譚紅偉 張旭敏 鄒 譽(yù) 周 建 李 瑩 邱建平 劉學(xué)波
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·臨床研究·
起源于左冠狀動(dòng)脈竇及右冠狀動(dòng)脈竇的室性早搏心電圖特征分析及射頻消融治療
譚紅偉張旭敏鄒譽(yù)周建李瑩邱建平劉學(xué)波
200120上海,同濟(jì)大學(xué)附屬東方醫(yī)院心內(nèi)科
【摘要】目的:比較左冠狀動(dòng)脈竇及右冠狀動(dòng)脈竇起源的室性早搏(室早)心電圖特征。方法:入選成功行主動(dòng)脈根部室早消融的患者20例,按消融部位分為左冠狀動(dòng)脈竇室早組(LCC組)15例、右冠狀動(dòng)脈竇室早組(RCC組)5例,比較兩組心電圖特征。結(jié)果:RCC組患者Ⅰ導(dǎo)聯(lián)均為R波;LCC組患者Ⅰ導(dǎo)聯(lián)4例為QS波,10例為RS或rs波,1例為R波(χ2=16.80,P<0.01)。與RCC組比較,LCC組患者Ⅲ導(dǎo)聯(lián)R波振幅增高 [(2.01± 0.45) mV對(duì)(1.45± 0.33) mV, P<0.05]、 aVL導(dǎo)聯(lián)QS波振幅加深[(1.20± 0.24) mV 對(duì)(0.65± 0.21) mV, P<0.01]、R波振幅Ⅲ/Ⅱ比值及QS波振幅aVL/aVR比值增大 (1.09± 0.12 對(duì) 0.80± 0.12,P<0.001; 1.31±0.35 對(duì) 0.60±0.24, P<0.001)、Ⅰ導(dǎo)聯(lián)QRS波時(shí)限縮短[(78± 32) ms 對(duì)(120± 13) ms,P<0.05]、aVL導(dǎo)聯(lián)QRS波時(shí)限延長(zhǎng) [(128±14) ms 對(duì)(100±24) ms, P<0.05]。除1例患者因起源點(diǎn)臨近左冠狀動(dòng)脈開(kāi)口而放棄消融外,其余均消融成功。平均隨訪(13 ± 6)個(gè)月,無(wú)復(fù)發(fā)病例及并發(fā)癥。結(jié)論:對(duì)于體表心電圖提示室早起源于左室流出道的患者,Ⅰ導(dǎo)聯(lián)R波提示RCC室早,Ⅰ導(dǎo)聯(lián)RS或rs波提示LCC室早;與RCC室早相比,LCC室早Ⅲ導(dǎo)聯(lián)R波振幅較高、aVL導(dǎo)聯(lián)QS波振幅較大、R波振幅Ⅲ/Ⅱ比值及QS波振幅aVL/aVR比值增大。
【關(guān)鍵詞】室性早搏;射頻消融;主動(dòng)脈根部;心電圖
Electrocardiography
特發(fā)性室性心律失常包括室性早搏(室早)及室性心動(dòng)過(guò)速(室速),主要起源于右室流出道,左室流出道也是其好發(fā)部位之一[1-2]。研究顯示左室流出道特發(fā)性室性心律失常最常見(jiàn)的部位是主動(dòng)脈竇部,少部分起源于左室間隔、二尖瓣環(huán)或左室頂部[3-6]。本研究對(duì)左冠狀動(dòng)脈竇(left coronary cusp, LCC)及右冠狀動(dòng)脈竇(right coronary cusp, RCC)起源室早的心電圖特征進(jìn)行比較,探討體表心電圖鑒別LCC及RCC室早的價(jià)值。
1對(duì)象與方法
1.1研究對(duì)象
入選2013年1月至2015年6月在我院行主動(dòng)脈根部室早射頻消融治療的患者20例,其中男性5例,平均年齡(56±16)歲。入選標(biāo)準(zhǔn):(1)年齡>18歲;(2)術(shù)前體表心電圖及24 h動(dòng)態(tài)心電圖(holter)均為頻發(fā)單形性室早;(3)有心悸、胸悶等癥狀,服用1種以上抗心律失常藥物療效不佳;(4)體表心電圖胸導(dǎo)聯(lián)移行在V3或V3以前;(5)術(shù)前體格檢查、胸片、超聲心動(dòng)圖除外器質(zhì)性心臟病。
1.2心電圖分析
記錄所有患者竇性心律及室早的12導(dǎo)聯(lián)同步心電圖,走紙速度100 mm/s。記錄心電圖時(shí)確保V1及V2導(dǎo)聯(lián)位于第4肋間以減少對(duì)體表心電圖特征的影響[7]。分析室早QRS波特征,指標(biāo)包括:(1)QRS波時(shí)限;(2)下壁導(dǎo)聯(lián)(Ⅱ、Ⅲ、aVF)及Ⅰ導(dǎo)聯(lián)R波振幅、時(shí)限及R波振幅Ⅲ/Ⅱ比值;(3)aVL、aVR導(dǎo)聯(lián)QS波振幅、時(shí)限及QS波振幅aVL/aVR比值;(4)胸導(dǎo)聯(lián)V1~V6 R波及S波振幅及時(shí)限。Q、R、S指相對(duì)高振幅的波(>5 mm),q、r、s指相對(duì)低振幅的波(≤5 mm)。QRS波時(shí)限指從12導(dǎo)聯(lián)同步記錄心電圖中QRS波群最早點(diǎn)測(cè)量至最晚點(diǎn)的時(shí)間。
1.3心內(nèi)電生理檢查和導(dǎo)管射頻消融
所有患者在停服抗心律失常藥物5個(gè)半衰期后行心內(nèi)電生理檢查。如患者無(wú)自發(fā)室早,則靜脈滴注異丙腎上腺素誘發(fā)。室早穩(wěn)定出現(xiàn)后,即開(kāi)始電生理標(biāo)測(cè)。所有患者均在Carto 3系統(tǒng)指導(dǎo)下行室早激動(dòng)標(biāo)測(cè)及起搏標(biāo)測(cè)。先經(jīng)右側(cè)股靜脈穿刺,行右室流出道激動(dòng)標(biāo)測(cè)。消融靶點(diǎn)選擇標(biāo)準(zhǔn)為:局部激動(dòng)領(lǐng)先體表心電圖室早QRS波起點(diǎn)至少20 ms以上和(或)起搏時(shí)至少11~12個(gè)導(dǎo)聯(lián)心電圖QRS波形態(tài)與自發(fā)室早完全相同[8]。消融靶點(diǎn)確定后,采用冷鹽水灌注消融導(dǎo)管,設(shè)置溫度43 ℃,功率30 W,鹽水流速20 mL/min試放電消融20 s。如該靶點(diǎn)消融有效,則繼續(xù)放電消融60~100 s,否則重新行激動(dòng)標(biāo)測(cè)及起搏標(biāo)測(cè)。如右室流出道未發(fā)現(xiàn)理想靶點(diǎn)或右室流出道消融無(wú)效,則行心大靜脈及左室流出道激動(dòng)標(biāo)測(cè)。如激動(dòng)標(biāo)測(cè)提示主動(dòng)脈瓣上領(lǐng)先,則行選擇性冠狀動(dòng)脈造影明確消融導(dǎo)管與左右冠狀動(dòng)脈開(kāi)口的關(guān)系,確保消融導(dǎo)管與左右冠狀動(dòng)脈開(kāi)口之間的距離>5 mm[9-10]。主動(dòng)脈根部消融能量設(shè)置與右室流出道相同。
消融成功標(biāo)準(zhǔn)為:反復(fù)多部位、多程序刺激均不能誘發(fā)與消融前形態(tài)一致的早搏;靜脈滴注異丙腎上腺素不能誘發(fā)與消融前形態(tài)一致的室早;觀察20~30 min,無(wú)自主出現(xiàn)的與消融前形態(tài)一致的室早。
1.4隨訪
所有患者術(shù)后服用阿司匹林100 mg/d,服用1個(gè)月。消融術(shù)后心電監(jiān)護(hù)24 h,次日復(fù)查動(dòng)態(tài)心電圖。消融術(shù)后1個(gè)月、6個(gè)月門診隨診,根據(jù)患者癥狀、心電圖和(或)動(dòng)態(tài)心電圖結(jié)果判定是否復(fù)發(fā)。
1.5統(tǒng)計(jì)學(xué)分析
應(yīng)用SPSS 16.0軟件進(jìn)行統(tǒng)計(jì)學(xué)分析。計(jì)量資料以均數(shù)±標(biāo)準(zhǔn)差表示,兩組間均數(shù)比較采用獨(dú)立樣本t檢驗(yàn);計(jì)數(shù)資料以率表示,率的比較采用χ2檢驗(yàn)。以P<0.05為差異有統(tǒng)計(jì)學(xué)意義。
2結(jié)果
2.1臨床特征
本研究共入選20例經(jīng)射頻消融治療證實(shí)起源于主動(dòng)脈根部室早患者,其中LCC組15例,RCC組5例,所有患者均無(wú)器質(zhì)性心臟病證據(jù)(見(jiàn)表1)。
表1 兩組患者臨床特征比較
注:NS為差異無(wú)統(tǒng)計(jì)學(xué)意義(以下相同)
2.2 心電圖特征比較
所有患者下壁導(dǎo)聯(lián)(Ⅱ、Ⅲ、aVF)均為R波,aVL及aVR導(dǎo)聯(lián)均為QS波。RCC組患者Ⅰ導(dǎo)聯(lián)均為R波;LCC組患者Ⅰ導(dǎo)聯(lián)4例為QS波,10例為RS或rs波,1例為R波(χ2=16.80,P<0.01)。RCC組患者V1導(dǎo)聯(lián)2例為QS波,4例為rS波;LCC組患者V1導(dǎo)聯(lián)4例為QS波,7例為rS波3例為qrS波,1例為R波。
與RCC組比較,LCC組Ⅲ導(dǎo)聯(lián)R波振幅增高 [(2.01± 0.45) mV 對(duì) (1.45± 0.33) mV,P<0.05];與RCC組比較,LCC組aVL導(dǎo)聯(lián)QS波振幅加深 [(1.20±0.24) mV 對(duì) (0.65±0.21) mV,P<0.01];與RCC組比較,LCC組R波振幅Ⅲ/Ⅱ比值及QS波振幅aVL/aVR比值增大 (1.09± 0.12 對(duì)0.80± 0.12,P<0.001;1.31±0.35 對(duì)0.60±0.24,P<0.001)(見(jiàn)表2)。
兩組QRS波時(shí)限比較無(wú)顯著性差異。與RCC組比較,LCC組Ⅰ導(dǎo)聯(lián)QRS波時(shí)限縮短[(78± 32) ms 對(duì)(120± 13) ms,P<0.05];與RCC組比較,LCC組aVL導(dǎo)聯(lián)QRS波時(shí)限顯著延長(zhǎng) [(128±14) ms 對(duì) (100±24) ms,P<0.05],見(jiàn)表2、3 。
典型的LCC室早和RCC室早體表心電圖見(jiàn)圖1。
2.3消融結(jié)果
本研究中,除1例患者因室早起源點(diǎn)距左冠狀動(dòng)脈開(kāi)口<5 mm,放棄消融外,其余患者均成功消融室早。術(shù)中及術(shù)后無(wú)嚴(yán)重并發(fā)癥。
表2 兩組患者心電圖肢體導(dǎo)聯(lián)指標(biāo)比較
表3 兩組患者心電圖胸導(dǎo)聯(lián)指標(biāo)比較
注:A為L(zhǎng)CC室早體表心電圖, Ⅰ導(dǎo)聯(lián)呈RS型,aVL/aVR>1.00;B為RCC室早體表心電圖, Ⅰ導(dǎo)聯(lián)呈R型,aVL/aVR<1.00
2.4隨訪結(jié)果
術(shù)后超聲心動(dòng)圖檢查顯示主動(dòng)脈瓣及瓣下結(jié)構(gòu)與功能均未受影響。門診平均隨訪(13 ± 6)個(gè)月,無(wú)復(fù)發(fā)病例,無(wú)并發(fā)癥發(fā)生。
3討論
本研究入選20例體表心電圖懷疑左室流出道起源室早的患者,結(jié)合射頻消融最終靶點(diǎn),分析左冠竇及右冠竇起源的室早的心電圖特征,結(jié)果發(fā)現(xiàn):(1)Ⅰ導(dǎo)聯(lián)R波提示RCC室早,Ⅰ導(dǎo)聯(lián)出現(xiàn)S或s波提示LCC室早;(2)與RCC室早相比,LCC室早Ⅲ導(dǎo)聯(lián)R波振幅較高、aVL導(dǎo)聯(lián)QS波振幅較大、R波振幅Ⅲ/Ⅱ比值及QS波振幅aVL/aVR比值增大;(3)經(jīng)導(dǎo)管射頻消融治療LCC及RCC室早是一種安全、有效的方法。
LCC與RCC室早具有不同心電圖特征,與其解剖有關(guān)。主動(dòng)脈根部位于心臟中心,由3個(gè)瓦氏竇組成,LCC及RCC與室間隔肌部相鄰,而無(wú)冠竇位于左右房之間,與房間隔相鄰[11-12]。研究證實(shí),心室肌延伸到主動(dòng)脈或肺動(dòng)脈-心室連接部以上,這些心室肌延伸可能是室早消融的靶點(diǎn)[12-13]。本研究發(fā)現(xiàn)RCC室早Ⅰ導(dǎo)聯(lián)均為R波,而LCC室早Ⅰ導(dǎo)聯(lián)均有S或s波;LCC室早Ⅲ導(dǎo)聯(lián)R波振幅及aVL導(dǎo)聯(lián)QS波振幅增加,其原因可能為L(zhǎng)CC較RCC的位置更高,且更偏左。
體表心電圖具有無(wú)創(chuàng)、簡(jiǎn)便等特點(diǎn),對(duì)于室早導(dǎo)管消融具有重要指導(dǎo)價(jià)值。Ouyang等[11]發(fā)現(xiàn),V1、V2導(dǎo)聯(lián)R/S比值及R波時(shí)限能較準(zhǔn)確區(qū)分右室流出道室早與主動(dòng)脈根部室早。Lin等[14]發(fā)現(xiàn),LCC室早胸導(dǎo)聯(lián)移行在V2導(dǎo)聯(lián),而RCC室早一般在V3。這些指標(biāo)也可以簡(jiǎn)便、較準(zhǔn)確地區(qū)分室早起源,但由于胸導(dǎo)聯(lián)受電極貼片位置影響較大,有局限性[7]。本研究發(fā)現(xiàn)對(duì)體表心電圖提示室早可能起源于主動(dòng)脈根部患者,Ⅰ導(dǎo)聯(lián)R波提示RCC室早,Ⅰ導(dǎo)聯(lián)RS或rs波提示LCC室早;Ⅲ導(dǎo)聯(lián)R波振幅較高、aVL導(dǎo)聯(lián)QS波振幅較深、R波振幅Ⅲ/Ⅱ比值及QS波振幅aVL/aVR比值增大提示室早起源于LCC。
本研究的局限性:(1)樣本量較??;(2)未納入無(wú)冠竇室早(無(wú)冠竇起源室早較少[10]);(3)未使用術(shù)中心腔內(nèi)超聲檢查,僅通過(guò)術(shù)中影像學(xué)檢查無(wú)法準(zhǔn)確定位部分起源于LCC和RCC交界處室早[15]。
參考文獻(xiàn)
[1]Prystowsky EN, Padanilam BJ, Joshi S, et al. Ventricular arrhythmias in the absence of structural heart disease [J]. J Am Coll Cardiol, 2012, 59(20):1733-1744.
[2]Chun KR, Satomi K, Kuck KH, et al. Left ventricular outflow tract tachycardia including ventricular tachycardia from the aortic cusps and epicardial ventricular tachycardia [J]. Herz, 2007, 32(3):226-232.
[3]Lin CY, Chung FP, Lin YJ, et al. Radiofrequency catheter ablation of ventricular arrhythmias originating from the continuum between the aortic sinus of Valsalva and the left ventricular summit: Electrocardiographic characteristics and correlative anatomy [J]. Heart Rhythm, 2016, 13(1):111-121.
[4]Yamada T, Litovsky SH, Kay GN. The left ventricular ostium: an anatomic concept relevant to idiopathic ventricular arrhythmias [J]. Circ Arrhythm Electrophysiol, 2008, 1(5):396-404.
[5]羅慶志,金奇,吳立群. 頻發(fā)室性早搏所致心肌病的電生理特征及其處理 [J]. 國(guó)際心血管病雜志, 2014,40(3): 137-139.
[6]宋衛(wèi)鋒,張嘉瑩,吳曉羽,等. Carto-3指導(dǎo)下射頻消融治療左室特發(fā)性室性心動(dòng)過(guò)速體會(huì) [J]. 國(guó)際心血管病雜志, 2014,40(2): 131-133.
[7]Anter E, Frankel DS, Marchlinski FE, et al. Effect of electrocardiographic lead placement on localization of outflow tract tachycardias [J]. Heart Rhythm, 2012, 9(5):697-703.
[8]Yoshida N, Yamada T, McElderry HT, et al. A novel electrocardiographic criterion for differentiating a left from right ventricular outflow tract tachycardia origin: the V2S/V3R index [J]. J Cardiovasc Electrophysiol, 2014, 25(7):747-753.
[9]Yamada T, McElderry HT, Doppalapudi H, et al. Idiopathic ventricular arrhythmias originating from the aortic root: prevalence, electrocardiographic and electrophysiologic characteristics, and results of radiofrequency catheter ablation [J]. J Am Coll Cardiol, 2008, 52(2):139-147.
[10]Yamada T, Lau YR, Litovsky SH, et al. Prevalence and clinical, electrocardiographic, and electrophysiologic characteristics of ventricular arrhythmias originating from the noncoronary sinus of Valsalva [J]. Heart Rhythm, 2013, 10(11):1605-1612.
[11]Ouyang F, Fotuhi P, Ho SY, et al. Repetitive monomorphic ventricular tachycardia originating from the aortic sinus cusp: electrocardiographic characterization for guiding catheter ablation [J]. J Am Coll Cardiol, 2002, 39(3):500-508.
[12]ada H. Catheter ablation of tachyarrhythmias from the aortic sinuses of Valsalva—when and how? [J].Circ J, 2012, 76(4):791-800.
[13]Hasdemir C, Aktas S, Govsa F, et al. Demonstration of ventricular myocardial extensions into the pulmonary artery and aorta beyond the ventriculo-arterial junction [J]. Pacing Clin Electrophysiol, 2007, 30(4):534-539.
[14]Lin D, Ilkhanoff L, Gerstenfeld E, et al. Twelve-lead electrocardiographic characteristics of the aortic cusp region guided by intracardiac echocardiography and electroanatomic mapping [J]. Heart Rhythm, 2008, 5(5):663-669.
[15]Bala R, Garcia FC, Hutchinson MD, et al. Electrocardiographic and electrophysiologic features of ventricular arrhythmias originating from the right/left coronary cusp commissure [J]. Heart Rhythm, 2010,7(3):312-322.
(收稿:2016-02-21修回:2016-04-25)
(本文編輯:梁英超)
·基礎(chǔ)研究·
通信作者:劉學(xué)波,Email:lxb70@hotmail.com
doi:10.3969/j.issn.1673-6583.2016.03.012
Electrocardiographic characteristics and radiofrequency catheter ablation of premature ventricular contractions originating from left and right coronary cusp
TANHongwei,ZHANGXumin,ZOUYu,ZHOUJian,LIYing,QIUJianping,LIUXuebo.
DepartmentofCaridology,ShanghaiEastHospitalaffiliatedtoTongjiUniversity,Shanghai200120,China
【Abstract】Objective:This study was undertaken to compare the electrocardiography characteristics of premature ventricular contractions (PVCs) from left coronary cusp (LCC) and right coronary cusp RCC. Methods:We studied 20 consecutive patients who underwent successful catheter ablation for PVCs originating from LCC (n=15) and RCC (n=5). Characteristics of 12-lead ECG were analyzed. Results:All patients with RCC PVCs presented R morphology in lead Ⅰ, whereas in patients with LCC PVCs, 4 presented QS morphology, 10 presented RS or rs and 1 presented R morphology (P<0.01). The R wave amplitude in lead Ⅲ were significantly higher [(2.01± 0.45) mV vs. (1.45± 0.33) mV, P<0.05] and the Q wave amplitude in aVL were significantly deeper [(1.20± 0.24) mV vs. (0.65± 0.21) mV, P<0.01] in patients with LCC PVCs than that in patients with RCC PVCs. Compared with RCC PVCs, the Ⅲ/Ⅱ ratio of R wave amplitude and aVL/aVR ratio of QS wave amplitude were significantly larger in patients with LCC PVCs (1.09± 0.12 vs. 0.80± 0.12; 1.31±0.35 vs. 0.60±0.24, both P<0.001).The QRS duration was significantly shorter in lead I [(78± 32) ms vs. (120± 13) ms, P<0.05] and longer in lead aVL [(128±14) ms vs. (100±24) ms, P<0.05] in patients with LCC PVCs than that in patients with RCC PVCs. The ablation procedures succeeded in all patients except far one whose ablation was not performed because the origin of the PVCs was identified close to the ostium of left coronary artery. There were no major procedural complications. No patient developed PVCs recurrence during a mean follow-up of (13 ± 6) months. Conclusion:In patients with left ventricular out-flow tract PVCs, a relatively large R wave in lead Ⅰ is seen in RCC PVCs while RS or rs wave in lead Ⅰ seen in LCC PCVCs. LCC PVCs shows higher R wave in lead Ⅲ, deeper Q wave in aVL, higher Ⅲ/Ⅱ ratio of R wave amplitude and aVL/aVR ratio of QS wave amplitude.
【Key words】Premature ventricular contractions; Radiofrequency ablation; Aortic root;