Mainigi Sumeet K, Greenspan Allan M
Section of Electrophysiology, Division of Cardiovascular Disease, The Institute for Heart and Vascular Health, Einstein Medical Center, Philadelphia, PA, USA.
J Innov Card Rhythm Manag. 2019 May 15;10(5):3642-3650. doi: 10.19102/icrm.2019.100501. eCollection 2019 May.
Contact impedance mapping can differentiate focal atrial tachyarrhythmias from macroreentry (atrial flutter) and localized reentry (atrioventricular nodal reentry tachycardia) by detecting different patterns of regional unipolar tissue impedance distribution. Specifically, focal atrial tachycardia (AT) is characterized by the finding of a contiguous low-impedance area (CLIA) adjacent to the site of origin, surrounded by normal tissue impedance levels. However, it remains unclear whether or not this finding could distinguish different mechanisms of focal AT. In the present study, we sought to determine whether impedance and voltage maps in patients with microreentrant AT differ from those created due to triggered activity. Consecutive patients undergoing electrophysiologic study and the ablation of AT were included. All patients underwent mapping and ablation procedures in a standard manner. Contact impedance and voltage maps were collected in the background and analyzed offline for comparison. A total of 50 patients with 75 focal ATs were studied and ablated, and the mechanism of AT (ie, triggered activity versus microreentry) was determined. The 41 ATs attributed to triggered activity in 30 patients all demonstrated a CLIA containing or adjacent to the successful ablation site, while the 34 ATs in the 20 patients attributed to microreentry demonstrated uniform impedance. In contrast, microreentrant AT patients were more likely to have scar located adjacent to the site of origin (88.9% versus 18.2%). Three-dimensional mapping employing both contact impedance mapping and voltage mapping can reliably identify the mechanism of focal AT.
接触阻抗标测可通过检测局部单极组织阻抗分布的不同模式,区分局灶性房性快速心律失常与大折返(心房扑动)和局限性折返(房室结折返性心动过速)。具体而言,局灶性房性心动过速(AT)的特征是在起源部位附近发现一个连续的低阻抗区域(CLIA),周围是正常组织阻抗水平。然而,这一发现能否区分局灶性AT的不同机制仍不清楚。在本研究中,我们试图确定微折返性AT患者的阻抗图和电压图是否与触发活动所致的图不同。纳入接受电生理检查和AT消融的连续患者。所有患者均以标准方式进行标测和消融操作。在背景状态下收集接触阻抗和电压图,并离线分析以进行比较。共研究并消融了50例患有75次局灶性AT的患者,并确定了AT的机制(即触发活动与微折返)。30例患者中归因于触发活动的41次AT均显示出一个包含成功消融部位或与之相邻的CLIA,而20例患者中归因于微折返的34次AT显示出均匀的阻抗。相比之下,微折返性AT患者更有可能在起源部位附近有瘢痕(88.9%对18.2%)。采用接触阻抗标测和电压标测的三维标测能够可靠地识别局灶性AT的机制。