|
大折返性房速和局灶性房速，可谓后房颤导管消融时代面临的主要问题，肺静脉电隔离术是目前导管消融治疗房颤的基石。但文献报道以及临床实践中发现，房颤导管消融术后的快速性房性心律失常的发生率较高（可达1.2%~25%），对于慢性持续性房颤，旨在终止房颤的消融手段（包括各类线性消融以及心房内碎裂电位CFAE消融）的过多应用，也会增加术后房速的发生。这类导管消融术后的房速往往伴有较快的心室率，且药物选择困难，心室率常控制不佳，部分患者短时间内可致心功能恶化，同时，如不及时终止这类房速恢复窦性心律，心房的基质改变又会影响房颤消融效果。 对于阵发性房颤，特别是术中提示有明确靶静脉的患者，单纯环肺静脉消融术后如发作房速多为局灶性，主要是由于靶静脉和左心房之间传导恢复所致，此外，还有不到10%的患者为其他部位的灶性触发和（或）驱动，如上腔静脉、左心耳等。而对于持续性房颤，术后房速多为大折返性，这是因为环肺静脉电隔离术（CPVI）后相当于人为在左房内增加了两圈传导屏障，这些人工的传导屏障和二尖瓣环一起，构成了术后左房内大折返性房速的电生理基础。因次，这类房速可以认为是一种医源性心律失常，常见的这类左房大折返性房速有两种，一种是围绕左房顶部的折返，另一种是围绕二尖瓣环的折返。此外，还有两种少见的形式，一种是左房顶部和二尖瓣峡部均参与的“8”字型折返，另一种是由于环肺静脉消融线遗留GAP造成的双GAP介导的折返性房速。 房速的主要标测方法有激动顺序标测以及拖带标测，有时需要联合应用，对于局灶性房速，其激动标测显示心内膜激动顺序由最早激动点向四周传播，所在心房的激动时间小于心动过速周长，对于局部微折返房速，粗标类似局灶性房速，但起源点常可见局部电位明显碎裂，持续时间可能会接近心动过速周长。 对于大折返性房速，感兴趣窗口（WOI）的设置如按De Pointe方法设置，CARTO激动图上首尾相接部位应为缓慢传导部位或关键部位。在CARTO激动顺序标测中，是否合理准确采点至为重要：①采点密度应适中，不留死角，但对感兴趣区应精细标测；②在心动过速节律或激动顺序发生变化时应重新设置WOI进行新标测；③避免在早搏时取点；④采点时应注意参考电极自动取点是否正确，否则应人工修正；⑤避免将干扰电位或远隔心腔的电位认作局部电位；⑥对于局部电位起始部不明的地方如疤痕、碎裂电位、双电位应作注解待事后总揽全图后再修正或判断。 拖带为另一重要的标测手段，拖带需要稳定的折返环路，如CL和PPI的差值在30 ms以内，说明起搏部位在主导折返环路附近，但不能判断是否为折返的关键部位。但拖带有其局限性：①拖带刺激有时会意外终止房速；②拖带刺激周围如存在传导延迟，则PPI 结果会不准确；③拖带频率过快，会造成起搏周围功能性阻滞，也会导致PPI不准确。为避免上述情况，拖带周长仅比心动过速周长短20~30 ms即可。 房速有时也会用到心房的基质标测，通常用于以下情况：①激动标测未能明确显示折返环路，如折返环路为局部折返而非常规大折返环路（如左房内顶部折返，二尖瓣峡部或三尖瓣峡部折返）或微折返，②心房内有明确瘢痕（如手术疤痕）或疤痕广泛且激动标测未能显示折返部位。此外，单极标测常用于验证局灶性房速的最早起源点而较少作为单一的标测方法。 对于三尖瓣峡部、二尖瓣峡部以及左房顶部线的消融，方法不再赘述，需要强调的是，对于二尖瓣峡部的消融，有高达近70%的患者需要冠状窦内远端的消融才能达到峡部的双向阻滞，对于一些局部的折返，消融的策略是用有效消融损伤连接疤痕和邻近的解剖电屏障阻断折返环路，如外科术后的右房环绕刀口疤痕的大折返性房速，可视消融的难易程度，消融线连接疤痕和三尖瓣环、下腔静脉或上腔静脉。 Mapping and ablation of macroreentrant atrial tachycardia and focal atrial tachycardia Shaowen Liu, Cardiology Department, Shanghai Jiao Tong University affiliated the First People’s Hospital, Shanghai, China The macroreentrant atrial tachycardia and focal atrial tachycardia are always concerned in post-atrial fibrillation ablation era. Pulmonary veins electrical isolation is the cornerstone for atrial fibrillation ablation, but atrial tachycardia is often encountered after procedures. The incidence of such atrial tachycardia varies from 1.2% to 25%. Some aggressive approaches aim to terminate atrial fibrillation (linear ablation or CFAE ablation e.g.) also increase onset of such atrial tachycardia. The atrial tachycardia is often associated fast ventricular rate which can further worsen heart performance, and if not terminated in time such atrial tachycardia causes atrial matrix remodeling which could perpetuate atrial fibrillation if recurrence happens. Atrial tachycardia after ablation for paroxysmal atrial fibrillation is often focal origin if target pulmonary veins are identified during procedure. The resumed target pulmonary vein-atrium connection conduction contributes its occurrence, and also less than 10% atrial tachycardia after procedure are focal origin for example SVC or left appendage. The macroreentrant atrial tachycardias are more prevalent in persistent atrial fibrillation after procedure. Many authors consider such atrial tachycardia an iatrogenic disease since two artificial circumferential PV rings combining mitral annula may comprise several reentrant pathways which contribute to genesis of atrial tachycardia. Frequently two type of macroreentrant atrial tachycardia are encountered. One is reentrant pathway surrounding roof of left atrium, and the other is surrounding left atrial isthmus. Another two sparse circumstance are number “8” type reentrant pathways with left atrial roof and mitral isthmus both engaged, and those mediated by two GAPs left in pulmonary veins. The activation sequence mapping and entrainment are two major approaches for atrial tachycardia after atrial fibrillation ablation. The activation type of an focal origin is concentric from an earliest point and atrial activation time is less than that of tachycardia cycle length (CL). For microreentrant atrial tachycardia, the panorama of left atrium activition is quite similar to a focal origin. But detailed mapping around earliest origin can reveal continuous local fragmented potential. The lasting time of such potential nearly equals to tachycardia CL. For macroreentrant atrial tachycardia, if WOI is set according De Pointe’s method the “Early Meet Late” will identify critical reentrant channel that means slow conduction area. During activation mapping with CARTO system proper point collection is very important with reasonable density and no place left. The area of interest should be mapped with detail. The WOI should be reset and begin a remap if tachycardia rate or sequence changes. The operator should confirm every point is picked right and avoid inappropriate point picking arising from interferential potential. Some potential with difficult discernable initial part should be labeled and wait for later reevaluation and revised. The entrainment is also a critical mapping approach for atrial tachycardia. The reentrant pathway should be stable or stimulation may terminate the tachycardia, or it make difficult to capture atrium. If difference between CL and PPI is within 30ms, it means the pacing site is just in the reentrant pathway or vicinity of it. But it doesn’t indicate the pacing site is in the critical reentrant channel. Sometimes the entrainment doesn’t work because of too fast pacing rate which induces functional exit blocking around. Entrainment cycle with 20-30ms less than tachycardia CL is enough. Matrix mapping is occasionally used for complex atrial tachycardia. Some unusual reentrant pathways arising from post cardiac surgery scar or primary extensive scars in atrial endocardium. For such cases the activation mapping sometimes can’t reveal a clear reentrant pathway. In this circumstance matrix mapping can provide additional valuable information. The unipolar mapping is often used to confirm the earliest origin in focal atrial tachycardia. The general principles, rationale, and working of the catheter ablation have been explained well in the existing literature. We should emphasize that about 70% of cases need intracoronary vein radiofrequency delivery to guarantee bidirectional mitral isthmus block. For some local reentrant atrial tachycardia, the strategy is to interrupt reentrant pathway by connecting the scar to a physiological electrical anatomic barrier such as SVC, IVC or an annula. |
|
|
