Lesson Eighty four Ventricular arrhythmias originating from papillary muscles in the right ventricle

Patient characteristics

Patients in this study consisted of eight consecutive patients with frequent premature ventricular complexes(PVCs)or both PVCs and ventricular tachycardia(VT)who had been referred for catheter ablation and whose arrhythmia was mapped to one of the right ventricular(RV)papillary muscles (PAPs).The control group consisted of 10 consecutive patients who were referred for ablation of symptomatic idiopathic arrhythmias originating in the right ventricle.Patients with RV PAP arrhythmias were predominantly men (seven of eight),while patients in the control group were all women(10/10).Four patients in the RV PAP group and one patient in the control group had an impaired left ventricular function before the procedure.Mean right ventricular ejection fraction was 0.53%±0.08%in the PAP group and 0.57%±0.10%in the control group.MRI did not reveal evidence of right ventricular dysplasia in any of the patients.One patient in the study group had nonsustained VT provoked by ventricular burst pacing,and four patients had inducible VT with burst pacing.Isoproterenol triggered nonsustained VT in one patient and increased the PVC frequency in two patients.In the control group,three of 10 patients had nonsustained VT triggered by isoproterenol infusion.During VT,entrainment could not be demonstrated.

Twelve-lead electrocardiogram

Twelve-lead electrocardiograms(ECGs)of the PVCs and VTs were analyzed for bundle branch block morphology,axis,QRS width,presence of notching in V1to V6(Figure 1),R-wave pattern in V1(rS,QS),and the transition point from predominantly negative S-wave to predominantly positive R-wave deflection in the precordium.An early transition was defined as transition in lead V4or earlier (Figure 1,left panel),and late transition was defined as a transition in V5or V6(Figure 1,right panel).Notches were defined as deflections in the QRS complex aside from1a triphasic pattern(Figure 1).

Pleomorphic PVCs were present in three of the eight RV PAP patients and in three of 10 patients in the control group.A total of 15 VAs were mapped to the RV PAPs.All RV PAP arrhythmias had an rS or QS pattern in lead V1and displayed a left bundle branch block morphology.The mean QRS width during ventricular ectopy was greater in the PAP group(163±21 ms)than in the control group(141±22 ms).In the PAP group,10 PVC morphologies had an inferior axis,and five had a superior axis.In the control group,all arrhythmias had an inferior axis.Notching in the precordial leads was present in 11 of 15 PVC morphologies in the RV PAP group and in five of 13 PVC morphologies in the control group.Late precordial transition (＞V4)was present in patients with posterior or anterior RV PAP arrhythmias.This corresponds to the more apical insertion of both anterior and posterior papillary muscles. Early precordial transition(≤V4)and an inferior axis occurred more often in arrhythmias originating in the septal RV PAP owing to2the more basal insertion of the septal papillary muscle.

Figure1 A:A 12-lead ECG of PVCs originating in a septal papillary muscle.Note the inferior axis,the early transition in lead V3,and the presence of notching.B:A 12-lead ECG of frequent PVCs originating in a posterior PAP.Note the superior axis and the late precordial transition in V5.

Mapping and Ablation(Figures 2 and 3)

Severalmultipolar electrode catheters were introduced into the right ventricle,right atrium,and His position.Programmed right ventricular stimulation was performed using up to four extrastimuli to assess for inducible VT.Programmed stimulation was repeated during infusion of isoproterenol at 2-20 μg/min.An electroanatomical mapping system(CARTO)was used to guide mapping.Activation mapping was performed during ventricular ectopy or VT.In the setting of infrequent ventricular ectopy,pace mapping was used to identify the site of origin.

Radiofrequency energy wasdelivered via a 4-mm-tip catheter or a 3.5-mm-tip irrigated-tip catheter at sites with the earliest endocardial activation during the VA and/or at matching pace-mapping sites.Radiofrequency energy was delivered in a temperaturecontrolled mode with a target temperature of 55℃at a power of≤50 W.With the irrigated-tip catheter,radiofrequency energy was applied at a power of 30-35 W and a maximal temperature of 45℃.Programmed ventricular stimulation with and without isoproterenol infusion was repeated at the end of the procedure.

Figure 2 A:Site of origin of a PVC originating in a posterior papillary muscle.A Purkinje potential is present during sinus rhythm(arrow).The endocardial activation time was-20 ms at the successful ablation site.B:Site of origin of a papillary muscle PVC without a recorded Purkinje potential.

The earliest endocardial activation time during VT orPVCswas23±8msbeforetheQRScomplexintheRV PAP patients and 28±4 ms in the control group.At the site of origin,there were matching pace maps compared with the targeted arrhythmia in the PAP group(a pace-mapmatchofatleast11/12leadswasfoundineight ofeightpatients)andinthenon-PAPgroup(apace-map matchofatleast11/12 leadswasfound in 10/10 patients).The site of origin of the arrhythmia was mapped to the right posterior papillary muscle (n=3),the anterior papillary muscle(n=4),or the septal muscle(n=8).A Purkinje potential at the effective ablation site was identified in two of eight patients in the RV PAP group andinnoneofthecontrolpatients.Themeanamplitudeof the ventricular electrogram at the site of origin of the arrhythmia during sinus rhythm was 2.1±1.4 mV in the RV PAPgroup and 2.9±2.4 mV in the control group.The mean power achieved was similar in the two groups,30.5±8.4 W and 30.4±5.8 W in the PAP and RVOT patients,respectively.The mean temperatures achieved during ablation were 35.5±7.3℃and 35.3±1.6℃in the PAP and RVOT groups and did not differ significantly.The mean impedance was higher in the PAP group(100.9±11.5 ohms)than in the control group (86.6±9.3ohms).Themeanablationtimewas8.9±2.3minutesin patients with single morphology papillary muscle ectopy and 16.9±9.1minutes in patients with two or more right papillary PVC/VT morphologies.The procedure time was longer in the PAP group as compared with in the control group(277±49vs.203±67minutes,respectively).

Real-time imaging

Intracardiac echocardiography was used during the procedures to identify the papillary muscles and to confirm catheter contact with the papillary muscle.Using intracardiac ultrasound the distinction of the site of origin was made between the septal PAP(insertion on the septum)and the anterior or posterior PAP(inserting in the RV free wall or apex).

Right-sided papillary muscle and arrhythmias

Prior studies described VAs originating in thepapillary muscles of the LV in patients with and without prior myocardial infarction.This study demonstrates that VAs also can arise in a RV PAP.Intracardiac echocardiography helped to identify the site of origin of arrhythmias originating from the right ventricle.Similar to arrhythmias originating from left-sided papillary muscles,adequate contact of the ablation catheter with the papillary muscle is important to assure a successful ablation.Structural abnormalities are often observed in patients with left-sided PAP arrhythmias.Scarring was occasionally observed even in the absence of prior myocardial infarction.

Figure 3 Schema of the right ventricle and the origin of PAP-related arrhythmias.

None of the patients in this series showed evidence of delayed enhancement on the preprocedural MRI.However,for the nulling of the MR signal,the signal from the healthy LV myocardium was used and right-sided abnormalities might have been missed owing to lower inversion times.The presence of a lower ejection fraction in half of the PAP patients,despite a similar baseline PVC burden in the control group,is intriguing butmighthave occurred by chance.Consistent with prior reports in patients with reduced ejection fraction and a high burden of PVCs,the LV ejection fraction improved after ablation in all patients with a reduced LV ejection fraction in this study.

Mechanism

RV PAP arrhythmias were not inducible by programmed atrial or ventricular stimulation.Sustained VT,if inducible,was provoked by isoproterenol or burst pacing,suggesting that the underlying mechanism is triggered activity.This is consistent with prior reports in patients with left-sided papillary muscle arrhythmias without prior infarction.Furthermore,VT could not be entrained or terminated by overdrive pacing,also supportingautomaticityinstead ofreentryasthe mechanism.Two of the eight patients in our study had a Purkinje potential at the successful site of ablation at the base of a papillary muscle,suggesting that the Purkinje fiber system might be involved in the arrhythmogenic substrate similar to left-sided papillary muscle arrhythmias.Failure to identify a Purkinje potential in the majority of the patients does not prove the absence of involvement of the Purkinje fiber system but may reflect the difficulty in achieving good contact with the arrhythmogenic papillary muscle.

詞 匯

provoke v.對(duì)...挑釁,激起,誘導(dǎo)

isoproterenol n.異丙腎上腺素

ectopy n.異位

insertion n.插入,插入物,嵌飾

multipolar adj.多極的

extrastimuli n.期外刺激

impedance n.阻抗

distinction n.區(qū)分,榮譽(yù),不同點(diǎn),差別

scar n.&v.疤痕,疤,斑疤,痕,巖礁,創(chuàng)傷；結(jié)疤

null n.&v.零,零位；使...無(wú)效

inversion n.反向,倒轉(zhuǎn)物,倒裝

intrigue n.&v.陰謀,情節(jié),私通；耍陰謀,吸引,使...困惑,私通

burden n.要旨,重負(fù),載重噸,重?fù)?dān),低聲部,負(fù)擔(dān)

automaticity n.自動(dòng)性

arrhythmogenic adj.致心律失常的

注 釋

1.aside from指“除…之外，偏離，暫置不論”，常置于句首，如Aside from their scavenger function,macrophages also possess destabilizing and thrombogenic properties。除了清除功能外，巨噬細(xì)胞也有引發(fā)不穩(wěn)定和促進(jìn)血栓形成特性。

2.owing to指“由于……”，醫(yī)學(xué)文獻(xiàn)中常用，特別強(qiáng)調(diào)因果關(guān)系或內(nèi)在聯(lián)系，可置于句首、句中或句尾，如Owing to the different release kinetics of cTnI and cTnT,the magnitude of rise or fall in the level of these proteins has to be established for every cTn assay individually。由于cTnI和cTnT的不同釋放動(dòng)力學(xué)，每個(gè)cTn試劑盒都必須確立這些蛋白濃度升高或下降的量值。

參考譯文

第84課 右心室乳頭肌起源室性心律失常

患者特征

研究對(duì)象（PAP組）系因頻發(fā)室性期前收縮（PVC）或PVC合并室性心動(dòng)過(guò)速而來(lái)行射頻導(dǎo)管消融手術(shù)（下稱消融），同時(shí)標(biāo)測(cè)到心律失常起源于右心室乳頭?。≒AP）的8例連續(xù)患者。對(duì)照組為因右心室起源特發(fā)性心律失常來(lái)行消融的連續(xù)10例癥狀性患者。右心室PAP心律失?；颊叨酁槟行裕?/8），而對(duì)照組全為女性（10/10）。術(shù)前右心室PAP組中4例和對(duì)照組中1例存在左心室功能障礙。PAP組平均射血分?jǐn)?shù)（0.53±0.08）%，對(duì)照組為（0.57±0.10）%。所有患者 MRI均無(wú)右心室發(fā)育不良跡象。研究組心室猝發(fā)起搏誘發(fā)非持續(xù)性室性心動(dòng)過(guò)速（VT）1例，猝發(fā)起搏誘發(fā)可誘發(fā)性VT 4例。異丙腎上腺素促發(fā)非持續(xù)性VT 1例，增加PVC頻率2例。對(duì)照組10例中的3例滴注異丙腎上腺素促發(fā)非持續(xù)性VT。VT時(shí)不能拖帶。

12導(dǎo)聯(lián)心電圖

對(duì)PVC和VT的12導(dǎo)聯(lián)心電圖的束支傳導(dǎo)阻滯圖形，心電軸，QRS 寬度，V1～V6導(dǎo)聯(lián)的切跡（圖 1），V1的 R 波形態(tài)（Rs,QS）以及胸導(dǎo)聯(lián)從負(fù)向S波為主轉(zhuǎn)為正向R波為主的移行點(diǎn)進(jìn)行分析。移行點(diǎn)位于V4或以前的為早移行（圖1A），位于V5V6的為晚移行（圖1B）。切跡是指不考慮三相波圖形的QRS波群中的反折（圖1）。

右心室PAP組8例中的3例、對(duì)照組10例中的3例出現(xiàn)多形性PVC。共標(biāo)測(cè)到15種室性心律失常源于右心室PAP。所有右心室PAP心律失常在V1表現(xiàn)為Rs或QS波，呈左束支傳導(dǎo)阻滯型。室性異位心律QRS波群平均寬度PAP組（163±21）ms大于對(duì)照組（141±22）ms。PAP 組中 10種PVC形態(tài)表現(xiàn)為心電軸向下，5種心電軸向上。對(duì)照組所有心律失常心電軸向下。右心室PAP組15種PVC中的11種、對(duì)照組13種PVC中的5種胸導(dǎo)聯(lián)存在切跡。右心室后或前乳頭肌起源心律失常胸導(dǎo)聯(lián)移行晚（＞V4）。這與前和后乳頭肌插入點(diǎn)更接近心尖相關(guān)。胸導(dǎo)聯(lián)早移行與向下電軸更多見于右心室間隔乳頭肌起源心律失常，這與間隔乳頭肌插入點(diǎn)更近基底部有關(guān)。

標(biāo)測(cè)與消融（圖 2、3）

多根多極電極導(dǎo)管置于右心室、右心房和希氏束部位。采用多達(dá)四個(gè)期外刺激的程控右心室刺激誘發(fā)VT。滴注異丙腎上腺素2～20 μg/min期間重復(fù)程控刺激。電解剖標(biāo)測(cè)系統(tǒng)（CARTO）用于標(biāo)測(cè)。室性異位搏動(dòng)或VT期間進(jìn)行激動(dòng)標(biāo)測(cè)。室性異位搏動(dòng)少見時(shí)采用起搏標(biāo)測(cè)確定起源點(diǎn)。

采用頭端4-mm的導(dǎo)管或3.5-mm的灌注導(dǎo)管，于室性心律失常時(shí)最早的心內(nèi)膜激動(dòng)點(diǎn)或匹配的起搏標(biāo)測(cè)點(diǎn)進(jìn)行消融。溫控55℃、功率≤50W釋放消融能量。灌注導(dǎo)管釋放能量30～35W、最大溫度45℃。消融結(jié)束時(shí)滴注或非滴注異丙腎上腺素下重復(fù)程控心室刺激。

VT或PVC時(shí)最早心內(nèi)膜激動(dòng)時(shí)間與QRS波群比較，RV PAP 組提前（23±8）ms，對(duì)照組提前（28±4）ms。在起源部位，起搏標(biāo)測(cè)圖與PAP組（全部8例起搏標(biāo)測(cè)圖匹配至少達(dá)11/12導(dǎo)聯(lián)）和非PAP組（全部10例起搏標(biāo)測(cè)圖匹配至少達(dá)11/12導(dǎo)聯(lián)）的目標(biāo)心律失常相匹配。標(biāo)測(cè)到心律失常起源點(diǎn)位于右后乳頭肌3例、前乳頭肌4例、間隔肌8例。右心室研究組8例中的2例有效消融靶點(diǎn)見到浦肯野電位，對(duì)照組10例均未見到浦肯野電位。竇性心律下心律失常起源點(diǎn)心室電圖平均電位右心室 PAP組（2.1±1.4）mV、對(duì)照組（2.9±2.4）mV。兩組消融達(dá)到的平均功率相近，PAP組與右心室流出道組分別為（30.5±8.4）W和（30.4±5.8）W。消融時(shí)達(dá)到的平均溫度PAP組和右心室流出道組分別為（35.5±7.3）℃和（35.3±1.6）℃，無(wú)明顯差異。平均阻抗PAP組（100.9±11.5）Ω高于對(duì)照組（86.6±9.3）Ω。平均消融時(shí)間單一形態(tài)乳頭肌異位搏動(dòng)（8.9±2.3）min，兩種或以上形態(tài)右乳頭肌PVC/VT（16.9±9.1）min。PAP 組手術(shù)時(shí)間（277±49）min大于對(duì)照組（203±67）min。

實(shí)時(shí)顯像

術(shù)中心腔內(nèi)心臟超聲識(shí)別乳頭肌并確定導(dǎo)管接觸乳頭肌。借助心腔內(nèi)超聲區(qū)分間隔乳頭?。ú迦朦c(diǎn)位于間隔）與前或后乳頭肌起源點(diǎn)（插入點(diǎn)位于右心室游離壁或心尖）。

右側(cè)乳頭肌與心律失常

以前報(bào)道過(guò)室性心律失常起源于伴或不伴心肌梗死患者的左心室乳頭肌。本研究證實(shí)室性心律失常也可源于右心室PAP。心腔內(nèi)心臟超聲有助于鑒別右心室心律失常的起源點(diǎn)。與左側(cè)乳頭肌起源心律失常相似，消融導(dǎo)管與乳頭肌充分接觸對(duì)于成功消融十分重要。左側(cè)乳頭肌心律失?；颊呓Y(jié)構(gòu)異常常見，既往無(wú)心肌梗死者偶爾也可見到瘢痕形成。

本系列患者中術(shù)前MRI檢查未見到延遲強(qiáng)化跡象。然而，MR信號(hào)的校零采用的是健康左心室心肌信號(hào)，右側(cè)的異?？梢蜉^低的反轉(zhuǎn)時(shí)間而遺漏。盡管對(duì)照組基線PVC負(fù)荷相近，PAP組患者半數(shù)存在較低的LVEF，這令人困惑，但也可能是偶然所致。與以前報(bào)道的LVEF下降和PVC負(fù)荷高的患者相一致，本研究中所有LVEF降低的患者，消融后LVEF均得到改善。

機(jī)制

右心室PAP心律失常不為心房或心室程控刺激所誘發(fā)。雖然異丙腎上腺素或猝發(fā)刺激可誘發(fā)持續(xù)性VT，提示基本機(jī)制為促發(fā)激動(dòng)。這與既往報(bào)道的不伴心肌梗死的左側(cè)乳頭肌心律失常相一致。另外，VT不能被超速起搏拖帶或中止，也支持自律性而非折返為其機(jī)制。本研究8例中的2例于成功消融點(diǎn)乳頭肌基部見到浦肯野電位，提示浦肯野纖維涉及致心律失?；|(zhì)，這與左側(cè)乳頭肌心律失常相似。未能在其余多數(shù)患者見到浦肯野電位不能證明未累及浦肯野纖維系統(tǒng)，但可反映難以達(dá)到良好接觸致心律失常的乳頭肌。

圖1A：間隔乳頭肌起源PVC 12導(dǎo)聯(lián)心電圖。電軸向下，早移行位于V3，并存在切跡。B：后乳頭肌起源PVC 12導(dǎo)聯(lián)心電圖。電軸向上，胸導(dǎo)聯(lián)晚移行位于V5

圖2A：后乳頭肌起源PVC的起源部位。竇性節(jié)律時(shí)出現(xiàn)浦肯野電位（箭頭所示）。成功消融部位心內(nèi)膜激動(dòng)時(shí)間提前20ms。B:乳頭肌PVC起源部位未記錄到浦肯野電位

圖3右心室和PAP相關(guān)心律失常起源的示意圖