Jeffrey Munro Win-Kuang Shen 劉曉宇 譯 王如興審校

非典型心房撲動(dòng)治療的實(shí)用方法

Jeffrey Munro Win-Kuang Shen 劉曉宇 譯 王如興審校

心房撲動(dòng)是一類具有不同表現(xiàn)的折返性房性心律失常，包括典型心房撲動(dòng)和非典型心房撲動(dòng)，其中典型心房撲動(dòng)是以下腔靜脈-三尖瓣峽部為關(guān)鍵傳導(dǎo)區(qū)域形成的折返性心律失常，而非典型心房撲動(dòng)的折返環(huán)多存在于左心房或右心房且與瘢痕和慢傳導(dǎo)區(qū)域有關(guān)。近年來，隨著心臟外科手術(shù)和房顫導(dǎo)管消融手術(shù)例數(shù)的增加，非典型心房撲動(dòng)的發(fā)病率也逐漸升高。典型心房撲動(dòng)的消融通常是沿下腔靜脈-三尖瓣峽部進(jìn)行線性消融，而非典型心房撲動(dòng)消融通常需要多種技術(shù)聯(lián)合應(yīng)用以明確關(guān)鍵傳導(dǎo)區(qū)域的位置，這些技術(shù)包括采用三維標(biāo)測(cè)系統(tǒng)行電解剖電壓標(biāo)測(cè)和激動(dòng)標(biāo)測(cè)及采用拖帶技術(shù)確定非典型心房撲動(dòng)發(fā)生的關(guān)鍵傳導(dǎo)區(qū)域。本文以一例既往行房顫導(dǎo)管消融術(shù)后發(fā)生非典型心房撲動(dòng)的患者為例，介紹我們是如何確定非典型心房撲動(dòng)折返環(huán)的組成，尤其是如何發(fā)現(xiàn)非典型心房撲動(dòng)發(fā)生的關(guān)鍵傳導(dǎo)區(qū)域并予以消融成功。

非典型心房撲動(dòng);電解剖電壓標(biāo)測(cè);激動(dòng)標(biāo)測(cè);拖帶;折返性心律失常;心房顫動(dòng)消融

1 引言

心房撲動(dòng)(房撲)，是一種具有折返機(jī)制的心律失常，通常分為兩種類型:典型房撲和非典型房撲(表1)。典型房撲，也稱為下腔靜脈-三尖瓣峽部(cavo-tricuspid isthmus，CTI)依賴型房撲，整個(gè)心動(dòng)過速折返環(huán)在右心房內(nèi)，CTI是折返環(huán)路中必要組成部分。從心尖角度來看，典型房撲是沿三尖瓣環(huán)形成的折返，且多呈逆時(shí)針方向而順時(shí)針方向少見。在折返環(huán)路較低的情況下，折返環(huán)仍以CTI作為傳導(dǎo)的關(guān)鍵區(qū)，激動(dòng)圍繞下腔靜脈傳導(dǎo)并通過界脊中間隙，而不是圍繞整個(gè)三尖瓣環(huán)進(jìn)行折返。沿房間隔和右心房側(cè)壁傳導(dǎo)的上行撲動(dòng)波，與下位折返環(huán)心房撲動(dòng)在高位右心房發(fā)生碰撞。目前已經(jīng)在解剖學(xué)上明確了典型房撲的環(huán)路，且絕大多數(shù)典型房撲可沿 CTI予以成功地線性消融［1－4］。所謂“非峽部依賴”的房撲出現(xiàn)較少，其可以在心房內(nèi)任何部位形成折返。盡管非典型房撲比典型房撲少見，但隨著先天性心臟病、冠心病和瓣膜性心臟病患者心房切開術(shù)例數(shù)，以及心房顫動(dòng)導(dǎo)管消融術(shù)造成心房瘢痕的患者數(shù)的增加，非典型房撲的發(fā)生率正不斷提高。相比于典型房撲的標(biāo)準(zhǔn)治療方法(即沿CTI行線性消融)較高的成功率，非典型房撲消融治療仍然具有挑戰(zhàn)性，主要原因是非典型房撲折返環(huán)的確定需要進(jìn)行復(fù)雜的標(biāo)測(cè)和電生理拖帶操作，故其消融成功率通常低于典型房撲［5－7］。

表1 心房撲動(dòng)的分類:根據(jù)是否下腔靜脈-三尖瓣峽部依賴主要分為典型房撲和非典型房撲兩類

典型心房撲動(dòng)體表心電圖的特點(diǎn)是出現(xiàn)沒有等電位線節(jié)段的持續(xù)不斷的鋸齒樣撲動(dòng)波，且其在心電圖下壁導(dǎo)聯(lián)Ⅱ、Ⅲ、aVF呈顯著的負(fù)向偏移;而逆鐘向心房撲動(dòng)心電圖表現(xiàn)為撲動(dòng)波在心前區(qū)導(dǎo)聯(lián)V1呈正向偏移，順鐘向(“逆向的”)心房撲動(dòng)心電圖則表現(xiàn)為撲動(dòng)波在下壁導(dǎo)聯(lián)呈正向偏移［圖1A:典型的沿三尖瓣環(huán)逆時(shí)針方向折返的心房撲動(dòng)，表現(xiàn)為下壁導(dǎo)聯(lián)(Ⅱ、Ⅲ、aVF)撲動(dòng)波倒置;圖1B:典型的沿三尖瓣環(huán)順時(shí)針方向折返的心房撲動(dòng)，表現(xiàn)為下壁導(dǎo)聯(lián)撲動(dòng)波直立］。在體表心電圖上，非典型房撲的撲動(dòng)波形態(tài)極其多變，對(duì)預(yù)測(cè)折返環(huán)的定位作用有限，而在室性心動(dòng)過速心電圖中，則可根據(jù)心電圖形態(tài)大致定位室性心動(dòng)過速的出口。此外，利用體表心電圖對(duì)有巨大折返環(huán)的非典型心房撲動(dòng)與局灶性房性心動(dòng)過速進(jìn)行辨別，臨床價(jià)值不是很大，原因在于這兩類撲動(dòng)波都可能存在較明顯的等電位線［圖2:12導(dǎo)聯(lián)體表心電圖提示為非典型房撲伴2︰1房室傳導(dǎo)(A);瘢痕相關(guān)性右心房非典型房撲(B);房顫消融患者行肺靜脈隔離和線性消融后在左心室形成的非典型房撲折返環(huán)(C)。圍繞二尖瓣環(huán)周圍的心房肌和左下肺靜脈附近的二尖瓣峽部是二尖瓣峽部依賴性房撲折返環(huán)的重要組成部分。沿房頂部線性消融所形成的間隙可能也是非典型房撲重要的折返傳導(dǎo)區(qū)域］。盡管借助體表心電圖來定位非典型房撲折返環(huán)存在不足，但目前已發(fā)現(xiàn)了一些利用體表心電圖定位非典型房撲的基本方法，然而精確定位仍需要采用更先進(jìn)的技術(shù)［8］。

在本文中，我們以一例非典型房撲患者的導(dǎo)管消融為例，介紹用于確定不典型房撲消融關(guān)鍵峽部的多種現(xiàn)代標(biāo)測(cè)技術(shù)，包括電壓標(biāo)測(cè)、激動(dòng)標(biāo)測(cè)和拖帶標(biāo)測(cè)。最后我們結(jié)合文獻(xiàn)總結(jié)了目前對(duì)于非典型房撲的病因、標(biāo)測(cè)和消融的認(rèn)識(shí)。

2 一例非典型房撲

患者男，52歲，既往有原發(fā)性高血壓、采用持續(xù)正壓通氣(continuous positive airway pressure，CPAP)治療阻塞性睡眠呼吸暫停綜合征和約5年的持續(xù)性心房顫動(dòng)病史。2012年年初患者在外院行微創(chuàng)迷宮手術(shù)治療，包括肺靜脈電隔離和心外膜神經(jīng)節(jié)叢消融并恢復(fù)正常竇性心律，同時(shí)使用40 mm封閉器行左心耳封堵。消融術(shù)后不久，患者心房顫動(dòng)復(fù)發(fā)并出現(xiàn)非典型房撲，先予以藥物治療6個(gè)月;2012年6月，在其他醫(yī)院接受了第二次消融治療，包括冷凍消融和左心房線性消融，但術(shù)后不久，房性心律失常再次復(fù)發(fā)。在以后的兩年中，患者持續(xù)應(yīng)用氟卡尼、地爾硫卓及一次同步電復(fù)律以維持竇性心律，但患者仍反復(fù)發(fā)作有癥狀的、持續(xù)性非典型房撲，伴有心悸、運(yùn)動(dòng)量下降和呼吸困難。

患者于2014年6月來我院住院，我們對(duì)患者的房性快速性心律失常進(jìn)行了評(píng)估和并決定采取相應(yīng)的治療方案。由于當(dāng)時(shí)患者仍存在運(yùn)動(dòng)量下降的表現(xiàn)，故可供選擇的治療方案包括:繼續(xù)控制患者心室律、再次電復(fù)律或心內(nèi)膜導(dǎo)管射頻消融。由于患者仍存在明顯癥狀及既往電復(fù)律無效。最終，由于出現(xiàn)活動(dòng)受限癥狀及之前嘗試電復(fù)律失敗，患者選擇再次進(jìn)行導(dǎo)管射頻消融。

術(shù)前心電圖(圖2)為具有等電位線及2︰1房室傳導(dǎo)的房性快速性心律失常。對(duì)具有不連續(xù)P波且伴有等電位線的房性心動(dòng)過速心電圖的鑒別診斷，應(yīng)考慮局灶機(jī)制或折返所致的非典型房撲。該患者心動(dòng)過速周長為240 ms且恒定。在患者冠狀靜脈竇放置二十極冠狀竇導(dǎo)管(Orbiter，Bard)，發(fā)現(xiàn)心房最早激動(dòng)點(diǎn)靠近冠狀竇導(dǎo)管近端，并向冠狀竇導(dǎo)管遠(yuǎn)端傳導(dǎo)。電生理檢查第一步通常是從右房到左房進(jìn)行多部位拖帶標(biāo)測(cè)(表2)。電生理診斷起搏導(dǎo)管分別置于高位右心房(圖3:在高位右心房對(duì)一例非典型房撲進(jìn)行顯性拖帶，其中，ABL:消融導(dǎo)管;CS:冠狀竇導(dǎo)管)、右心房房間隔上部、右心房側(cè)壁和三尖瓣峽部。在所有部位成功進(jìn)行顯性拖帶，結(jié)果發(fā)現(xiàn)起搏后間期與心動(dòng)過速周長之差(PPI－TCL)均＞20 ms，且右心房側(cè)壁的PPI－TCL最長，而越接近房間隔，PPITCL逐漸變短，提示右心房不在折返環(huán)所在的區(qū)域。進(jìn)行房間隔穿刺前，在冠狀竇口進(jìn)行拖帶標(biāo)測(cè)，結(jié)果顯示隱匿拖帶伴有長PPI－TCL，提示此處是接近關(guān)鍵峽部的慢傳導(dǎo)區(qū)，但不是折返環(huán)的關(guān)鍵傳導(dǎo)區(qū)。在冠狀靜脈竇中部進(jìn)行拖帶標(biāo)測(cè)時(shí)，PPI－TCL較短，刺激波與撲動(dòng)波之間的間期為零，且和腔內(nèi)心電圖(EGM)顯示刺激到撲動(dòng)波的間期相同，提示拖帶處為出口且折返環(huán)包含左心房。

表2 本例患者非典型心房撲動(dòng)不同部位拖帶標(biāo)測(cè)結(jié)果

通過兩次房間隔穿刺，分別將消融導(dǎo)管和二十極Lasso導(dǎo)管送入左心房。Lasso導(dǎo)管分別送入至四根肺靜脈，證實(shí)肺靜脈完全隔離。接著，利用消融導(dǎo)管在左心房不同部位進(jìn)行拖帶標(biāo)測(cè)，其中左心房后壁為顯性拖帶，而左心耳殘端，二尖瓣瓣環(huán)10點(diǎn)、12點(diǎn)位置及左心房房間隔下部均表現(xiàn)為隱匿性拖帶，PPI－TCL較短并逐漸縮短至接近體表撲動(dòng)波周期，所有腔內(nèi)心電圖顯示的撲動(dòng)波周期均與體表心電圖撲動(dòng)波周期一致。在二尖瓣環(huán)11點(diǎn)位置，我們發(fā)現(xiàn)一個(gè)低振幅的碎裂電位，且符合瘢痕處慢傳導(dǎo)區(qū)和電位傳導(dǎo)間隙的表現(xiàn)(圖4:沿二尖瓣環(huán)11點(diǎn)鐘位置標(biāo)測(cè)到碎裂低振幅雙極電位，提示為慢傳導(dǎo)區(qū)，予以成功消融)。

在二尖瓣環(huán)10點(diǎn)位置的腔內(nèi)局部電位距離體表心電圖撲動(dòng)波為84 ms，此時(shí)心動(dòng)過速周長為241 ms，因此占心動(dòng)過速周長的35%(圖5:沿二尖瓣環(huán)10點(diǎn)位置的隱匿性拖帶，其中，ABL:消融導(dǎo)管;CS:冠狀竇電極)。二尖瓣環(huán)12點(diǎn)位置和左心房間隔下部腔內(nèi)局部電位到體表撲動(dòng)波的距離分別為159 ms和54 ms，分別占心動(dòng)過速周長的66%和22%。

應(yīng)用CARTO三維標(biāo)測(cè)系統(tǒng)(Biosense Webster)進(jìn)行激動(dòng)標(biāo)測(cè)和電壓標(biāo)測(cè)［圖6:左房激動(dòng)標(biāo)測(cè)(A)和左房電壓標(biāo)測(cè)(B);從二尖瓣環(huán)11點(diǎn)位置至右上肺靜脈進(jìn)行線性消融，在此過程中房撲發(fā)作終止;然后再沿慢傳導(dǎo)區(qū)存在潛在間隙的低電壓區(qū)，包括房頂線、左上肺靜脈至二尖瓣環(huán)線和右下肺靜脈至二尖瓣環(huán)線進(jìn)行補(bǔ)充線性消融］。激動(dòng)標(biāo)測(cè)圖表明激動(dòng)傳導(dǎo)是占心動(dòng)過速周期大部分且圍繞二尖瓣環(huán)的大折返環(huán)，而不是局部最早激動(dòng)并向外圍擴(kuò)散的局灶性房性心動(dòng)過速。電壓標(biāo)測(cè)圖表明;環(huán)繞肺靜脈開口處存在許多低電壓區(qū)域;除了左心房頂部以外，從肺靜脈到二尖瓣環(huán)11點(diǎn)和3點(diǎn)位置之間存在線性低電壓區(qū)。

二尖瓣峽部依賴的非典型房撲的診斷是在左心耳基底進(jìn)行隱匿性拖帶標(biāo)測(cè)，刺激波到體表心房撲動(dòng)波之間的長度占心動(dòng)過速周長的66%，則為折返形成的關(guān)鍵峽部。消融應(yīng)用3.5 mm灌注消融導(dǎo)管(SmartTouch，Biosense Webster)，輸出功率35 W，溫度上限45℃。消融策略為沿二尖瓣游離壁峽部進(jìn)行線性消融，消融損傷從二尖瓣環(huán)至左上肺靜脈，與前次環(huán)肺靜脈消融瘢痕處相連(圖6A)。第一次線性消融結(jié)束后，心動(dòng)過速周長從240 ms延長到254 ms。第二次線性消融是由二尖瓣環(huán)11點(diǎn)前方開始向右上肺靜脈進(jìn)行，消融過程中心動(dòng)過速周長延長至320 ms并最終停止(圖7:從右上肺靜脈至二尖瓣環(huán)線性消融中，不典型房撲開始減慢和終止圖形，房撲終止并恢復(fù)竇性心律)。接著，繼續(xù)延長第二消融線，消融方向是從左心房房頂?shù)阶笮亩撞?圖6B)。消融結(jié)束后，進(jìn)行心房程序刺激，給予多達(dá)三次期前刺激也無法誘發(fā)任何房性快速性心律失常。

激動(dòng)標(biāo)測(cè)圖表明本例患者心動(dòng)過速似乎是圍繞二尖瓣環(huán)折返并為二尖瓣峽部依賴性。第一次行二尖瓣峽部線性消融后，患者心動(dòng)過速周長延長，考慮可能的原因是折返環(huán)內(nèi)環(huán)被阻滯，但沒有影響關(guān)鍵傳導(dǎo)區(qū)，折返激動(dòng)順序改變，折返可能沿左心房后壁進(jìn)行，或形成“8”字形的復(fù)合折返。最終，在二尖瓣環(huán)11點(diǎn)處消融，終止了心動(dòng)過速的發(fā)作，此處有先前電壓標(biāo)測(cè)時(shí)發(fā)現(xiàn)的碎裂低電壓電位，表明對(duì)關(guān)鍵峽部進(jìn)行了消融，從而不能再次誘發(fā)非典型房撲。

3 非典型心房撲動(dòng)的文獻(xiàn)回顧

3.1 病因和發(fā)病率

非典型房撲，有時(shí)也被稱為非局灶性房性心動(dòng)過速，具有折返機(jī)制，通常見于有心房瘢痕形成病史的患者，這些瘢痕往往是由心臟外科手術(shù)，以及外科或?qū)Ч芟谥委熜姆款潉?dòng)所致(圖2B和圖2C)。有報(bào)道稱，心房顫動(dòng)射頻消融術(shù)后的左房撲動(dòng)患者，77%有器質(zhì)性心臟病，23%無明顯器質(zhì)性心臟?。?］。在最近一個(gè)多中心回顧性研究分析中，Coffey等［5］報(bào)道在91例非典型心房撲動(dòng)患者中，65%的患者曾接受心房導(dǎo)管消融治療;27%的患者既往有心臟手術(shù)治療史，其中12%的患者接受迷宮手術(shù)，8%的患者存在與非典型房撲相關(guān)的特發(fā)性瘢痕，提示這8%的患者可能有心房心肌病。

隨著先天性心臟病外科手術(shù)例數(shù)的增多和心房顫動(dòng)射頻消融術(shù)的日益普及，非典型房撲的發(fā)生率可能會(huì)相應(yīng)升高。在一項(xiàng)前瞻性研究中，67例患者接受了心房顫動(dòng)射頻消融術(shù)，手術(shù)方式為環(huán)肺靜脈隔離和線性消融，其中，43%的患者術(shù)后有房性心動(dòng)過速發(fā)生，其中69%是以折返為機(jī)制的非典型房撲;在消融后的第3、第6和第12個(gè)月，應(yīng)用連續(xù)7 d Holter進(jìn)行監(jiān)測(cè)，發(fā)現(xiàn)31%的患者存在持續(xù)性房性快速性心律失常［6］。盡管包括非典型房撲在內(nèi)的房性心動(dòng)過速發(fā)生率較高，但經(jīng)過心房顫動(dòng)導(dǎo)管消融治療后，相當(dāng)比例的房性心動(dòng)過速表現(xiàn)出自限性。Chugh等［7］報(bào)道，在接受心房顫動(dòng)射頻消融的349例患者中，有24%在約1年的隨訪期間發(fā)生以大折返為機(jī)制的房性心動(dòng)過速，其中33%的房性心動(dòng)過速有自愈性且通常發(fā)生在最初消融術(shù)后的5個(gè)月內(nèi)，因此他們建議術(shù)后短期內(nèi)對(duì)這類患者予以密切觀察。

3.2 標(biāo)測(cè)

應(yīng)用于非典型心房撲動(dòng)的主要標(biāo)測(cè)方法有拖帶標(biāo)測(cè)、電壓標(biāo)測(cè)和激動(dòng)標(biāo)測(cè)。使用拖帶標(biāo)測(cè)技術(shù)的目的是尋找隱匿性拖帶位點(diǎn)，并確認(rèn)非典型房撲折返環(huán)的關(guān)鍵峽部。通過構(gòu)建右心房和/或左心房電壓標(biāo)測(cè)圖，有助于確定低電壓區(qū)，這些區(qū)域往往代表作為折返環(huán)邊界的瘢痕區(qū)域。激動(dòng)標(biāo)測(cè)則可以將三維標(biāo)測(cè)系統(tǒng)中折返性心動(dòng)過速的大部分周長與心房解剖結(jié)構(gòu)關(guān)聯(lián)起來。另外，雙電位或高度碎裂的局部電位所在區(qū)域，可能分別代表阻滯線、阻滯區(qū)或各向異性傳導(dǎo)。每種標(biāo)測(cè)技術(shù)均有自身的局限性，因此把采用這些技術(shù)所得到的信息整合起來，對(duì)成功標(biāo)測(cè)和消融非常重要。

3.2.1 拖帶標(biāo)測(cè) 拖帶標(biāo)測(cè)已成為用于明確折返環(huán)存在的重要手段，研究證明其有助于確定陣發(fā)性室上性心動(dòng)過速和非典型房撲折返環(huán)的構(gòu)成，并用于室性心動(dòng)過速的標(biāo)測(cè)。拖帶標(biāo)測(cè)的基本操作方法是，當(dāng)心動(dòng)過速發(fā)作時(shí)從感興趣位點(diǎn)以短于心動(dòng)過速周長10～30 ms的間期進(jìn)行心房超速起搏，確認(rèn)拖帶后停止起搏，心動(dòng)過速仍繼續(xù)存在。Waldo等［10］提出了拖帶標(biāo)測(cè)的4條準(zhǔn)則，并報(bào)道了拖帶方法在典型心房撲動(dòng)標(biāo)測(cè)中的應(yīng)用。

在心房的某個(gè)區(qū)域?qū)Ψ堑湫头繐溥M(jìn)行拖帶，起搏后周期與心動(dòng)過速周長之差(PPI－TCL)＜20 ms，則認(rèn)為該拖帶區(qū)域在折返環(huán)路上。此外，當(dāng)出現(xiàn)隱匿性拖帶時(shí)，即體表心電圖自身撲動(dòng)波和腔內(nèi)心電圖心房波激動(dòng)順序與拖帶后的撲動(dòng)波相同，則認(rèn)為起搏導(dǎo)管頂端位于關(guān)鍵性慢傳導(dǎo)區(qū)域內(nèi)。起搏標(biāo)測(cè)部位(PPI－TCL)＜20 ms，呈隱匿性拖帶且刺激波到體表撲動(dòng)波的間期逐漸縮短，表明起搏標(biāo)測(cè)點(diǎn)逐漸靠近折返環(huán)的出口。

拖帶標(biāo)測(cè)對(duì)非典型房撲折返環(huán)的定位提供了一個(gè)總體思路，但應(yīng)該與其他標(biāo)測(cè)方法聯(lián)合使用。Morton等［11］對(duì)這些標(biāo)測(cè)方法應(yīng)用于典型房撲消融的敏感性和特異性進(jìn)行了研究。以比撲動(dòng)波周期短10 ms的起搏間期進(jìn)行隱匿性拖帶標(biāo)測(cè)，對(duì)關(guān)鍵性峽部判斷的敏感性和特異性分別為100%和54%;如果逐漸縮短起搏間期，敏感性下降、特異性提高［11］。Triedman 等［12］將舒張期局部低電壓碎裂電位鑒別技術(shù)和拖帶標(biāo)測(cè)技術(shù)應(yīng)用于先天性心臟病術(shù)后發(fā)生房性折返性心動(dòng)過速的射頻消融治療，急性期成功率為73%;隨訪平均4個(gè)月，復(fù)發(fā)率為53%。雖然這些研究沒有針對(duì)非典型心房撲動(dòng)進(jìn)行研究，但他們指出了拖帶標(biāo)測(cè)在準(zhǔn)確預(yù)測(cè)峽部位置和充分定位折返環(huán)構(gòu)成方面還存在問題，而心動(dòng)過速終止和心動(dòng)過速周期變化也限制了拖帶標(biāo)測(cè)應(yīng)用于存在多個(gè)折返環(huán)和彌散傳導(dǎo)機(jī)制的患者。

3.2.2 電解剖(電壓和激動(dòng))標(biāo)測(cè) 非典型房撲患者的心房中通常存在瘢痕組織，這些組織幾乎沒有任何電活動(dòng)，表現(xiàn)為低電壓區(qū)及局部電信號(hào)消失。在心房內(nèi)電壓標(biāo)測(cè)中，通常建議將瘢痕組織或無電活動(dòng)區(qū)域定義為一些雙極電壓振幅＜0.05 mV，且輸出電流為20 mA時(shí)無法奪獲心房組織的點(diǎn)［9］。瘢痕和低電壓區(qū)可以在三維標(biāo)測(cè)系統(tǒng)的心房解剖結(jié)構(gòu)模型中標(biāo)測(cè)出來，這對(duì)阻滯區(qū)域邊界和可能的慢傳導(dǎo)區(qū)域的判斷提供了指導(dǎo)，而這些區(qū)域可能就是非典型房撲發(fā)生的關(guān)鍵性峽部。在局部阻滯區(qū)域經(jīng)常可以發(fā)現(xiàn)雙電位，這對(duì)尋找線性消融的消融線之間的間隙提供了進(jìn)一步指導(dǎo)。此外，復(fù)雜的碎裂電位往往提示慢傳導(dǎo)區(qū)，在標(biāo)測(cè)中可以將其作為關(guān)鍵性峽部的候選區(qū)域予以標(biāo)記。

激動(dòng)標(biāo)測(cè)應(yīng)用三維標(biāo)測(cè)系統(tǒng)，在心動(dòng)過速發(fā)作時(shí)顯示相對(duì)于參考電極上某一點(diǎn)的局部電位激動(dòng)時(shí)間，參考電極通常選擇冠狀竇電極。局部電位激動(dòng)時(shí)間與參考電極之間的時(shí)間差被指定為顏色光譜中的某種顏色，紅色表示最早激動(dòng)時(shí)間而紫色代表最晚激動(dòng)時(shí)間，這樣可鑒別占心動(dòng)過速周期至少90%的激動(dòng)時(shí)間間隔。在精確激動(dòng)標(biāo)測(cè)過程中，可能的關(guān)鍵峽部可通過慢傳導(dǎo)區(qū)加以鑒別，在激動(dòng)標(biāo)測(cè)圖上表現(xiàn)為在一定的區(qū)域內(nèi)顏色的快速變化。在激動(dòng)標(biāo)測(cè)過程中，一項(xiàng)有用的發(fā)現(xiàn)是當(dāng)最早的局部激動(dòng)固定在一個(gè)較小的區(qū)域內(nèi)，則提示該心律失常的發(fā)生機(jī)制可能是局灶或局部折返所致，且最早激動(dòng)點(diǎn)即為消融靶點(diǎn)。多極導(dǎo)管和高密度標(biāo)測(cè)的發(fā)展為快速標(biāo)測(cè)非持續(xù)性房性心動(dòng)過速提供了有效方法。

Nakagawa等［13］報(bào)道了利用電壓和激動(dòng)標(biāo)測(cè)技術(shù)對(duì)13例有先天性心臟病修補(bǔ)術(shù)病史的患者行射頻消融，在這些患者中共發(fā)現(xiàn)15個(gè)持續(xù)性的大折返性右心房房性心動(dòng)過速。應(yīng)用電解剖標(biāo)測(cè)，他們確定了瘢痕區(qū)以及折返通路，并以這些通路作為消融靶點(diǎn)進(jìn)行治療，最終15個(gè)心動(dòng)過速均成功終止，所有患者在射頻消融術(shù)后均不能誘發(fā)持續(xù)性房性心動(dòng)過速。應(yīng)用電解剖標(biāo)測(cè)系統(tǒng)對(duì)心房顫動(dòng)消融術(shù)后的非典型房撲做進(jìn)一步研究，所得結(jié)果與上述類似［5－7，14－15］。

3.3 折返環(huán)特點(diǎn)

非典型房撲折返環(huán)可根據(jù)許多變量進(jìn)行分類，這些變量包括折返環(huán)的位置、大小、形態(tài)以及與之相關(guān)的既往線性消融產(chǎn)生的間隙。與既往消融相關(guān)的非典型房撲通常可根據(jù)折返環(huán)大小進(jìn)一步分類:大折返環(huán)定義為折返環(huán)＞2～3 cm或涉及兩個(gè)或更多的心房節(jié)段，并且利用激動(dòng)標(biāo)測(cè)可對(duì)占心動(dòng)過速周期至少90%的折返環(huán)進(jìn)行定位識(shí)別;而小折返環(huán)定義為折返環(huán)＜2～3 cm或折返位于術(shù)者定義的單一心房節(jié)段。實(shí)際上，局灶性房性心動(dòng)過速在激動(dòng)標(biāo)測(cè)中表現(xiàn)為有一個(gè)最早激動(dòng)點(diǎn)，且激動(dòng)以該點(diǎn)為中心以離心性擴(kuò)散的方式傳導(dǎo)［6，9，16］。

心房撲動(dòng)折返環(huán)的解剖定位幾乎包括左房或右房中的任何結(jié)構(gòu)。在有心房顫動(dòng)消融病史的患者中，以大折返為機(jī)制的非典型房撲，其關(guān)鍵峽部在二尖瓣峽部的占25% ～42%，在左心房頂部的占13%～20%，在間隔的占13%;而微折返或局灶機(jī)制的房性心動(dòng)過速常見于肺靜脈前庭、左心房前后壁、左心耳基底部、左心房間隔和冠狀竇［14－15］。

常見的折返環(huán)形態(tài)是單環(huán)折返和多環(huán)折返以及微折返。Linton等［17］采用在兩個(gè)不同位置依次進(jìn)行超速起搏，通過測(cè)量這兩個(gè)位置的起搏后間期，鑒別折返環(huán)是單一環(huán)路還是雙重環(huán)路。在雙環(huán)路折返的情形下，首先在具有最短起搏后間期(拖帶過程中幾乎和心動(dòng)過速周期相等)的峽部進(jìn)行消融;如果心動(dòng)過速?zèng)]有終止，則在下一個(gè)最短起搏后間期部位消融。

折返環(huán)穿過之前消融線的房性心動(dòng)過速稱為間隙相關(guān)性房性心動(dòng)過速，據(jù)文獻(xiàn)［7］報(bào)道其占折返性房性心動(dòng)過速的96%以上。這充分說明在線性消融過程中，對(duì)消融線完全阻滯可潛在避免這些心律失常的發(fā)生。當(dāng)然，雖然線性消融損傷能提高持續(xù)性心房顫動(dòng)患者的消融成功率，但隨之帶來的是術(shù)后隨訪期間房性心動(dòng)過速發(fā)生率升高［18］。

3.4 消融終點(diǎn)和成功率

總體說來，不典型房撲導(dǎo)管消融急性期成功率較高，但長期隨訪成功率稍差。消融靶點(diǎn)在房間隔區(qū)域時(shí)，急性和長期成功率明顯偏低。研究報(bào)道消融成功率還與所使用的導(dǎo)管不同有關(guān)。房撲折返環(huán)的房間隔部位之所以難以消融，是因?yàn)樵搮^(qū)域解剖結(jié)構(gòu)關(guān)系復(fù)雜且可能難以輸送適當(dāng)?shù)纳漕l能量。Coffey等［5］進(jìn)行回顧性病例分析，射頻消融術(shù)后發(fā)生房性心律失常的患者進(jìn)行(16±12)個(gè)月的隨訪，急性期成功率97%、長期成功率77%，而非間隔部和間隔部的成功率分別為82%和67%。同時(shí)，他們還發(fā)現(xiàn)，長期成功率的不同與瘢痕可能的成因有關(guān):消融治療外科手術(shù)形成的瘢痕相關(guān)性房性心動(dòng)過速，長期成功率為88%;導(dǎo)管消融術(shù)形成的瘢痕為75%;特發(fā)性心房瘢痕為57%。其他研究表明，這類房性心動(dòng)過速導(dǎo)管消融的急性和長期成功率均較低，原因可能是這些研究通常使用消融導(dǎo)管進(jìn)行激動(dòng)標(biāo)測(cè)而非多電極導(dǎo)管標(biāo)測(cè)，由此可能造成標(biāo)測(cè)時(shí)所取點(diǎn)的密度較低［7，14－15］。

消融導(dǎo)管類型的選擇也可能影響非典型房撲射頻消融的急性和長期成功率。一項(xiàng)隨機(jī)研究表明，應(yīng)用3.5 mm冷鹽水灌注導(dǎo)管和8 mm非灌注導(dǎo)管對(duì)非典型房撲進(jìn)行消融，急性期成功率分別為94%和77%;隨訪10個(gè)月，采用48 h動(dòng)態(tài)心電圖在3、6和9個(gè)月進(jìn)行檢查，發(fā)現(xiàn)長期成功率分別為92%和59%，所以鹽水灌注消融導(dǎo)管成功率更高［19］。

4 結(jié)論

隨著接受心房顫動(dòng)射頻消融的患者以及在心臟手術(shù)中切開心房的患者尤其是先天性心臟病患者越來越多，非典型房撲正在成為一種越來越常見的心律失常。綜合運(yùn)用包括拖帶標(biāo)測(cè)和高級(jí)標(biāo)測(cè)在內(nèi)的系統(tǒng)性方法，以及隨著人們對(duì)電解剖基質(zhì)認(rèn)識(shí)的提高，射頻消融術(shù)治療上述頗具臨床挑戰(zhàn)性的心律失常的成功率可達(dá)90%。影響消融結(jié)果的因素較多，包括患者的手術(shù)和消融病史、折返環(huán)的位置和特點(diǎn)以及標(biāo)測(cè)技術(shù)和消融導(dǎo)管。盡管目前對(duì)于非典型房撲消融還無具體研究報(bào)道，但消融成功率和并發(fā)癥的發(fā)生率，通常與術(shù)者的臨床經(jīng)驗(yàn)及各中心開展這種復(fù)雜性心律失常的手術(shù)數(shù)量有關(guān)。

(圖和參考文獻(xiàn)請(qǐng)查閱前面的英文原文)

【致謝】 衷心感謝南京醫(yī)科大學(xué)附屬無錫人民醫(yī)院心內(nèi)科的劉曉宇博士和王如興教授在百忙中分別承擔(dān)了本文的翻譯和審校工作。

A practical approach to atypical atrial flutter

Jeffrey Munro Win-Kuang Shen

Atrial flutter is a heterogeneous group of re-entrant atrial arrhythmias including typical atrial flutter where the cavo-tricuspid isthmus is a critical zone of conduction and atypical atrial flutter in which the re-entrant circuit can exist in the right or left atrium associated with scar and a slow zone of conduction.The prevalence of atypical atrial flutter is increasing as the number of cardiac surgery and catheter based ablations of atrial fibrillation is more widespread.Typical atrial flutter ablation typically involves a linear ablation along the cavo-tricuspid isthmus as opposed to atypical atrial flutter usually requiring an integrated approach of electroanatomical voltage mapping and activation mapping in a computer based 3D mapping system as well as entrainment techniques for determining critical zones of conduction.In this article we present a case of atypical atrial flutter that we have employed these tools to determine the components of an atypical atrial flutter circuit，specifically the critical zone of conduction which was targeted with radiofrequency ablation for termination of atypical atrial flutter in a patient with a prior ablation for atrial fibrillation.

atypical atrial flutter;electroanatomical voltage mapping;activation mapping;entrainment;re-entrant arrhythmias;atrial fibrillation ablation

10.13308/j.issn.2095 －9354.2015.04.001

R541.75

A

2095－9354(2015)04－0229－16

10.13308/j.issn.2095 －9354.2015.04.001

【編者按】 近年來，隨著心臟外科手術(shù)和房顫導(dǎo)管消融手術(shù)例數(shù)的增加，非典型心房撲動(dòng)的發(fā)病率逐漸升高。本期特邀世界頂級(jí)醫(yī)院美國梅奧醫(yī)學(xué)中心(Mayo Clinic)心電生理專家Jeffrey Munro博士和Win-Kuang Shen(沈文光)教授結(jié)合臨床病例，探討在非典型心房撲動(dòng)消融中如何聯(lián)合運(yùn)用電解剖電壓標(biāo)測(cè)、激動(dòng)標(biāo)測(cè)及拖帶技術(shù)等多種技術(shù)，明確關(guān)鍵傳導(dǎo)區(qū)域位置?！癇rugada擬表型”是2012年由Adrian Baranchuk等首次提出的一個(gè)新術(shù)語，其有助于鑒別先天Brugada綜合征，可防止學(xué)術(shù)上概念的混淆，且準(zhǔn)確識(shí)別Brugada綜合征與Brugada擬表型，有助于合理治療，令更多的患者獲益。本期奉上該術(shù)語的首次提出者，加拿大金斯頓綜合醫(yī)院的Adrian Baranchuk教授的最新綜述，首次向國內(nèi)讀者全面介紹Brugada擬表型的相關(guān)前沿問題，以期推動(dòng)我國心血管病研究領(lǐng)域?qū)υ搯栴}的關(guān)注。

2015－05－12)

(本文編輯:顧艷)

海外論壇

1 Introduction

Atrial flutter，an arrhythmia with a reentrant mechanism，is often classified by subdividing it into two types:typical and atypical(Tab.1).Typical atrial flutter，otherwise known as cavo-tricuspid isthmus(CTI)dependent，with the entire tachycardia circuit within the right atrium uses the CTI as an obligatory component of the reentrant circuit.The wavefront in typical atrial flutter rotates around the tricuspid annulus in a counterclockwise or less commonly clockwise direction，from the perspective of the apex.In the case of lower loop

Author Unit:85054 Phoenix，Arizona，U.S.，Department of Cardiovascular Diseases，Division of Cardiac Electrophysiology，Mayo Clinic

Author Brief Introduction:Jeffrey Munro，D.O.，fellow of clinical cardiac electrophysiology;research interests:atrial fibrillation，atypical atrial flutter，ventricular tachycardiafibrillation，E-mail:Munro.Jeffrey@mayo.edureentry，the reentrant circuit again involves the CTI as the critical zone of conduction and the wavefront propagates around the inferior vena cava with conduction occurring through a gap in the crista terminalis rather than around the entire tricuspid annulus.The ascending wavefront along the septum and lateral right atrium collide in the high right atrium with lower loop reentry atrial flutter.The anatomic barriers of the circuit have been well defined and the site of successful ablation almost always involves a linear ablation along the CTI［1－4］.Less commonly，atrial flutter can involve a circuit anywhere else within the atrium，the so called“non-isthmus dependent”atrial flutter.Although less common than typical atrial flutter，the atypical variant is increasing in prevalence with an increasing number of individuals with an atriotomy from surgery related to congenital heart disease，coronary disease and valvular heart disease as well as atrial scar related to atrial fibrillation ablation procedures.In contrast to the well-defined approach，with a high success rate，of linear ablation along the cavo-tricuspid isthmus for typical atrial flutter，ablation procedures targeting atypical atrial flutter remains a challenging procedure involving complex mapping and entrainment maneuvers to define components of the circuit at times with success rates generally less than those seen with typical atrial flutter［5－7］.

Tab.1 A classification of atrial flutter:two main types of atrial flutter are typical and atypical atrial flutter，as determined by the role of the cavo-tricuspid isthmus

Typical atrial flutter is characterized on the surface electrocardiogram as having a continuously undulating flutter wave without an isoelectric segment with a predominantly negative deflection in the inferior ECG leads(Ⅱ，Ⅲ，aVF)and a positive deflection in precordial lead V1for the counterclockwise variant and positive deflection in the inferior leads in the case ofthe clockwise(“reverse”)variant(Fig.1A，F(xiàn)ig.1B).The flutter wave morphology on a surface ECG for atypical atrial flutter is highly variable and is limited in its role for prediction of the circuit location as opposed to ventricular tachycardia where ECG morphology is useful for a general localization of exit sites.Additionally，using the surface ECG to distinguish atypical atrial flutter with a macro-reentrant circuit from a focal atrial tachycardia is not particularly valuable as the flutter waves of either type may have significant isoelectric intervals(Fig.2).Despite the shortcomings of surface ECG for prediction of circuit location some general rules have been developed but precise determination requires more sophisticated techniques［8］.

In this article we present a case of atypical atrial flutter that demonstrates many of the contemporary techniques for mapping including voltage，activation and entrainment to identify the critical isthmus for ablation.A literature review follows summarizing the current understanding of atypical atrial flutter，including etiology，mapping and ablation.

2 A case of atypical atrial flutter

Our case is of a 52 year old male with a history of essential hypertension，obstructive sleep apnea treated with continuous positive airway pressure(CPAP)therapy，and persistent atrial fibrillation for approximately 5 years.He had undergone a minimally invasive Maze procedure at an outside institution in early 2012 including pulmonary vein isolation，ganglionated plexus ablation epicardially with restoration of normal sinus rhythm and left atrial appendage closure with a 40 mm atrial clip.Shortly after the ablation procedure the patient had recurrence of atrial fibrillation and atypical atrial flutter and was treated medically for 6 months.He underwent a second ablation procedure at another outside institution in mid-2012 with cryoablation and a linear ablation within the left atrium，but again had recurrent atrial arrhythmias shortly after the procedure.Over the following 2 years，treatment with flecainide and diltiazem was continued for rhythm control in addition to a synchronized external cardioversion but the patient continued to have persistent symptomatic atypical atrial flutter with palpitations，reduced functional capacity and dyspnea.

He presented to us in mid-2014 for evaluation and management of his atrial tachyarrhythmias.At that time he was still experiencing reduced functional capacity and alternatives were discussed including a continued rate control approach，an additional attempt at cardioversion orendocardialradiofrequency energy catheter ablation.The patient opted for a repeat ablation because of the limiting symptoms and failed prior attempt at cardioversion.

The initial ECG(Fig.2)showed an atrial tachyarrhythmia with an isoelectric interval and 2︰1 AV conduction.The differential-diagnosis of discrete P waves with an isoelectric interval includes an atrial tachycardia with a focal mechanism or an atypical flutter with a reentrant mechanism.The cycle length of the tachycardia was 240 ms with no variability of the cycle length.A duodecapolar catheter(Orbiter，Bard)was placed in the coronary sinus and atrial activation was the earliest in the proximal poles with activation proceeding distally.The first maneuver in the electrophysiology lab was entrainment mapping from multiple locations throughout the right atrium and left atrium(Tab.2).The diagnostic pacing catheter was positioned at the high right atrium(Fig.3)，superior right atrial septum，and lateral right atrium and cavo-tricuspid isthmus and entrainment maneuvers performed.All sites showed manifest entrainment with post pacing interval minus tachycardia cycle length interval(PPI－TCL)＞20 ms with the greatest interval at the lateral right atrium and progressively shorter intervals moving closer to the septum suggesting that the right atrium was not part of the reentrant circuit.Prior to transeptal puncture，entrainment was performed at the coronary sinus ostium showing concealed entrainment but long PPI－TCL suggestive of a slow zone of conduction contiguous with the critical isthmus but not a zone of critical conduction of the reentry circuit.Entrainment at the mid coronary sinus had a short PPI－TCL with a stimulus to flutter wave interval that was zero，equaling the local electrogram(EGM)to flutter wave，consistent with an exit site and a circuit that involved the left atrium.

Tab.2 Entrainment mapping at different sites for the presented case of atypical atrial flutter

Two transeptal punctures were made for advancing the ablation catheter and duodecapolar Lasso catheter into the left atrium.The Lasso catheter was advanced into each of the pulmonary veins demonstrating isolation of all four.Next，the ablation catheter was positioned and entrainment maneuvers were performed at the posterior wall of the left atrium，with manifest entrainment，at the base of the left atrial appendage remnant，both 12 o’clock and 10 o’clock positions of the mitral annulus，and inferior septum of the left atrium(LA)with concealed entrainment and short PPI－TCL with progressively shorter stimulus to surface flutter wave intervals，all matching the local EGM to surface flutter wave intervals.A low-amplitude fractionated electrogram was identified at the 11 o’clock position of the mitral annulus consistent with a slow zone of conduction and potential conduction gap in scar(Fig.4).

The local EGM to the surface flutter wave at the 10 o’clock mitral annulus position was 84 ms at which time the tachycardia cycle length was 241 ms，hence representing 35%of the tachycardia cycle length(Fig.5).The 12 o’clock mitral annular position and LA inferoseptal local EGM’s to surface flutter waves were 159 ms and 54 ms，representing 66%and 22%of the tachycardiac cycle length，respectively.

Both an activation map and voltage map was constructed using the CARTO 3D-mapping system(Biosense Webster)(Fig.6).The activation map demonstrated an activation sequence consistent with a macro-reentrant circuit with the majority of the tachycardia cycle length identified around the mitral annulus，rather than a discrete area of early activation and centrifugal spread as one would expect with a focal tachycardia.The voltage map demonstrated a number of low voltage areas around the ostia of the pulmonary veins and linear areas from the pulmonary veins to the mitral annulus at the 11 o’clock and 3 o’clock areas in addition to along the roof of the LA.

Mitral-isthmus dependent atypical atrial flutter was diagnosed with concealed entrainment at the base of the left atrial appendage having a stimulus to surface flutter wave interval representing 66%of the tachycardia cycle length，consistent with a critical isthmus site.A 3.5 mm irrigated tip ablation catheter(SmartTouch，Biosense Webster)was used for all ablation lesions with a power output of 35 W and temperature limit of 45℃.Ablation was performed along the mitral isthmus with the creation of a linear ablation lesion from the mitral annulus to the left superior pulmonary vein，connecting to the scar of prior circumferential ablation(Fig.6A).With completion of the first linear ablation，the tachycardia cycle length increased from 240 ms to 254 ms.A second linear ablation lesion was made from the mitral annulus at 11 o’clock anteriorly toward the right superior pulmonary vein with lengthening of the tachycardia to 320 ms followed by termination(Fig.7).This linear lesion was extended across the roof to the base of the left atrial appendage(Fig.6B).Post ablation，programmed stimulation of the atrium using up to triple extra-stimuli was unable to induce any further atrial tachyarrhythmias.

The activation map demonstrated a tachycardia that appeared to involve the mitral annulus and was mitral isthmus dependent.After the initial ablation along the mitral isthmus，the lengthening of the tachycardia cycle length was consistent with an alteration in the circuit with possibilities being ablation of an inner loop but not the critical zone of conduction，changing the activation of the circuit to then include the posterior wall，or a multiple loop reentry circuit such as a figure of 8.Finally，ablation at the 11 o’clock position of the mitral annulus with previously identified fractionated low-voltage electrograms had terminated the tachycardia，consistent with ablation of the critical isthmus and resultant noninducibility.

3 Literature review on atypical atrial flutter

3.1 Etiologies and incidence

Atypical atrial flutter，sometimes called non-focal atrial tachycardia(AT)，has a reentrant mechanism and most commonly presents with a history of cardiac surgery，or prior atrial ablation procedure from either a surgical or catheter based approach with presence of atrial scar(Fig.2B，F(xiàn)ig.2C).In a report of patients with left atrial flutter prior to widespread use of catheter ablation for atrial fibrillation 77%had evidence of structural heart disease with the remaining 23%having no obvious structural heart disease［9］.In a more contemporary retrospective multi-center review of 91 patients with atypic al atrial flutter，Coffey et al［5］reported that 65%had prior catheter ablation of the atrial tissue，27%had prior cardiac surgery including a Maze procedure in 12%and idiopathic scar related atypical atrial flutter was found in 8%suggestive of an atrial cardiomyopathy.

The incidence of atypical atrial flutter is likely to increase with more individuals living with congenital heart disease after surgery as well as catheter ablation of atrial fibrillation becoming an increasingly common procedure.In a prospective study of 67 patients undergoing catheter ablation of atrial fibrillation with pulmonary vein isolation and linear ablation，43%of patients had experienced atrial tachycardia，of which 69% had a reentrant mechanism consistent with an atypical atrial flutter，and 31%had sustained atrial tachyarrhythmias using 7-day Holter monitors at 3，6 and 12 months post ablation for screening［6］.Although there is a significant incidence of atrial tachycardias including atypical atrial flutter，after catheter ablation of atrial fibrillation a significant proportion of them are self-limited.Chugh et al［7］reported an experience of 349 patients who underwent catheter ablation for atrial fibrillation with 24%developing macro-reentrant atrial tachycardia during follow-up of approximately 1 year，with 33%of these being are self-resolving，commonly within 5 months after the original ablation procedure，and a strategy for shortterm monitoring may be considered.

3.2 Mapping

The primary tools for mapping an atypical atrial flutter are entrainment，voltage，and activation mapping.The entrainment technique is used to identify sites of concealed entrainment and define the critical isthmus of the circuit for atypical atrial flutter.Constructing a voltage map of the right and/or left atrium help define the low voltage areas that represent scar and can serve as boundaries for the re-entrant circuit.Activation mapping helps define the majority of the cycle length of a reentrant tachycardia on a 3D-mapping system in relation to the atrial anatomy.Additionally areas of double potentials or highly fractionated local electrograms may define lines or block or slow anisotropic conduction，respectively.Each of these techniques has its limitations and an approach integrating all of the information available is important for successful mapping and ablation.

3.2.1 Entrainment mapping Entrainment mapping has become an important tool for interrogating reentrant circuits，and has proven helpful in paroxysmal supraventricular tachycardias as well as defining components of atypical atrial flutter circuits similar to the employment of this technique in mapping ventricular tachycardia.Atrial overdrive pacing from a site of interest during the tachycardia at a cycle length of 10－30 ms shorter than the tachycardia with cessation of pacing and resumption of the tachycardia is the basic maneuver involved in entrainment.Waldo et al［10］proposed 4 criteria for entrainment and has reported the use of entrainment for mapping typical atrial flutter.

Entrainment of an atypical atrial flutter at a location within the atria with the difference between the post-pacing intervaland tachycardia cycle length(PPI－TCL)less than 20 ms is suggestive of the location being within the re-entrant circuit.Furthermore，if there is concealed entrainment where the spontaneous flutter waves on the surface electrocardiogram and activation sequence of the intracardiac atrial electrograms are identical to those seen while pacing during entrainment，the position of the pacing catheter tip is within the critical slow zone of conduction.Mapping locations with a(PPI－TCL)of less than 20 ms，concealed entrainment and progressively shorter stimulus to surface flutter wave intervals is consistent with points progressively closer to exit site of the circuit.

Entrainment provides a general idea of the location of the components of an atypical atrial flutter circuit but should be used in conjunction with other mapping modalities.The sensitivity and specificity of these maneuvers for typical atrial flutter have been investigated by Morton et al［11］.The sensitivity and specificity for concealed entrainment，and hence isthmus identification，pacing a cycle length 10 ms shorter than the flutter cycle length were 100%and 54%respectively，with declining sensitivity and improved specificity with progressively shorter cycle lengths of overdrive［11］.Triedman et al［12］reported acute success rates of 73%and recurrence rates of 53%at a mean of 4 months for ablation of intraatrial reentrant tachycardias in patients with congenital heart disease using identification of low-voltage fractionated diastolic electrograms and entrainment mapping techniques.Although these studies have not addressed atypical atrial flutter specifically，they raise questions about the usefulness of entrainment to accurately predict the location of the isthmus and fully define the circuit involved.Termination of the tachycardia and alteration of the cycle length with entrainment maneuvers also limit its utility in patients with multiple reentrant circuits and diffuse substrate.

3.2.2 Electroanatomical(voltage and activation)mapping Atypical atrial flutters usually have areas of scar tissue that have little or no electrical activity and are identified by the very low voltage or absence of local electrograms.It has been suggested that scar，or electrically silent areas，for a voltage map within the atria be defined as points with a bipolar amplitude of＜0.05 mV and inability to capture atrial tissue with a power output of 20 mA［9］.Visualization of scar and low voltage areas can be achieved by annotating these areas on a computer generated anatomical 3D-map and provides a guide for boundaries of block and potential zones of slow conduction that could represent a critical isthmus.Double potentials are often found at zones of local block and can provide further guidance when assessing gaps in linear ablation lines.Additionally，complex fractionated electrograms representing slow conduction zones can be marked within the map as candidates for a critical isthmus.

Activation mapping uses a 3D-mapping computer system to display local activation time during tachycardia of the atrium relative to a reference point，usually a catheter in the coronary sinus.The difference in the local activation time as compared to the reference point is assigned a color based on the color spectrum with red representing the earliest activation time and violet the latest activation time，with identified activation times spanning 90%or more of the tachycardia cycle length.With an accurate activation map，a potential critical isthmus may be identified by slow zone of conduction，seen on an activation map by a rapid change in color in a confined area.A useful finding of activation mapping is when the earliest local activation is confined to a very small area，suggestive of a focal mechanism or localized reentry circuit which can be approached with targeting ablation at the earliest activation point.Multipole catheters have been developed and provide an effective means for rapidly mapping non-sustained atrial tachycardias as well as high density mapping.

Nakagawa et al［13］reported using voltage and activation mapping for ablation of 15 sustained macroreentrant right atrial tachycardias in 13 patients with a history of surgical repair of congenital heart disease.With electroanatomical mapping they were able to identify areas of scar as well as channels for propagation which were targeted with radiofrequency ablation and successful termination of all 15 tachycardias and inability to induce sustained atrial tachycardia in any patient post-ablation.Further studies using electroanatomical mapping systems for atypical atrial flutter after atrial fibrillation ablation have yielded similar results［5－7，14－15］.

3.3 Circuit characteristics

The circuits of atypical atrial flutter can be categorized by a number of variables including circuit location，circuit size，morphology，and association with a gap in a previous linear ablation.Atypical atrial flutter related to a prior ablation procedure is often subdivided by size of the circuit with macro-reentrant being defined as a re-entrant circuit size ＞2－3 cm or involving 2 or more atrial segments with activation mapping identifying 90% or more of the tachycardia cycle length，small reentrant defined the tachycardia cycle length is mapped in an area ＜2－3 cm or within 1 atrial segment depending on author.Truly focal atrial tachycardias have a point source and centrifugal spread of the wavefront on activation mapping［6，9，16］.

Anatomical location of a flutter circuit can involve nearly any structure within the left or right atrium.In patients having a history of atrial fibrillation ablation the isthmus is identified most commonly at the mitral isthmus in 25%－42%，left atrial roof in 13%－20%and septal in 13%for macro-reentrant mechanisms;at the antrum of the pulmonary veins，the anterior and posterior wall，base of the LAA，left septum and coronary sinus for small reentrant circuits and focal AT［14－15］.

The common circuit morphologies are single-loop reentry and multiple-loop reentry as well as microreentrant circuits.Linton et al［17］have developed a technique for distinguishing whether a circuit involves a single or double loop reentrant mechanism by measuring the post pacing intervals at two separate locations after sequentially overdrive pacing at each of these locations.In the case of double-loop reentry，the isthmus having the shortest post-pacing interval approximating the tachycardia cycle length with entrainment is ablated initially and the next shortest site targeted if termination of the tachycardia is not achieved.

Reentrant circuits involving conduction across a prior ablation line have been termed gap-related AT’s with up to 96%of re-entrant AT’s being reported as gaprelated［7］.This highlights the importance of complete block across a linear ablation to potentially avoid occurrence of these arrhythmias.Certainly，linear ablation lesions potentially offer higher success rates in patients with persistent atrial fibrillation，but come with the additional cost of higher AT occurrence on follow-up［18］.

3.4 Ablation end-points and success rates

In general，acute success rates are high with freedom from recurrence with long-term follow-up only marginally worse.Septal locations are associated with significantly lower acute and long-term success rates for ablation.Different success rates have also been reported depending on ablation catheter type used.A septal location of flutter circuits are often more resistant to ablation with complex anatomical relationships and potential difficulty of delivering adequate radiofrequency energy in those locations.Coffey et al［5］reported in their review of cases，an acute success rate of 97%and longterm success rates of 77%，being any post-procedure AT during(16±12)months follow-up，of 82%and 67%for non-septal and septal location atrial tachycardias，respectively.Furthermore they found that long-term success rates varied depending on the likely etiology of scar with freedom from AT of 88%with surgical scar，75%for those with a history of catheter ablation and 57%for individuals with idiopathic atrial scarring.Other studies have reported lower acute and long-term success rates but often used the ablation catheter for activation mapping rather than a multi-electrode catheter which may have resulted in a lower density of points when mapping［7，14－15］.

Choice of catheter type may also play a role in acute and long-term success rates with radiofrequency ablation of atypical atrial flutter.A randomized study comparing 3.5 mm open-irrigated tip catheters to 8 mm non-irrigated tip catheters for ablation of atypical atrial flutter showed that acute(94%vs.77%)and long-term success at 10 months follow-up，using 48-hour Holter monitors at 3，6，and 9 months，(92%vs.59%)was higher with the irrigated tip catheter［19］.

4 Conclusion

Atypical atrial flutter is becoming an increasingly prevalent problem as more atrial fibrillation ablations are performed and a larger number of individuals are living after cardiac surgery with atriotomy especially in patients with congenital heart disease.With a systematic approach including entrainment，advanced mapping，and improved understanding of the electroanatomical substrate，the success rates of radiofrequency ablation can approach 90%for this clinically challenging arrhythmia.A number of factors are related to ablation outcomes，including the patient’s surgical and ablation history，location and characteristics of the reentrant circuits，and mapping and ablation catheters.Although not specifically reported for the atypical atrial flutter ablation，success and complications outcomes are often associated with the experience of the operator and the procedural volumes of the medical center for these complex interventional procedures.

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