 1639-1648.
4. Klein G, GiraudonG, Sharma A, et al. Demonstration of macroreentry and feasibility of operative therapy in the common type of atrial flutter. Am J Cardiol 1986; 57: 587-591.
5. Spach MS , Dolber PC , Heidlage J F, et al. Related articles in fluence of the passive anisotropic properties on directional differences in propagation following modification of the sodium conductance in human atrial muscle : a model of reentry based on anisotropic discontinuous propagation. Circ, Res 1988; 62: 811-832.
6. Yamabe H, Misumi I, Fukushima H, et al. Conduction properties of the crista terminalis and its influence on the right atrial activation sequence in patients with typical atrial flutter. PACE 2002; 25: 132-141.
7. Kanter RJ, Garson AJ. Atrial arrhythmias during chronic follow - up of surgery for complex congenital heart disease. PACE 1997; 20: 502-511.
8. Akar JG, Kok LC, Haines DE, et al. Coexistence of type I atrial flutter and intra-atrial reentrant tachycardia in patients with surgically corrected congenital heart disease. J Am Coll Cardiol 2001; 38: 377-384.
9. Cauchemez B, Haissaguerre M, Fischer B, et al. Electrophysiological effects of catheter ablation of inferior vena cava-tricuspid annulus isthmus in common atrial flutter. Circulation 1996; 93: 284-294.
10. Poty H, Saoudi N, Haissaguerre M, et ah Radiofrequency catheter ablation of atrial flutter: Further insights in to the various types of isthmus block: Application to ablation during sinus rhythm. Circulation 1996; 94: 3198-3203.
1. Cosio FG, Lopez GM, Goicolea A, et al. Electrophysiologic studies in atrial flutter. Clin Cardiol 1992; 15: 667-673.
2. Olshansky B, Okumura K, Hess PG, et al Demonstration of an area of slowconduction in human atrial flutter. J Am Coll Cardioal 1990; 16:1639-1648.
3. Klein G, Giraudon G, Sharma A, et al. Demonstration of macroreentry and feasibility of operative therapy in the common type of atrial flutter. Am J Cardiol 1986; 57: 587- 591.
4. Willems S, Weiss C, Ventura R, et al. Catheter ablation of atrial flutter guided by electroanatomic mapping (CARTO): a randomized comparison to the conventional approach. J Cardiovasc Electrophysiol 2000; 11: 1223-1230.
5. Kottkamp H, Hugl B, Krauss B, et al. Electromagnetic versus fluoroscopic mapping of the inferior isthmus for ablation of typical atrial flutter: a prospective randomized study. Circulation 2000; 102: 2082-2086.
6. Kall J, Rubenstein DS, Kopp DE, et al. Atypical atrial flutter originating in the right atrial free wall. Circulation 2000; 101: 270-279.
7. Nakagawa H, Shah N, Matsudaira K, et al: Characterization of reentrant circuit in macroreentrant right atrial tachycardia after surgical repair of congenital heart disease: isolated channels between scars allow "focal" ablation. Circulation 2001; 103: 699-709.
8. Akar JG, Kok LC, Haines DE, et al. Coexistence of type I atrial flutter and Intra-atrial reentrant tachycardia in patients with surgically corrected congenital heart disease. J Am Coll Cardiol 2001; 38: 377- 384.
9. Kalman JM, VanHare GF, Olgin JF, et al. Ablation of "incisional reentrant atrial tachycardia complicating surgery for congenital heart disease. Use of entrainment to define a critical isthmus of conduction. Circulation 1996; 93: 502-512.
10. Tai CT, Liu TY, Lee PC, et al. Non-contact mapping to guide radiofrequency ablation of atypical right atrial flutter. J Am Coll Cardiol 2004; 44: 1080-1086.
11. Nabar C, Timmermans A, Medeiros K, et al. Radiofrequency ablation of atrial arrhythmias after previous open-heart surgery. Europace 2005; 7:40-49.
12. Spach MS, Dolber PC, Heidlage J F. et al. Related articles influence of the passive anisotropic properties on directional differences in propagation following modification of the sodium conductance in human atrial muscle : a model of reentry based on anisotropic discontinuous propagation. Circ, Res 1988; 62: 811-832.
1. Lundstrom T, Ryden L. Chronic atrial fibrillation. Long-term results of direct current conversion. Acta Med Scand 1988; 223: 53-59.
2. Arora R, Verheule S, Scott L, et al. Arrhythmogenic substrate of the pulmonary veins assessed by high resolution optical mapping. Circulation 2003; 107: 1816-1821.
3. Mandapati R, Skailes A, Chen J, et al. Stable microreentrant sources as a mechanism of atrial fibrillation in the isolated sheep heart. Circulation 2000; 101: 194-199.
4. Jalife J, Berenfeld O, Mansour M. Mother rotors and fibrillatory conduction: A mechanism of atrial fibrillation . Cardiovasc Res 2002; 54: 204-216.
5. Cappato R, Calkins H, Chen SA, et al. Worldwide survey on the methodes, efficacy, and safety of catheter ablation for human atrial fibrillation. Circulation 2005; 111: 1100-1105.
6. Gerstenfeld EP, Callans DJ, Dixit S, et al. Mechanisms of Organized Left Atrial Tachycardias Occurring After Pulmonary Vein Isolation. Circulation 2004; 110: 1351-1357.
7. Chugh A, Oral H, Lemola K, et al. Prevalence, mechanisms, and clinical significance of macroreentrant atrial tachycardia during and following left atrial ablation for atrial fibrillation. Heart Rhythm 2005; 2:464-471.
8. Deisenhofer I, Estner H, Zrenner B, et al. Left atrial tachycardia after circumferential pulmonary vein ablation for atrial fibrillation: incidence, electrophysiological characteristics and results of radiofrequency ablation. Europace 2006; 8: 573-582.
9. Raviele A, Themistoclakis S, Rossillo A, et al. Iatrogenic postatrial fibrillation ablation left atrial tachycardiaP flutter : How to prevent and treat it? J Cardiovase Electrophysiol 2005; 16 : 298-301.
10. Mesas CE, Pappone C, Lang CCE, et al. Left atrial tachycardia after circumferential pulmonary vein ablation for atrial fibrillation: Electroanatomic characterization and treatment. J Am Coll Cardiol 2004; 44: 1071-1079.
11.Poppone C, Rosanio S , Oreto G, et al . Circumferential radiofrequency ablation of pulmonary veins ostia. A new anatomic approach for curing atrial fibrillation. Circulation 2000; 102: 2619-2628.
12. Ouyang F, Antz M, Ernst S, et al. Recovered pulmonary vein conduction as a dominant factor for recurrent atril tachyarrhythmias after complete circular isolation of the pulmonary veins : lessons from double lasso technique. Circulation 2005; 111: 127-135.
13. Pappone C, Manguso F, Vicedomini G, et al. Prevention of ratrogenic atrial tachycardia after ablation of atrial fibrillation: A prospective randomized study comparing circumferential pulmonary vein ablation with a modified approach. Circulation 2004; 110: 3036-3042.
14. Jais P, Hocini M, Hsu L-F, et al. Technique and Results of Linear Ablation at the Mitral Isthmus. Circulation 2004; 110: 2996-3002.
15. Fred H.M. Wittkamp F, Matthijs F. et al. Where to draw the mitral isthmus line in catheter ablation of atrial fibrillation: histological analysis. European Heart Journal 2005; 26: 689-695.
16. Becker A. Left atrial isthmus: Anatomic aspects relevant for linear catheter ablation procedures in humans. J Cardiovasc Electrophysiol 2004; 15:809-812.
1. Haissaguerre M, Jais P, Shah DC, et al. Spontaneous initiation of atrial fibrillation by ectopic beats originating in the pulmonary veins. N Eng J Med 1998; 339: 659-666.
2. Poppone C, Rosanio S, Oreto G, et al. Circumferential radiofrequency ablation of pulmonary veins ostia. A new anatomic approach for curing atrial fibrillation. Circulation 2000; 102: 2619-2628.
3. Gerstenfeld EP, Callans DJ, Dixit S, et al. Mechanisms of organized left tachycardias occurring after pulmonary vein isolation. Circulation 2004; 110: 1351-1357.
4. Chae H, Oral H, Good E, et al. Atrial Tachycardia After Circumferential Pulmonary Vein Ablation of Atrial Fibrillation: Mechanistic Insights, Results of Catheter Ablation, and Risk Factors for Recurrence. J Am Cardiol 2007; 50: 1781-1787.
5. Ouyang F, Antz M, Ernst S, et al. Recovered pulmonary vein conduction as a dominant factor for recurrent atrial tachyarrhythmias after complete circular isolation of the pulmonary veins: lessons from double Lasso technique. Circulation 2005; 111: 127-135.
6. Nademanee K, McKenzie J, Kosar E, et al. A approach for catheter ablation of atrial fibrillation: mapping of the electrophysiologic substrate. J Am Coll Cardiol 2004; 43: 2044-2053.
7. Haissaguerre M, Hocini M, Sanders P, et al. Catheter ablation of long-lasting persistent atrial fibrillation: Clinical outcome and mechanism of subsequent arrhythmia. J Cardiovasc Electrophysiol 2005; 16: 1138-1145
8. Pappone C, Manguso F, Vicedomini G, et al. Prevention of ratrogenic atrial tachycardia after ablation of atrial fibrillation: A prospective randomized study comparing circumferential pulmonary vein ablation with a modified approach. Circulation 2004; 110: 3036-3042.
9. Jais P, Hocini M, Hsu LF, et al. Technique and results of linear ablation at the mitral isthmus. Circulation 2004; 110: 2996-3002.
10. Oral H, Chugh A, Lemola K, et al. Noninducibility of atrial fibrillation and an end oint of left atrial circumferential ablation for paroxysmal atrial fibrillation. A randomized study. Circulation 2004; 110:2797-2801.
11. Hashimoto T, Tada H, Naito N, et al. Prevalence and characteristics of left atrial tachycardia following left atrial catheter ablation. PACE 2007; 30: S94-97.
12. Chugh AC, Oral H, Lemola K, et al. Prevalence, mechanisms, and clinical significance of macroreentrant atrial tachycardia during and following leftatrial ablation for atrial fibrillation. Heart Rhythm 2005; 2: 464-471.
13. Daoud EG, Weiss R, et al. Proarrhythmia of circumferential left atrial lesions for management of atrial fibrillation. J Cardiovasc Electrophsiol 2005; 16: 1160-1165.
14. Fred H.M. Wittkamp F, Matthijs F. et al. Where to draw the mitral isthmus line in catheter ablation of atrial fibrillation: histological analysis. European Heart Journal 2005; 26: 689-695.
15. Becker A. Left atrial isthmus: Anatomic aspects relevant for linear catheter ablation procedures in humans. J Cardiovasc Electrophysiol 2004; 15:809-812.
16. Takahashi Y, Jais P, Hocini M, et al. Acute occlusion of the left circumflex cornary artery during mitral isthmus linear ablation. J Cardiovasc Electrophysiol 2005; 16: 1104-1107.
17. Deisenhofer H, Estner B, Zrenner J, et al. Left atrial tachycardia after circumferential pulmonary vein ablation for atrial fibrillation: incidence, electrophysiological characteristics, and results of radiofrequency ablation. Europace 2006; 8: 573-582.
2. Cosio FG, Lopez GM, Goicolea A, et al. Electrophysiologic studies in atrial flutter. Clin Cardiol 1992; 15: 667-673.
3. Olshansky B, Okumura K, Hess PG, et al. Demonstration of an area of slow conduction in human atrial flutter. J Am Coll Cardioal 1990; 16: 1639-1648.
4. Klein G, GiraudonG, Sharma A, et al. Demonstration of macroreentry and feasibility of operative therapy in the common type of atrial flutter. Am J Cardiol 1986; 57: 587-591.
5. Spach MS , Dolber PC , Heidlage J F, et al. Related articles in fluence of the passive anisotropic properties on directional differences in propagation following modification of the sodium conductance in human atrial muscle : a model of reentry based on anisotropic discontinuous propagation. Circ, Res 1988; 62: 811-832.
6. Yamabe H, Misumi I, Fukushima H, et al. Conduction properties of the crista terminalis and its influence on the right atrial activation sequence in patients with typical atrial flutter. PACE 2002; 25: 132-141.
7. Kanter RJ, Garson AJ. Atrial arrhythmias during chronic follow - up of surgery for complex congenital heart disease. PACE 1997; 20: 502-511.
8. Akar JG, Kok LC, Haines DE, et al. Coexistence of type I atrial flutter and intra-atrial reentrant tachycardia in patients with surgically corrected congenital heart disease. J Am Coll Cardiol 2001; 38: 377-384.
9. Cauchemez B, Haissaguerre M, Fischer B, et al. Electrophysiological effects of catheter ablation of inferior vena cava-tricuspid annulus isthmus in common atrial flutter. Circulation 1996; 93: 284-294.
10. Poty H, Saoudi N, Haissaguerre M, et ah Radiofrequency catheter ablation of atrial flutter: Further insights in to the various types of isthmus block: Application to ablation during sinus rhythm. Circulation 1996; 94: 3198-3203.
1. Cosio FG, Lopez GM, Goicolea A, et al. Electrophysiologic studies in atrial flutter. Clin Cardiol 1992; 15: 667-673.
2. Olshansky B, Okumura K, Hess PG, et al Demonstration of an area of slowconduction in human atrial flutter. J Am Coll Cardioal 1990; 16:1639-1648.
3. Klein G, Giraudon G, Sharma A, et al. Demonstration of macroreentry and feasibility of operative therapy in the common type of atrial flutter. Am J Cardiol 1986; 57: 587- 591.
4. Willems S, Weiss C, Ventura R, et al. Catheter ablation of atrial flutter guided by electroanatomic mapping (CARTO): a randomized comparison to the conventional approach. J Cardiovasc Electrophysiol 2000; 11: 1223-1230.
5. Kottkamp H, Hugl B, Krauss B, et al. Electromagnetic versus fluoroscopic mapping of the inferior isthmus for ablation of typical atrial flutter: a prospective randomized study. Circulation 2000; 102: 2082-2086.
6. Kall J, Rubenstein DS, Kopp DE, et al. Atypical atrial flutter originating in the right atrial free wall. Circulation 2000; 101: 270-279.
7. Nakagawa H, Shah N, Matsudaira K, et al: Characterization of reentrant circuit in macroreentrant right atrial tachycardia after surgical repair of congenital heart disease: isolated channels between scars allow "focal" ablation. Circulation 2001; 103: 699-709.
8. Akar JG, Kok LC, Haines DE, et al. Coexistence of type I atrial flutter and Intra-atrial reentrant tachycardia in patients with surgically corrected congenital heart disease. J Am Coll Cardiol 2001; 38: 377- 384.
9. Kalman JM, VanHare GF, Olgin JF, et al. Ablation of "incisional reentrant atrial tachycardia complicating surgery for congenital heart disease. Use of entrainment to define a critical isthmus of conduction. Circulation 1996; 93: 502-512.
10. Tai CT, Liu TY, Lee PC, et al. Non-contact mapping to guide radiofrequency ablation of atypical right atrial flutter. J Am Coll Cardiol 2004; 44: 1080-1086.
11. Nabar C, Timmermans A, Medeiros K, et al. Radiofrequency ablation of atrial arrhythmias after previous open-heart surgery. Europace 2005; 7:40-49.
12. Spach MS, Dolber PC, Heidlage J F. et al. Related articles influence of the passive anisotropic properties on directional differences in propagation following modification of the sodium conductance in human atrial muscle : a model of reentry based on anisotropic discontinuous propagation. Circ, Res 1988; 62: 811-832.
1. Lundstrom T, Ryden L. Chronic atrial fibrillation. Long-term results of direct current conversion. Acta Med Scand 1988; 223: 53-59.
2. Arora R, Verheule S, Scott L, et al. Arrhythmogenic substrate of the pulmonary veins assessed by high resolution optical mapping. Circulation 2003; 107: 1816-1821.
3. Mandapati R, Skailes A, Chen J, et al. Stable microreentrant sources as a mechanism of atrial fibrillation in the isolated sheep heart. Circulation 2000; 101: 194-199.
4. Jalife J, Berenfeld O, Mansour M. Mother rotors and fibrillatory conduction: A mechanism of atrial fibrillation . Cardiovasc Res 2002; 54: 204-216.
5. Cappato R, Calkins H, Chen SA, et al. Worldwide survey on the methodes, efficacy, and safety of catheter ablation for human atrial fibrillation. Circulation 2005; 111: 1100-1105.
6. Gerstenfeld EP, Callans DJ, Dixit S, et al. Mechanisms of Organized Left Atrial Tachycardias Occurring After Pulmonary Vein Isolation. Circulation 2004; 110: 1351-1357.
7. Chugh A, Oral H, Lemola K, et al. Prevalence, mechanisms, and clinical significance of macroreentrant atrial tachycardia during and following left atrial ablation for atrial fibrillation. Heart Rhythm 2005; 2:464-471.
8. Deisenhofer I, Estner H, Zrenner B, et al. Left atrial tachycardia after circumferential pulmonary vein ablation for atrial fibrillation: incidence, electrophysiological characteristics and results of radiofrequency ablation. Europace 2006; 8: 573-582.
9. Raviele A, Themistoclakis S, Rossillo A, et al. Iatrogenic postatrial fibrillation ablation left atrial tachycardiaP flutter : How to prevent and treat it? J Cardiovase Electrophysiol 2005; 16 : 298-301.
10. Mesas CE, Pappone C, Lang CCE, et al. Left atrial tachycardia after circumferential pulmonary vein ablation for atrial fibrillation: Electroanatomic characterization and treatment. J Am Coll Cardiol 2004; 44: 1071-1079.
11.Poppone C, Rosanio S , Oreto G, et al . Circumferential radiofrequency ablation of pulmonary veins ostia. A new anatomic approach for curing atrial fibrillation. Circulation 2000; 102: 2619-2628.
12. Ouyang F, Antz M, Ernst S, et al. Recovered pulmonary vein conduction as a dominant factor for recurrent atril tachyarrhythmias after complete circular isolation of the pulmonary veins : lessons from double lasso technique. Circulation 2005; 111: 127-135.
13. Pappone C, Manguso F, Vicedomini G, et al. Prevention of ratrogenic atrial tachycardia after ablation of atrial fibrillation: A prospective randomized study comparing circumferential pulmonary vein ablation with a modified approach. Circulation 2004; 110: 3036-3042.
14. Jais P, Hocini M, Hsu L-F, et al. Technique and Results of Linear Ablation at the Mitral Isthmus. Circulation 2004; 110: 2996-3002.
15. Fred H.M. Wittkamp F, Matthijs F. et al. Where to draw the mitral isthmus line in catheter ablation of atrial fibrillation: histological analysis. European Heart Journal 2005; 26: 689-695.
16. Becker A. Left atrial isthmus: Anatomic aspects relevant for linear catheter ablation procedures in humans. J Cardiovasc Electrophysiol 2004; 15:809-812.
1. Haissaguerre M, Jais P, Shah DC, et al. Spontaneous initiation of atrial fibrillation by ectopic beats originating in the pulmonary veins. N Eng J Med 1998; 339: 659-666.
2. Poppone C, Rosanio S, Oreto G, et al. Circumferential radiofrequency ablation of pulmonary veins ostia. A new anatomic approach for curing atrial fibrillation. Circulation 2000; 102: 2619-2628.
3. Gerstenfeld EP, Callans DJ, Dixit S, et al. Mechanisms of organized left tachycardias occurring after pulmonary vein isolation. Circulation 2004; 110: 1351-1357.
4. Chae H, Oral H, Good E, et al. Atrial Tachycardia After Circumferential Pulmonary Vein Ablation of Atrial Fibrillation: Mechanistic Insights, Results of Catheter Ablation, and Risk Factors for Recurrence. J Am Cardiol 2007; 50: 1781-1787.
5. Ouyang F, Antz M, Ernst S, et al. Recovered pulmonary vein conduction as a dominant factor for recurrent atrial tachyarrhythmias after complete circular isolation of the pulmonary veins: lessons from double Lasso technique. Circulation 2005; 111: 127-135.
6. Nademanee K, McKenzie J, Kosar E, et al. A approach for catheter ablation of atrial fibrillation: mapping of the electrophysiologic substrate. J Am Coll Cardiol 2004; 43: 2044-2053.
7. Haissaguerre M, Hocini M, Sanders P, et al. Catheter ablation of long-lasting persistent atrial fibrillation: Clinical outcome and mechanism of subsequent arrhythmia. J Cardiovasc Electrophysiol 2005; 16: 1138-1145
8. Pappone C, Manguso F, Vicedomini G, et al. Prevention of ratrogenic atrial tachycardia after ablation of atrial fibrillation: A prospective randomized study comparing circumferential pulmonary vein ablation with a modified approach. Circulation 2004; 110: 3036-3042.
9. Jais P, Hocini M, Hsu LF, et al. Technique and results of linear ablation at the mitral isthmus. Circulation 2004; 110: 2996-3002.
10. Oral H, Chugh A, Lemola K, et al. Noninducibility of atrial fibrillation and an end oint of left atrial circumferential ablation for paroxysmal atrial fibrillation. A randomized study. Circulation 2004; 110:2797-2801.
11. Hashimoto T, Tada H, Naito N, et al. Prevalence and characteristics of left atrial tachycardia following left atrial catheter ablation. PACE 2007; 30: S94-97.
12. Chugh AC, Oral H, Lemola K, et al. Prevalence, mechanisms, and clinical significance of macroreentrant atrial tachycardia during and following leftatrial ablation for atrial fibrillation. Heart Rhythm 2005; 2: 464-471.
13. Daoud EG, Weiss R, et al. Proarrhythmia of circumferential left atrial lesions for management of atrial fibrillation. J Cardiovasc Electrophsiol 2005; 16: 1160-1165.
14. Fred H.M. Wittkamp F, Matthijs F. et al. Where to draw the mitral isthmus line in catheter ablation of atrial fibrillation: histological analysis. European Heart Journal 2005; 26: 689-695.
15. Becker A. Left atrial isthmus: Anatomic aspects relevant for linear catheter ablation procedures in humans. J Cardiovasc Electrophysiol 2004; 15:809-812.
16. Takahashi Y, Jais P, Hocini M, et al. Acute occlusion of the left circumflex cornary artery during mitral isthmus linear ablation. J Cardiovasc Electrophysiol 2005; 16: 1104-1107.
17. Deisenhofer H, Estner B, Zrenner J, et al. Left atrial tachycardia after circumferential pulmonary vein ablation for atrial fibrillation: incidence, electrophysiological characteristics, and results of radiofrequency ablation. Europace 2006; 8: 573-582.