謝啟應(yīng) 孫澤琳 楊天倫
研究證實,心臟再同步化治療(cardiac resynchronization therapy,CRT)可改善多數(shù)患者左心室射血分?jǐn)?shù)(left ventricular ejection fractions,LVEF),改善伴QRS 波群增寬心力衰竭患者的心功能和預(yù)后[1-2],對心電圖呈典型完全性左束支傳導(dǎo)阻滯、QRS 波群寬度≥150 ms、肺動脈壓較低和LVEF 顯著降低等特征的患者應(yīng)答率更高,尤其是女性[3-4]。目前,常規(guī)CRT 是將左心室導(dǎo)線經(jīng)冠狀靜脈竇(coronary sinus,CS)置入到左心室外膜靜脈分支中,從心外膜起搏左心室。然而,因靜脈解剖結(jié)構(gòu)差異(如CS 開口畸形、靶靜脈缺如、血管嚴(yán)重迂曲或狹窄)及閾值過高、膈神經(jīng)刺激等原因,5% ~10%患者無法經(jīng)冠狀靜脈竇途徑置入左心室導(dǎo)線,術(shù)后亦有20% ~30%患者對CRT 無應(yīng)答[5]。部分患者采用經(jīng)開胸置入左心室心外膜導(dǎo)線或采用心室多部位起搏等方法取得了較好的療效[6-8]。正常情況下,左心室激動由內(nèi)膜向外膜擴(kuò)布,因此,理論上左心室心內(nèi)膜起搏更符合生理,較心外膜起搏更具優(yōu)勢。近年來,國內(nèi)外嘗試對經(jīng)CS 置入左心室導(dǎo)線失敗和CRT 術(shù)后無應(yīng)答的患者采用多種方法行左心室心內(nèi)膜起搏,提高了CRT 成功率和應(yīng)答率[9-16]。2014年美國心律學(xué)會公布的ALSYNC 研究[17]顯示,經(jīng)左心室心內(nèi)膜起搏使約50%的CRT 無應(yīng)答患者獲益。因而,對常規(guī)經(jīng)CS 行CRT 術(shù)失敗或CRT 術(shù)后無應(yīng)答的患者,改用左心室心內(nèi)膜起搏不失為一種可行的辦法。
經(jīng)CS 送導(dǎo)線入左心室外膜靜脈分支是目前常規(guī)CRT手術(shù)的關(guān)鍵點和難點。導(dǎo)線常因血管徑路受限而置入失敗:(1)先天性心臟病或后天獲得性靜脈嚴(yán)重狹窄/閉塞導(dǎo)致手術(shù)難度異乎尋常[18],成功率較低。(2)CS 開口異常(如開口在左心房、畸形、嚴(yán)重狹窄)、竇口(Thebesian 瓣)阻擋或心臟擴(kuò)大后心臟轉(zhuǎn)位等可導(dǎo)致鞘管、導(dǎo)線不能進(jìn)入CS[19-20];部分患者分支開口嚴(yán)重成角或嚴(yán)重迂曲、靶血管分支缺如等導(dǎo)致無法置入導(dǎo)線[9]。(3)CS 分支個體差異較大,多數(shù)患者冠狀靜脈有多條分支,但僅有44.4%患者存在超過1 支以上適合置入起搏導(dǎo)線的靜脈分支[5];因前次手術(shù)刺激靜脈分支閉塞導(dǎo)致再次手術(shù)時無理想靶靜脈;部分患者分支部位因膈神經(jīng)刺激或起搏閾值過高而缺乏靶血管。左心室心內(nèi)膜起搏則較少受上述因素限制,理論上可選擇左心室任何部位置入導(dǎo)線。
左右膈神經(jīng)均走行于心臟表面,置入左心室外膜靜脈分支的導(dǎo)線與左側(cè)膈神經(jīng)相鄰,可刺激膈神經(jīng)導(dǎo)致膈肌跳動。CRT 術(shù)中膈神經(jīng)刺激發(fā)生率為13.0%,術(shù)后為7.5%,多數(shù)發(fā)生在導(dǎo)線置入左心室側(cè)壁中部、后壁中部和心尖部位[21]。因為側(cè)壁中部、后壁中部往往是激動最延遲部位,血流動力學(xué)更優(yōu)[22-23],所以膈神經(jīng)刺激影響導(dǎo)線的置入,降低手術(shù)成功率和術(shù)后應(yīng)答率。而左心室心內(nèi)膜起搏離膈神經(jīng)遠(yuǎn),且不受血管分布限制,可選擇起搏部位多,故極少發(fā)生膈神經(jīng)刺激。
經(jīng)CS 置入左心室心外膜導(dǎo)線多采用被動電極,靶血管較粗大、平直、缺乏固定導(dǎo)線結(jié)構(gòu)及活動過度等易導(dǎo)致術(shù)中、術(shù)后導(dǎo)線移位甚至脫落。左心室心內(nèi)膜起搏,因心內(nèi)膜起搏閾值較外膜低,且采用的螺旋電極穩(wěn)定性較好,導(dǎo)線可達(dá)左心室壁任何區(qū)域,不受靜脈分布限制,可選擇閾值更低的部位起搏。
左心室瘢痕是影響起搏閾值和應(yīng)答率的重要因素。存在左心室瘢痕的患者僅47%CRT 治療有效,而無瘢痕患者則為83%[24]。左心室內(nèi)膜起搏可避開瘢痕區(qū)域,獲得更好的起搏閾值和血流動力學(xué)效應(yīng)。收縮力的生理性跨壁梯度由心內(nèi)膜指向心外膜,內(nèi)膜起搏時左心室心肌收縮力較外膜起搏增加[25]。在左心室最佳部位起搏可獲得最好的血流動力學(xué)效應(yīng),無應(yīng)答率最低。最佳起搏部位因人而異,并不一定是左心室最晚激動部位,可分布在內(nèi)膜和外膜,內(nèi)膜分布居多,但都遠(yuǎn)離心肌瘢痕和電傳導(dǎo)阻滯區(qū)[26-27]。在最佳起搏部位內(nèi)膜起搏較外膜起搏具有更優(yōu)的血流動力學(xué)效應(yīng)[28]。
正常情況下,電激動由左心室內(nèi)膜向外膜擴(kuò)布。左心室心內(nèi)膜起搏電傳導(dǎo)快,符合正常的激動順序。外膜起搏時激動由外往內(nèi)擴(kuò)布,逆轉(zhuǎn)了左心室跨壁激動順序,心內(nèi)膜的除極和復(fù)極延遲,跨壁復(fù)極離散度和QT 間期延長,可導(dǎo)致室性心律失常發(fā)生[29-30]。而心內(nèi)膜起搏時心室內(nèi)傳導(dǎo)時間和跨壁傳導(dǎo)時間顯著快于心外膜起搏,能有效減小左心室的跨壁復(fù)極離散度,具有降低室性心律失常風(fēng)險的潛在優(yōu)勢。
經(jīng)房間隔入徑導(dǎo)線穿過二尖瓣有可能影響瓣膜裝置的完整性和閉合[31],引起或加重二尖瓣反流[32]。經(jīng)主動脈逆行途徑則可能影響主動脈的閉合,導(dǎo)致主動脈瓣反流[33]。而瓣膜反流能導(dǎo)致心臟擴(kuò)大,心力衰竭加重,嚴(yán)重時需要換瓣處理。外徑較細(xì)小的導(dǎo)線有可能減少對瓣膜的影響。
左心室內(nèi)膜導(dǎo)線相關(guān)血栓形成的發(fā)生率高達(dá)37%[31-32]。血栓脫落或經(jīng)房間隔穿刺口/房間隔缺損相關(guān)反常性栓塞可導(dǎo)致卒中等嚴(yán)重臨床事件發(fā)生[9,34]。術(shù)中穿刺間隔或撤出CRT 相關(guān)鞘管可發(fā)生血栓、空氣栓塞,術(shù)后停用口服抗凝劑可導(dǎo)致血栓栓塞事件發(fā)生[9]。右心系統(tǒng)置入導(dǎo)線亦可引起血栓栓塞,但左心室內(nèi)導(dǎo)線相關(guān)血栓栓塞常導(dǎo)致卒中等嚴(yán)重臨床不良反應(yīng)。盡管有患者因存在房間隔缺損、卵圓孔未閉等誤將導(dǎo)線置入左心室,長期隨訪無血栓形成和栓塞事件發(fā)生[35]。實際上,導(dǎo)線存在致使血栓的發(fā)生率遠(yuǎn)高于臨床出現(xiàn)癥狀。故建議術(shù)后終身口服抗凝劑。
心臟植入式電子裝置術(shù)后感染發(fā)生率為2.2%,口服抗凝劑是發(fā)生術(shù)后感染的危險因素之一[36]。左心室內(nèi)膜導(dǎo)線感染可致導(dǎo)線與臨近結(jié)構(gòu)形成贅生物及膿腫、感染性心內(nèi)膜炎、二尖瓣損害等。因感染等原因需要拔除導(dǎo)線時,會面臨贅生物和包繞導(dǎo)線的纖維脫落、二尖瓣裝置損害和心肌撕裂等風(fēng)險。與拔出右心導(dǎo)線不同,盡管超聲未發(fā)現(xiàn)血栓的患者可安全經(jīng)皮拔除左心室內(nèi)膜導(dǎo)線[33],但仍建議首選外科手術(shù)。
經(jīng)穿刺或消融房間隔置入左心室心內(nèi)膜導(dǎo)線是目前最常用的技術(shù),因方法和器械不同而存在多種手術(shù)方式。根據(jù)靜脈入徑不同,可分為三種方式:(1)上、下腔靜脈混合法是目前最常用的術(shù)式。該方法經(jīng)下腔靜脈穿刺房間隔后留置導(dǎo)絲作為標(biāo)識,再經(jīng)上腔靜脈利用射頻消融大頭、可控彎鞘(3830 起搏電極系統(tǒng))或在心臟三維標(biāo)測系統(tǒng)、心臟內(nèi)超聲等引導(dǎo)下將可撕開鞘經(jīng)房間隔送至左心室,沿鞘送入導(dǎo)線固定在左心室理想靶目標(biāo)[9]。手術(shù)的難點在于尋找原來的房間隔穿刺口,易導(dǎo)致手術(shù)失敗。故部分術(shù)者采用經(jīng)上腔靜脈送入圈套器套在由股靜脈送入的房間隔穿刺針上,穿刺成功后將圈套器送入左心房建立導(dǎo)線輸送軌道[37],或經(jīng)股靜脈穿刺房間隔后送起搏導(dǎo)線至左心室固定,后建立軌道將導(dǎo)線尾端經(jīng)上腔靜脈拉出體外連接脈沖發(fā)生器[38]。(2)上腔靜脈法[39]。穿刺鎖骨下靜脈等經(jīng)上腔靜脈送入穿刺針穿刺房間隔,成功后沿導(dǎo)絲送入撕開鞘,將導(dǎo)線固定在左心室內(nèi)膜。此方法房間隔穿刺難度較大。(3)下腔靜脈法。穿刺髂/股靜脈送入穿刺針穿刺房間隔,沿導(dǎo)絲送入可撕開鞘和導(dǎo)線入左心室固定,再由下腔靜脈送入其他導(dǎo)線。此方法所有的導(dǎo)線均由下腔靜脈置入,脈沖發(fā)生器置于腹部,有增加囊袋感染的風(fēng)險[40]。由房間隔入徑導(dǎo)線要經(jīng)過二尖瓣裝置,故有可能影響二尖瓣功能導(dǎo)致二尖瓣反流,為避免血栓栓塞,需終身口服抗凝藥物。
Gamble 等[12]首次報道了經(jīng)穿刺室間隔植入左心室內(nèi)膜電極。手術(shù)簡要過程為:穿刺成功后經(jīng)上腔靜脈沿導(dǎo)絲送Agilis 鞘至右心室,方向指向室間隔,左心室造影確認(rèn)。送Brockenbrough 針或通過射頻能量穿刺室間隔,沿導(dǎo)絲送撕開鞘入左心室,送導(dǎo)線入左心室內(nèi)固定。術(shù)后平均LVEF 增加(14 ±8)%,無血栓栓塞、出血、導(dǎo)線相關(guān)感染事件發(fā)生[11]。該術(shù)式導(dǎo)線不經(jīng)過二尖瓣,故不會影響左心房室瓣功能,但仍然有可能形成血栓,術(shù)中穿刺時要注意室性心動過速、心室顫動的發(fā)生。
目前,尚無臨床應(yīng)用該方式置入左心室內(nèi)膜導(dǎo)線,僅有植入起搏器時誤穿刺動脈,經(jīng)主動脈瓣入左心室置入導(dǎo)線的病例報告[33-34]。Irvine 等[33]報道1 例患者在起搏器植入術(shù)后2 周出現(xiàn)藥物無效的干咳,超聲發(fā)現(xiàn)心室電極誤植入到左心室內(nèi)膜,導(dǎo)線附著血栓。開胸手術(shù)發(fā)現(xiàn)導(dǎo)線穿透左鎖骨下靜脈后入動脈,經(jīng)主動脈瓣至左心室內(nèi)。直接經(jīng)動脈拔除導(dǎo)線,未發(fā)生血栓栓塞事件和影響主動脈瓣功能。Reising等[34]報道1 例植入心室單腔起搏器4 個月的患者出現(xiàn)右上肢無力、臉部麻木等卒中表現(xiàn)。超聲提示起搏導(dǎo)線在左心室,未見血栓,側(cè)位胸片提示心室導(dǎo)線靠后,尖端指向脊柱。順利經(jīng)皮拔除起搏電極后未見相關(guān)并發(fā)癥發(fā)生。Reinig等[41]穿刺豬頸動脈經(jīng)主動脈瓣置入左心室內(nèi)膜導(dǎo)線,6 個月后顯示LVEF 正常,無血栓形成,但主動脈瓣存在輕、中度反流。導(dǎo)線經(jīng)過主動脈瓣有可能影響瓣膜功能,嚴(yán)重的主動脈瓣反流可引起心臟擴(kuò)大、心力衰竭。因而,該術(shù)式安全性和可行性尚需進(jìn)一步研究。
最早在2008 年由Kassai 等[14-15]報道其在經(jīng)胸小切口直視下從心尖部穿刺將導(dǎo)線置入左心室心內(nèi)膜。小切口切開皮膚后經(jīng)胸超聲定位心尖,從心尖穿刺送導(dǎo)線至左心室側(cè)壁固定。該方法和穿刺室間隔途徑一樣,避免了對二尖瓣的影響,但仍然有潛在血栓栓塞和起搏裝置感染的風(fēng)險。目前病例數(shù)較少,有效性和長期安全性尚需進(jìn)一步研究。
Auricchio 等[13]首次報道了3 例CRT 患者植入利用超聲換能激動無導(dǎo)線的左心室內(nèi)膜電極(WiCSw-LV)系統(tǒng)?;颊叻謩e為埋藏式心臟復(fù)律除顫器(ICD)升級CRTD、經(jīng)CS 置入導(dǎo)線失敗和CRTD 術(shù)后無應(yīng)答。穿刺右股動脈,經(jīng)主動脈逆行途徑在左心室游離壁心內(nèi)膜放置9 mm 無導(dǎo)線起搏電極,由經(jīng)胸超聲和心室內(nèi)造影確認(rèn)電極位置及穩(wěn)定性后釋放電極。電極由超聲發(fā)射器激活后與常規(guī)經(jīng)靜脈置入的右心室、右心房導(dǎo)線同步起搏。3 例均成功植入,隨訪發(fā)現(xiàn)心功能均顯著改善,未見并發(fā)癥發(fā)生。2015 年美國心律學(xué)會上報道了SELECT-LV 研究,該研究納入了39 例不適合行CRT或?qū)鹘y(tǒng)CRT 治療無應(yīng)答的心力衰竭患者?;颊咧踩氤暉o線心臟刺激系統(tǒng),結(jié)果顯示左心室起搏比心外起搏可能更為有效。而更大規(guī)模的WiSE-CRT 研究(歐洲多中心臨床試驗,100 例患者)將有望對該系統(tǒng)的有效性和安全性提供更多臨床證據(jù)。
左心室心內(nèi)膜起搏較外膜起搏更符合生理性電激動傳導(dǎo)方式,具有更優(yōu)的血流動力學(xué)作用,在增加手術(shù)成功率和CRT 應(yīng)答率、減少室性心律失常等方面具有一定優(yōu)勢。由于行左心室內(nèi)膜起搏操作復(fù)雜、可能影響左側(cè)房室瓣瓣膜功能、潛在血栓栓塞及感染性心內(nèi)膜風(fēng)險、長期口服抗凝藥物的風(fēng)險和依從性差,目前CRT 選擇行左心室心內(nèi)膜起搏主要為經(jīng)冠狀靜脈竇和(或)經(jīng)胸心外膜置入心外膜導(dǎo)線失敗的補(bǔ)救措施[9],以及CRT 心外膜導(dǎo)線置入術(shù)后無應(yīng)答的患者[7],但病例數(shù)較少、隨訪時間較短。因此,左心室心內(nèi)膜起搏能否作為CRT 的常規(guī)術(shù)式尚需進(jìn)一步改進(jìn)器械、簡化操作方法,以及大規(guī)模臨床試驗和長期隨訪資料證實。
[1]Goldenberg I,Kutyifa V,Klein HU,et al. Survival with cardiacresynchronization therapy in mild heart failure. N Engl J Med,2014,370:1694-1701.
[2]Stavrakis S,Lazzara R,Thadani U. The benefit of cardiac resynchronization therapy and QRS duration:a meta-analysis. J Cardiovasc Electrophysiol,2012,23:163-168.
[3]Killu AM,Grupper A,F(xiàn)riedman PA,et al. Predictors and outcomes of " super-response" to cardiac resynchronization therapy. J Card Fail,2014,20:379-386.
[4]鄒彤,楊杰孚.心臟再同步化治療新指南要點及進(jìn)展. 中國介入心臟病學(xué)雜志,2014,22:538-542.
[5]Khan FZ,Virdee MS,Gopalan D,et al. Characterization of the suitability of coronary venous anatomy for targeting left ventricular lead placement in patients undergoing cardiac resynchronization therapy. Europace,2009,11:1491-1495.
[6]周宏,李振,賀貴寶,等. 左室心外膜電極起搏在冠狀靜脈竇左室電極植入失敗時的應(yīng)用. 江蘇實用心電學(xué)雜志,2012,21:162-164.
[7]秦勝梅,宿燕崗,陳海燕,等. 心臟再同步化治療無反應(yīng)者的治療— —升級為左室雙部位起搏(附二例報道). 中國心臟起搏與心電生理雜志,2015,29:18-23.
[8]Zanon F,Baracca E,Pastore G,et al. Multipoint pacing by a left ventricular quadripolar lead improves the acute hemodynamic response to CRT compared with conventional biventricular pacing at any site. Heart Rhythm,2015,12:975-981.
[9]謝啟應(yīng),孫澤琳,楊天倫,等. 經(jīng)房間隔穿刺左心室內(nèi)膜起搏心臟再同步化治療并文獻(xiàn)分析. 中國現(xiàn)代醫(yī)學(xué)雜志,2015,25:88-93.
[10]Domenichini G,Diab I,Campbell NG,et al. A highly effective technique for transseptal endocardial left ventricular lead placement for delivery of cardiac resynchronization therapy. Heart Rhythm,2015,12:943-949.
[11]Betts TR,Gamble JH,Khiani R,et al. Development of a technique for left ventricular endocardial pacing via puncture of the interventricular septum. Circ Arrhythm Electrophysiol,2014,7:17-22.
[12]Gamble JH,Bashir Y,Rajappan K,et al. Left ventricular endocardial pacing via the interventricular septum for cardiac resynchronization therapy:first report. Heart Rhythm,2013,10:1812-1814.
[13]Auricchio A,Delnoy PP, Regoli F,et al. First-in-man implantation of leadless ultrasound-based cardiac stimulation pacing system: novel endocardial left ventricular resynchronization therapy in heart failure patients. Europace,2013,15:1191-1197.
[14]Kassai I,F(xiàn)riedrich O,Ratnatunga C,et al. Feasibility of percutaneous implantation of transapical endocardial left ventricular pacing electrode for cardiac resynchronization therapy.Europace,2011,13:1653-1657.
[15]Kassai I,F(xiàn)oldesi C,Szekely A,et al. New method for cardiac resynchronization therapy: transapical endocardial lead implantation for left ventricular free wall pacing. Europace,2008,10:882-883.
[16]宿燕崗,聶振寧,秦勝梅,等. 經(jīng)房間隔穿刺行左心室內(nèi)膜植入心臟再同步治療除顫器一例. 中華心律失常學(xué)雜志,2012,16:384-386.
[17]John Morgan.ALSYNC:LV Endocardial Pacing Could Help in CRT Nonresponse.[C/OL]2012-05-12.http://www.medscape.com/viewarticle/824972.
[18]Niazi I,Dhala A,Choudhuri I,et al. Cardiac resynchronization therapy in patients with challenging anatomy due to venous anomalies or adult congenital heart disease. Pacing Clin Electrophysiol,2014,37:1181-1188.
[19]Mondoly P,Marachet MA,Massabuau P,et al. Transseptal implantation of a left ventricular pacing lead for an ectopic location of the coronary sinus ostium in the left atrium. Pacing Clin Electrophysiol,2013,36:e51-e52.
[20]Holda MK,Klimek-Piotrowska W,Koziej M,et al. Anatomical variations of the coronary sinus valve (Thebesian valve):implications for electrocardiological procedures. Europace,2015,17:921-927.
[21]Biffi M,Exner DV,Crossley GH,et al. Occurrence of phrenic nerve stimulation in cardiac resynchronization therapy patients:the role of left ventricular lead type and placement site.Europace,2013,15:77-82.
[22]Rickard J,Kumbhani DJ,Popovic Z,et al. Characterization of super-response to cardiac resynchronization therapy. Heart Rhythm,2010,7:885-889.
[23]Merchant FM,Heist EK,McCarty D,et al. Impact of segmental left ventricle lead position on cardiac resynchronization therapy outcomes. Heart Rhythm,2010,7:639-644.
[24]Chalil S,Stegemann B, Muhyaldeen SA,et al. Effect of posterolateral left ventricular scar on mortality and morbidity following cardiac resynchronization therapy. Pacing Clin Electrophysiol,2007,30:1201-1209.
[25]Derumeaux G,Ovize M, Loufoua J,et al. Assessment of nonuniformity of transmural myocardial velocities by color-coded tissue Doppler imaging:characterization of normal,ischemic,and stunned myocardium. Circulation,2000,101:1390-1395.
[26]Derval N,Steendijk P,Gula LJ,et al. Optimizing hemodynamics in heart failure patients by systematic screening of left ventricular pacing sites:the lateral left ventricular wall and the coronary sinus are rarely the best sites. J Am Coll Cardiol,2010,55:566-575.
[27]Padeletti L,Pieragnoli P,Ricciardi G,et al. Acute hemodynamic effect of left ventricular endocardial pacing in cardiac resynchronization therapy:assessment by pressure-volume loops.Circ Arrhythm Electrophysiol,2012,5:460-467.
[28]Sohal M,Shetty A,Niederer S,et al. Delayed trans-septal activation results in comparable hemodynamic effect of left ventricular and biventricular endocardial pacing:insights from electroanatomical mapping. Circ Arrhythm Electrophysiol,2014,7:251-258.
[29]Tayeh O,F(xiàn)arouk W,Elazab A,et al. Potential pro-arrhythmic effect of cardiac resynchronization therapy. J Saudi Heart Assoc,2013,25:181-189.
[30]Mykytsey A,Maheshwari P, Dhar G,et al. Ventricular tachycardia induced by biventricular pacing in patient with severe ischemic cardiomyopathy. J Cardiovasc Electrophysiol,2005,16:655-658.
[31]Konings TC,Koolbergen DR,Bouma BJ,et al. Iatrogenic perforation of the posterior mitral valve leaflet: a rare complication of pacemaker lead placement. J Am Soc Echocardiogr,2008,21:512. e5-e7.
[32]Rodriguez Y,Baltodano P,Tower A,et al. Management of symptomatic inadvertently placed endocardial leads in the left ventricle. Pacing Clin Electrophysiol,2011,34:1192-1200.
[33]Irvine JN,LaPar DJ,Mahapatra S,et al. Treatment of a malpositioned transcutaneous ventricular pacing lead in the left ventricle via direct aortic puncture. Europace,2011,13:1207-1208.
[34]Reising S,Safford R,Castello R,et al. A stroke of bad luck:left ventricular pacemaker malposition. J Am Soc Echocardiogr,2007,20:1316.e1-e3.
[35]Wedekind H,Muller JG. Visual diagnosis in cardiology:malposition of dual-chamber pacemaker lead. Anaesth Intensive Care,2007,35:806.
[36]Lekkerkerker JC,van Nieuwkoop C,Trines SA,et al. Risk factors and time delay associated with cardiac device infections:Leiden device registry. Heart,2009,95:715-720.
[37]Lau EW. Yoked catheter positioning in transseptal endocardial left ventricular lead placement. Pacing Clin Electrophysiol,2011,34:884-893.
[38]Elencwajg B,López Cabanillas N,Cardinali EL,et al. The Jurdham procedure:endocardial left ventricular lead insertion via a femoral transseptal sheath for cardiac resynchronization therapy pectoral device implantation. Heart Rhythm,2012,9:1798-1804.
[39]Calvo N,Arguedas H,Canepa JP,et al. Endocardial left ventricular lead placement from the left subclavian vein approach. Europace,2014,16:1857-1859.
[40]Moria-Vázquez P,Barba-Pichardo R, Gamero JV,et al.Implantation via the femoral vein of a biventricular defibrillator with transseptal endocardial left ventricular pacing. Rev Esp Cardiol,2009,62:1503-1505.
[41]Reinig M,White M,Levine M,et al. Left ventricular endocardial pacing:a transarterial approach. Pacing Clin Electrophysiol,2007,30:1464-1468.