Lesson Sixty-five EHRA/HRS/APHRS expert consensus on p remature ventricular comp lexes and non-sustained ventricular tachycard ia

●心電學英語

Lesson Sixty-five EHRA/HRS/APHRS expert consensus on p remature ventricular comp lexes and non-sustained ventricular tachycard ia

Premature ventricular com plexes

Premature ventricular complexes(PVCs)are common both in patients with and without structural heart disease(SHD)and may be asymptomatic even for patientswith high frequency of these beats.Other patients may be highly symptomatic with relatively few ectopic beats.

Several studies have demonstrated an association between frequent PVCsand a potentially reversible cardiomyopathy,which in selected patients resolves after catheter ablation.The number of PVCs/24 h that is associated with impaired LV function has generally been reported atburdens above 15-25%of the total cardiac beats,though thismay be as low as 10%.However, since PVCs may be the result of an underlying cardiomyopathy,itmay be difficult to prospectively determine which of these sequences is operative in a given patient.Importantly,the vastmajority of patients with frequentPVCswillnotgo on to develop cardiomyopathy but currently available data do not allow for accurate risk prediction.

Diagnostic evaluation

Electrocardiogram and ambulatorymonitoring

The vastmajority ofpatientswithoutSHDwhohave PVCs have a benign prognosis.An exceptionmay be a very small subsetofpatientswith PVCs thathavea short coupling interval(＜300ms)between the prematureand the preceding beats,a finding which suggests the short QT syndrome and increases the risk ofmalignant VAs. Aswith other VAs,the first step in the evaluation of a patientwith PVCs is to determine the presence or absenceof SHD.For patientswith arrhythmic orother cardiac symptoms,a resting 12-lead ECG is very helpful to evaluate the presence ofmyocardial scar(Q-waves or fractionated QRScomplexes),the QT interval,ventricular hypertrophy,and other evidence of SHD.An echocardiogram provides assessment of right ventricular (RV)and LV structureand function,valvularabnormalities,and pulmonary artery systolic pressure and is recommended for patients with symptomatic PVCs,a high frequency of PVCs(＞10%burden),orwhen the presenceofSHD issuspected.

Exercise testing

For selected patients,especially when there is a suggestion of symptoms associated with exercise,exercise stress testing should be considered to determine whether PVCsare potentiated or suppressed by exercise, to assesswhether longer duration VAs are provoked.A negative exercise test can decrease the probability that catecholaminergic polymorphic ventricular tachycardia (CPVT)is the underlying cause.Premature ventricular complexes thatworsen with exercise should prompt further investigation as these patientsaremore likely to require treatment.

Imaging investigations

Although themajority ofpatientswith PVCs can beaccurately assessed with a 12-lead ECG and echocardiography,contrast-enhanced MRImay provide additional diagnostic and prognostic datawhen the presence or absence of SHD remains in doubt.While thereare no large-scale studies investigating which patients should undergo MRI,themanagementof several forms of SHD associated with PVCsmay be guided by MRI,including dilated cardiomyopathy,hypertrophic cardiomyopathy (HCM),sarcoidosis,amyloidosis,and arrhythmogenic rightventricular cardiomyopathy(ARVC).In these conditions,the presence of ventricular wallmotion abnormalities or myocardial scar detected by delayed gadolinium enhancementmay provide useful prognostic information.In selected patients for whom the diagnosis of ARVC is suspected,the signal-averaged ECG may provide useful information and forms aminor diagnostic criterion for thisdisorder.

Treatment

Indications for treatment in patients without structural heartdisease

In the absence of SHD,themost common indication for treating PVCs remains the presenceofsymptoms thatarenot improved by explanation of theirbenign nature and reassurance from the physician.Some patients may require treatment for frequentasymptomatic PVCs if longitudinal imaging surveillance reveals an interval decline in LV systolic function or an increase in chamber volume.For patientswith＞10 000 PVCs/24 h,follow-up with repeatechocardiography and Holtermonitoring should be considered.It should also be recognized thatPVCburden often fluctuatesover time.

Indications for treatment in patientswith structuralheart disease

In patientswith SHD,symptoms form the primary grounds for considering whether treatment is indicated. Elimination of high burden PVCs(＞10%)in patients with impaired LV function can be associated with significant improvementof LV function,evenwhen significant scarring is present.Catheter ablation may also be helpful when frequent PVCs interfere with cardiac resynchronization therapy.

Medical therapy

For patients whose symptoms are not effectively managed by explanation of their benign nature and reassurance from the physician,a trialofbeta-blockers or non-dihydropyridine calcium antagonistsmay be considered though the efficacy of these agents is quite limited with only 10-15%of patients achieving＞90% PVC suppression.Whilemembrane-active antiarrhythmic drugs(AADs)aremore effective to suppress PVCs, the risk-benefit ratiohasnotbeen carefully evaluated in patients without SHD.Nevertheless,these agents are highly effectiveandmay significantly improve symptoms inmarkedly symptomatic patients.Because these agents may increase the risk ofmortality in patientswith significant SHD,perhapswith theexception ofamiodarone, caution is advised before using them for PVC suppression.

Catheterablation

Catheter ablation of PVCs is recommended for highly selected patients who remain very symptomatic despite conservative treatment or for those with very high PVC burdens associated with a decline in LV systolic function.Multiple studies indicate high efficacy of ablation with PVC elimination in 74-100%of patients. However,procedural successmay be dependent on site oforiginwith lowerefficacy reported for coronary venous and epicardial foci than for other sites.The efficacy of catheter ablationmay be reduced for patientswithmultiplemorphologiesof PVCs or those forwhom the clinical PVCmorphology cannot be induced at the time of the procedure.Although complete PVC elimination is the goal of ablation,it should be noted that partial successmay still be associated with significant improvement in LV systolic function.The published complication rates of catheter ablation for PVC suppression are generally low(～1%).

Non-sustained ventricular tachycardia

Non-sustained ventricular tachycardia(NSVT)is defined as runs ofbeats arising from the ventricleswith duration between 3 beatsand 30 sand with cycle length of＜600ms(＞100 b.p.m.).Similar to PVCs,NSVT is a relatively common finding in patients with either structurally normal or abnormal hearts.NSVT is foundin nearly 6%of patients evaluated for palpitations.In general,therapy for the underlying cardiac disease is indicated rather than for the arrhythmia itself.However, the findingof NSVTshould always trigger furtherevaluation of the patient.

Non-susta ined ventricular tachycardia in the structurally normalheart

Exercise-related NSVT is relatively common and appears to be associated with aworse prognosiswhen it occursduring recovery.Polymorphic NSVT requiresextensive evaluation in both symptomatic and asymptomatic patientswith carefulassessment for the presence of coronary ischaemia.An important inherited arrhythmia which may present as exercise-induced NSVT is CPVT.This condition is typicallymanifested by polymorphic or bidirectional VT which are triggered by sympathetic stimulation and exercise(commonly occurringatan exercise levelof120-130 b.p.m.)and isassociated with an increased risk of sudden death.The underlyingmechanism of CPVT is calcium overload leading to delayed afterdepolarizations as a result ofmutations in the genes coding for ryanodine receptor or calsequestrin proteins.Non-sustained ventricular tachycardia is a relatively common finding among athletes.Other causes of NSVT in the absence of SHD include QT interval prolongation caused bymutations in proteins regulating repolarizing currents or electrolyte abnormalities.Athleteswith NSVT should be evaluated for the presence of HCM,a diagnosiswhichmay overlap with some degree of LVH as an adaptation to exercise. Becauseof this challenging distinction,expertconsultation should be obtained if this diagnosis is suspected. Although only limited data are available regarding the significance of NSVT in athletes without a structural cardiac disease,discontinuation of training isnotgenerally recommended.

Non-sustain ed ventricular tachycardia in structuralheartdisease

Non-sustained ventricular tachycardia is common in ischaemic heart disease and can be recorded in 30-80%of patients during long-term ECGmonitoring where it is usually asymptomatic.No studies have demonstrated amortality benefit of suppressing NSVT with either AADs or catheter ablation and treatment is usually not indicated in asymptomatic patients.A range of studies have demonstrated thatNSVT occurring during the first few days after an acute coronary eventhas noadverse long-term prognostic significance1.However, when NSVT occurs 48 h ormore after MI,there is an increased mortality and morbidity even when asymptomatic.For a patientwith non-ischaemic dilated cardiomyopathy,the prognostic significance of NSVT is uncertain and no studies have provided precise guidance for treatmentin thisgroup ofpatients.

The occurrence of NSVT in patientswith an implanted ICD isassociatedwith an increased frequency of shocks and all-causemortality.For these patients,programming the ICD to a long VT detection time and a high ventricular fibrillation(VF)detection ratemay be especially important.

Diagnostic evaluation

For patientswith an apparently normal heart,the 12-lead ECG should be scrutinized forevidenceof typicaloutflow tractVT,polymorphic VT(PMVT),including torsadesde pointes(TdP),oran inherited arrhythmia syndrome,such as the long QT,short QT,Brugada,or early repolarization syndromes.Outflow tract VAs typically have an inferior axiswith either RV or LV origin. When the precordial transition is＜V3and the ratio of the R-and S-waves in lead V2during PVCs or VT divided by this ratio during sinus rhythm exceeds 0.6,a LV outflow tractorigin isstrongly suggested.In addition to the ECG,an echocardiogram to assess the presence or absence of SHD should also be considered for all patientswith NSVT.For caseswhereSHD issuspected but cannotbe definitively diagnosed with echocardiography, cardiac MRImay be especially useful to confirm the presence or absence ofmyocardial scar or wallmotion abnormalities.

Treatment

Non-sustained ventricular tachycardia in the absence of structuralheartdisease

Most short-lastingmonomorphic NSVTs originate from the RV or LV outflow tracts.These arrhythmiasonly require treatment if they are symptomatic,incessant,or produce LV dysfunction.Sudden death is very rare in patientswith outflow tract VT.The treatmentof these arrhythmias iseithermedicalwith abeta-blocker, anon-hydropyridine calcium blocker,class IC drugs,or with catheter ablation.Non-sustained ventricular tachycardiawith a focalmechanismmay also occur from the papillarymuscles and respond to beta-blockers or catheterablation.In addition,reentrant LV VT utilizing false tendons can be treated with verapamil,though with a relatively high recurrence risk on oral therapy. Catheter ablation is effective for idiopathic reentrant LV VT and should be considered even when this sustained arrhythmia is terminated by intravenous verapamil. Catheter ablation can be recommended for patientswith idiopathic NSVT that is highly symptomatic and drug refractory,especially if itisexercise-induced.

Non-sustained ventricular tachycardia in patients with structuralheartdisease

The recordingofpolymorphic NSVT should prompt a thorough evaluation for the presence of coronary ischaemia as the primary therapy for this arrhythmia should be directed to improving coronary perfusion.If non-sustained PMVT can be classified as a CPVT,the risk of life-threatening arrhythmia is high and beta-blockade therapywith potentialplacementofan ICD is recommended.In cases of TdPVT,anymedication or electrolyte disturbance that prolongs repolarization should beaddressed.

Although an ICD should be considered for all patientswith a significantly reduced LVEF(＜0.35),there may be a role for programmed electrical stimulation in selected patients with NSVT and ischaemic heart disease who have less severe LV dysfunction(LVEF＜0.40).Implantable cardioverter-defibrillator implantation is recommended in this group of patients if VF or sustained VT is inducible with programmed electrical stimulation.Similarly,if NSVT is observed in a patient with a priorMI,a history ofsyncope,and LVEF＞40%, EPS is generally recommended to guide treatment,usuallywith ICD implantation,should sustained VT be inducible2.Non-sustained ventricular tachycardia in an asymptomatic patient with a LVEF＞40%does not usually require specific antiarrhythmic therapy,and the goal is optimized treatmentof the underlying heart disease.In the setting of HCM,ICD therapy is an appropriate consideration if NSVT is presentwith or without othermajor risk factors.In general,AAD therapy may be considered for patients with SHD who experience symptomatic,recurrent NSVT not resolved by revascularization,optimization ofmedical therapy,or treatment of reversible factors.

詞匯

potentiate v.起加強作用,使...強有力

provoke v.對...挑釁,激起,誘導

sarcoidosis n.肉樣瘤病

amyloidosis n.淀粉樣變性

gadolinium n.釓

reassurance n.再保證,勸慰,再保險

surveillance n.監(jiān)視,監(jiān)督

conservative adj.&n.保守,保守的,保守黨,穩(wěn)當?shù)?保守者,防腐劑

trigger n.&v.扳機,導火索;觸發(fā),發(fā)動,使...觸發(fā)

scrutinize v.詳細檢查

incessant adj.不停的,沒完沒了

注釋

1.A range of指“一系列，一套”，如A lthough still debated,a range of potentialmechanisms through which cocoam ightexert its benefitson cardiovascular health have been proposed.雖然仍存爭議，已提出可有益于心血管健康的一系列潛在機制。

2.句子“...usually with ICD implantation,should sustained VT be inducible.”中，“should sustained VT be inducible”是虛擬語氣的一種倒裝結構，完整的句子應是“if sustained VT should be inducibe”。當虛擬從句中包含有助動詞、情態(tài)動詞、動詞be或have時，可省略if，并把上述動詞提到主語之前。

參考譯文

第65課室性期前搏動和陣發(fā)性室性心動過速EHRA/HRS/APHRS專家共識

室性期前搏動

室性期前搏動（PVC）常見于伴或不伴結構性心臟疾?。⊿HD）患者，有患者PVC頻發(fā)而無癥狀，另有患者癥狀明顯而異位搏動較少。

多個研究證實頻發(fā)PVC與潛在可逆性的心肌病之間存在關聯(lián)，所選患者心肌病在導管消融后消失。已報道與左心室功能障礙相關的24h PCV數(shù)即負荷值通常達到總心搏數(shù)的15%～25%以上，盡管可低達10%。然而，鑒于PVC可為心肌病的結果，因此，對于特定的患者難以前瞻性地確定這種因果關系。重要的是大多數(shù)頻發(fā)PVC患者不會發(fā)展為心肌病，但現(xiàn)有的可用資料并不能做出正確的危險預測。

診斷性評估

大多數(shù)無SHD的PVC患者預后良好。極少數(shù)PVC患者例外，期前搏動與其前的心搏之間的偶聯(lián)間期短（＜300ms），提示短QT綜合征，增加惡性室性心律失常的危險。如同其它室性心律失常，PVC患者評估的第1步是確定是否存在SHD。對于心律失?；蚱渌呐K癥狀的患者，靜息12導聯(lián)心電圖非常有助于評估心臟瘢痕的存在（Q波或碎裂QRS波群）、Q-T間期、心室肥大和SHD的其他跡象。超聲心動圖可供評估右心室與左心室結構和功能、瓣膜異常和肺動脈收縮壓，建議用于癥狀性PVC患者、頻發(fā)PVC（負荷＞10%）患者或疑有SHD的患者。

運動試驗

對所選患者，特別當癥狀與運動存在關聯(lián)時，應考慮運動試驗以確定運動是促進或抑制PVC，評估是否誘發(fā)較長時程的室性心律失常。運動試驗陰性可降低兒茶酚胺性多形性室性心動過速（CPVT）作為基本病因的可能性。隨運動而惡化的室性期前搏動應予進一步檢查，這些患者很可能需要治療。

影像學檢查

雖然多數(shù)PVC患者12導聯(lián)心電圖和超聲心動圖能作出正確評估，對不能確定有無SHD者，增強MRI能提供額外的診斷和預后數(shù)據(jù)。盡管沒有大范圍研究調查哪些患者應行MRI檢查，MRI可指導多種伴發(fā)PVC的SHD，包括擴張型心肌病，肥厚型心肌?。℉CM），肉樣瘤病，淀粉樣變性和致心律失常右心室心肌?。ˋRVC）的治療。由延遲釓增強檢測到的心室壁運動異常和心肌疤痕為這些情況提供有用的預后信息。對于擬診ARVC的患者，信號平均心電圖提供有用的信息，并成為這種疾病診斷的次要標準。

治療

無結構性心臟病患者的治療指征

經(jīng)醫(yī)師解釋并確保良性特性后臨床癥狀不緩解是無SHDPVC治療的最常見指征。對于縱向影像監(jiān)測提示階段性左心室收縮功能下降或心室容量增加的一些患者，無癥狀的頻發(fā)PVC需要治療。對于PVC＞10 000/24h患者，應作超聲心動圖和24h動態(tài)心電圖隨訪復查，應了解PVC負荷隨時間而波動。

結構性心臟病患者的治療指征

對于SHD患者，癥狀成為是否考慮治療的主要理由。對于伴有心功能障礙的患者，消除高負荷PVC后左心室功能明顯改善，即使存在明顯的瘢痕形成。當頻發(fā)PVC干擾心臟再同步化治療時，導管消融也是有助的。

藥物治療

醫(yī)師解釋并確保良性特性后癥狀仍然不能有效控制的患者，可考慮試用倍他阻斷劑或非二氫吡啶類鈣拮抗劑，但療效非常有限，只有10%～15%患者PVC抑制達到＞90%。雖然膜活性抗心律失常藥物（AAD）抑制PVC更有效，但對風險-獲益比尚未做過認真評估。盡管如此，這些藥物是高效的，對于癥狀明顯的患者能顯著改善癥狀。由于這些藥物可增加有明顯SHD患者的死亡風險，在使用它們抗PVC之前應謹慎考慮，胺碘酮例外。

導管消融

對于那些經(jīng)保守治療癥狀仍然很明顯或高負荷PVC伴左心室收縮功能下降的高度選擇患者，建議導管消融。多項研究表明消融效率高，70%～100%患者PVC消除。然而，手術的成功依賴于起源部位，冠狀竇或心外膜起源療效低于其他部位。多形性PVC或手術中無法誘發(fā)臨床PVC圖形的患者，導管消融療效降低。雖然完全消除PVC是消融的目標，應注意到部分成功仍然伴隨明顯的左心室收縮功能改善。已發(fā)表的PVC導管消融并發(fā)癥發(fā)生總體低（≤1%）。

陣發(fā)性室性心動過速（NSVT）

NSVT定義為心室起源搏動在3個至30s之間，周長＜600ms（＞100次/min）。類同于PVC，NSVT較常見于心臟結構正?；虍惓５幕颊摺Ｒ娪诮?%因心悸而檢查的患者。通常，治療基礎心臟病而非心律失常本身。然而，發(fā)現(xiàn)NSVT總應該對對患者作進一步檢查。

心臟結構正常的NSVT

運動相關的NSVT相對常見，當出現(xiàn)于恢復期時，似乎預后更差。癥狀性或非癥狀性多形性NSVT患者需要全面評估，認真分析冠狀動脈缺血。CPVT是一種重要的遺傳性心律失常，可表現(xiàn)為運動相關的NSVT。通常表現(xiàn)為多形性或雙向性室性心動過速，由交感刺激或運動誘發(fā)（通常于運動心率達120～130次/min時發(fā)生），伴隨猝死危險性增加。CPVT的基本機制是鈣超載導致延遲后除極，由編碼蘭尼堿受體或隱鈣素蛋白的基因突變所致。NSVT較常見于運動員。無SHD時，NSVT的其他病因包括調節(jié)復極電流的蛋白突變或電解質異常引起的Q-T間期延長。NSVT運動員應作HCM診斷鑒別，因其可與運動相適應的一定程度左心室肥厚重疊。這種鑒別具有挑戰(zhàn)性，當考慮這一診斷時應咨詢專家。盡管有關無結構性心臟病NSVT運動員的可用資料有限，通常不建議中止訓練。

結構性心臟病的NSVT

NSVT常見于缺血性心臟病，長期心電監(jiān)測顯示達30%～80%，通常無癥狀。沒有研究證實抗心律失常藥物或導管消融抑制NSVT能降低死亡率，無癥狀患者通常無需治療。一系列研究已經(jīng)證實發(fā)生于急性冠狀動脈事件最初幾天的NSVT對長期預后無不利影響。然而，NSVT發(fā)生在心肌梗死48h或之后的，即使無癥狀，死亡率也增加。對于非缺血性擴張型心肌病患者，NSVT的預后意義不確定，至今尚無研究為這一群患者提供清晰的治療指南。

植入ICD患者NSVT的發(fā)生伴隨著電擊頻次及所有原因死亡率的增加。對這些患者，程控ICD，延長室性心動過速（VT）探測時間和提高心室顫動探測頻率特別重要。

診斷性評估

對于看起來心臟正常的患者，應作12導聯(lián)心電圖仔細核查典型的流出道VT，多形性VT，包括尖端扭轉型VT，遺傳性心律失常綜合征如長QT，短QT，Brugada，或早復極綜合征的跡象。無論右心室或左心室起源，流出道室性心律失常心電軸向下。當胸導聯(lián)移行區(qū)＜V3且V2上的PVC或VT的R/S與竇性心律相應值對比＞0.6時，高度提示左心室流出道起源。除了心電圖，對所有NSVT患者應作超聲心動圖檢查評估有無SHD。對于疑有SHD但超聲心動圖又不能確診的，MRI特別有助于確定是否存在心肌瘢痕或心室壁運動異常。

治療

無結構性心臟病的NSVT

多數(shù)短陣的單形性NSVT起源于右心室或左心室流出道。當這些心律失常有癥狀、持續(xù)發(fā)作或引起左心室功能不全時需要治療。流出道VT猝死極為罕見。這些心律失?？尚兴幬镏委?，如β受體阻滯劑或非二氫吡啶類鈣通道阻斷劑、Ic類抗心律失常藥物，或導管消融。局灶機制的NSVT也可發(fā)生于乳頭肌，β受體阻滯劑或導管消融有效。另外，利用假腱束的折返性左心室VT可用異搏定治療，盡管口服治療有較高的復發(fā)率。導管消融對特發(fā)性折返性左心室VT有效，當這種持續(xù)性心律失常經(jīng)靜注異搏定中止后應考慮消融。對于癥狀明顯、藥物無效、特別是運動誘發(fā)的特發(fā)性NSVT患者，應行導管消融。

結構性心臟病患者的NSVT

記錄到多形性NSVT應徹底評估冠狀動脈缺血，因為這種心律失常根本的治療是直接改善冠狀動脈灌注。如陣發(fā)性PMVT可歸類為CPVT，危及生命心律失常的危險性高，建議倍他阻斷劑治療及植入ICD。對于尖端扭轉型VT患者，應處理延長復極的任何藥物或電解質紊亂。

雖然所有LVEF（＜0.35）明顯下降的患者考慮植入ICD,對于NSVT合并缺血性心臟病而左心室功能障礙不那么嚴重（LVEF＜0.40）的患者，程控電刺激有用。程控電刺激能誘發(fā)心室顫動或持續(xù)性VT患者，建議置入ICD。同樣，如NSVT見于既往有心肌梗死、暈厥病史而LVEF＞40%的患者，通常建議行電生理檢查指導治療，只要誘發(fā)出VT，通常需植入ICD。無癥狀且LVEF＞40%的患者，NSVT通常不需要特別的抗心律失常治療，目標是充分治療基礎心臟病。伴或不伴其他主要危險因素的HCM患者,發(fā)生NSVT時考慮ICD治療是合適的?？傊?，對于有癥狀的SHD患者，再血管化、充分的藥物治療或控制可逆性因素后NSVT反復發(fā)作，應考抗心律失常藥物治療。

[1]Pedersen C T,Kay G N,Kalman J,et al.EHRA/HRS/APHRS expert consensus on ventricular arrhythmias[J].Europace,2014, 16∶1257-1283.

（童鴻）