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

●心电学英语

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.

词汇

potentiate v.起加强作用,使...强有力

provoke v.对...挑衅,激起,诱导

sarcoidosis n.肉样瘤病

amyloidosis n.淀粉样变性

gadolinium n.钆

reassurance n.再保证,劝慰,再保险

surveillance n.监视,监督

conservative adj.&n.保守,保守的,保守党,稳当的;保守者,防腐剂

trigger n.&v.扳机,导火索;触发,发动,使...触发

scrutinize v.详细检查

incessant adj.不停的,没完没了

注释

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.虽然仍存争议，已提出可有益于心血管健康的一系列潜在机制。

2.句子“...usually with ICD implantation,should sustained VT be inducible.”中，“should sustained VT be inducible”是虚拟语气的一种倒装结构，完整的句子应是“if sustained VT should be inducibe”。当虚拟从句中包含有助动词、情态动词、动词be或have时，可省略if，并把上述动词提到主语之前。

参考译文

第65课室性期前搏动和阵发性室性心动过速EHRA/HRS/APHRS专家共识

室性期前搏动

室性期前搏动（PVC）常见于伴或不伴结构性心脏疾病（SHD）患者，有患者PVC频发而无症状，另有患者症状明显而异位搏动较少。

多个研究证实频发PVC与潜在可逆性的心肌病之间存在关联，所选患者心肌病在导管消融后消失。已报道与左心室功能障碍相关的24h PCV数即负荷值通常达到总心搏数的15%～25%以上，尽管可低达10%。然而，鉴于PVC可为心肌病的结果，因此，对于特定的患者难以前瞻性地确定这种因果关系。重要的是大多数频发PVC患者不会发展为心肌病，但现有的可用资料并不能做出正确的危险预测。

诊断性评估

大多数无SHD的PVC患者预后良好。极少数PVC患者例外，期前搏动与其前的心搏之间的偶联间期短（＜300ms），提示短QT综合征，增加恶性室性心律失常的危险。如同其它室性心律失常，PVC患者评估的第1步是确定是否存在SHD。对于心律失常或其他心脏症状的患者，静息12导联心电图非常有助于评估心脏瘢痕的存在（Q波或碎裂QRS波群）、Q-T间期、心室肥大和SHD的其他迹象。超声心动图可供评估右心室与左心室结构和功能、瓣膜异常和肺动脉收缩压，建议用于症状性PVC患者、频发PVC（负荷＞10%）患者或疑有SHD的患者。

运动试验

对所选患者，特别当症状与运动存在关联时，应考虑运动试验以确定运动是促进或抑制PVC，评估是否诱发较长时程的室性心律失常。运动试验阴性可降低儿茶酚胺性多形性室性心动过速（CPVT）作为基本病因的可能性。随运动而恶化的室性期前搏动应予进一步检查，这些患者很可能需要治疗。

影像学检查

虽然多数PVC患者12导联心电图和超声心动图能作出正确评估，对不能确定有无SHD者，增强MRI能提供额外的诊断和预后数据。尽管没有大范围研究调查哪些患者应行MRI检查，MRI可指导多种伴发PVC的SHD，包括扩张型心肌病，肥厚型心肌病（HCM），肉样瘤病，淀粉样变性和致心律失常右心室心肌病（ARVC）的治疗。由延迟钆增强检测到的心室壁运动异常和心肌疤痕为这些情况提供有用的预后信息。对于拟诊ARVC的患者，信号平均心电图提供有用的信息，并成为这种疾病诊断的次要标准。

治疗

无结构性心脏病患者的治疗指征

经医师解释并确保良性特性后临床症状不缓解是无SHDPVC治疗的最常见指征。对于纵向影像监测提示阶段性左心室收缩功能下降或心室容量增加的一些患者，无症状的频发PVC需要治疗。对于PVC＞10 000/24h患者，应作超声心动图和24h动态心电图随访复查，应了解PVC负荷随时间而波动。

结构性心脏病患者的治疗指征

对于SHD患者，症状成为是否考虑治疗的主要理由。对于伴有心功能障碍的患者，消除高负荷PVC后左心室功能明显改善，即使存在明显的瘢痕形成。当频发PVC干扰心脏再同步化治疗时，导管消融也是有助的。

药物治疗

医师解释并确保良性特性后症状仍然不能有效控制的患者，可考虑试用倍他阻断剂或非二氢吡啶类钙拮抗剂，但疗效非常有限，只有10%～15%患者PVC抑制达到＞90%。虽然膜活性抗心律失常药物（AAD）抑制PVC更有效，但对风险-获益比尚未做过认真评估。尽管如此，这些药物是高效的，对于症状明显的患者能显著改善症状。由于这些药物可增加有明显SHD患者的死亡风险，在使用它们抗PVC之前应谨慎考虑，胺碘酮例外。

导管消融

对于那些经保守治疗症状仍然很明显或高负荷PVC伴左心室收缩功能下降的高度选择患者，建议导管消融。多项研究表明消融效率高，70%～100%患者PVC消除。然而，手术的成功依赖于起源部位，冠状窦或心外膜起源疗效低于其他部位。多形性PVC或手术中无法诱发临床PVC图形的患者，导管消融疗效降低。虽然完全消除PVC是消融的目标，应注意到部分成功仍然伴随明显的左心室收缩功能改善。已发表的PVC导管消融并发症发生总体低（≤1%）。

阵发性室性心动过速（NSVT）

NSVT定义为心室起源搏动在3个至30s之间，周长＜600ms（＞100次/min）。类同于PVC，NSVT较常见于心脏结构正常或异常的患者。见于近6%因心悸而检查的患者。通常，治疗基础心脏病而非心律失常本身。然而，发现NSVT总应该对对患者作进一步检查。

心脏结构正常的NSVT

运动相关的NSVT相对常见，当出现于恢复期时，似乎预后更差。症状性或非症状性多形性NSVT患者需要全面评估，认真分析冠状动脉缺血。CPVT是一种重要的遗传性心律失常，可表现为运动相关的NSVT。通常表现为多形性或双向性室性心动过速，由交感刺激或运动诱发（通常于运动心率达120～130次/min时发生），伴随猝死危险性增加。CPVT的基本机制是钙超载导致延迟后除极，由编码兰尼碱受体或隐钙素蛋白的基因突变所致。NSVT较常见于运动员。无SHD时，NSVT的其他病因包括调节复极电流的蛋白突变或电解质异常引起的Q-T间期延长。NSVT运动员应作HCM诊断鉴别，因其可与运动相适应的一定程度左心室肥厚重叠。这种鉴别具有挑战性，当考虑这一诊断时应咨询专家。尽管有关无结构性心脏病NSVT运动员的可用资料有限，通常不建议中止训练。

结构性心脏病的NSVT

NSVT常见于缺血性心脏病，长期心电监测显示达30%～80%，通常无症状。没有研究证实抗心律失常药物或导管消融抑制NSVT能降低死亡率，无症状患者通常无需治疗。一系列研究已经证实发生于急性冠状动脉事件最初几天的NSVT对长期预后无不利影响。然而，NSVT发生在心肌梗死48h或之后的，即使无症状，死亡率也增加。对于非缺血性扩张型心肌病患者，NSVT的预后意义不确定，至今尚无研究为这一群患者提供清晰的治疗指南。

植入ICD患者NSVT的发生伴随着电击频次及所有原因死亡率的增加。对这些患者，程控ICD，延长室性心动过速（VT）探测时间和提高心室颤动探测频率特别重要。

诊断性评估

对于看起来心脏正常的患者，应作12导联心电图仔细核查典型的流出道VT，多形性VT，包括尖端扭转型VT，遗传性心律失常综合征如长QT，短QT，Brugada，或早复极综合征的迹象。无论右心室或左心室起源，流出道室性心律失常心电轴向下。当胸导联移行区＜V3且V2上的PVC或VT的R/S与窦性心律相应值对比＞0.6时，高度提示左心室流出道起源。除了心电图，对所有NSVT患者应作超声心动图检查评估有无SHD。对于疑有SHD但超声心动图又不能确诊的，MRI特别有助于确定是否存在心肌瘢痕或心室壁运动异常。

治疗

无结构性心脏病的NSVT

多数短阵的单形性NSVT起源于右心室或左心室流出道。当这些心律失常有症状、持续发作或引起左心室功能不全时需要治疗。流出道VT猝死极为罕见。这些心律失常可行药物治疗，如β受体阻滞剂或非二氢吡啶类钙通道阻断剂、Ic类抗心律失常药物，或导管消融。局灶机制的NSVT也可发生于乳头肌，β受体阻滞剂或导管消融有效。另外，利用假腱束的折返性左心室VT可用异搏定治疗，尽管口服治疗有较高的复发率。导管消融对特发性折返性左心室VT有效，当这种持续性心律失常经静注异搏定中止后应考虑消融。对于症状明显、药物无效、特别是运动诱发的特发性NSVT患者，应行导管消融。

结构性心脏病患者的NSVT

记录到多形性NSVT应彻底评估冠状动脉缺血，因为这种心律失常根本的治疗是直接改善冠状动脉灌注。如阵发性PMVT可归类为CPVT，危及生命心律失常的危险性高，建议倍他阻断剂治疗及植入ICD。对于尖端扭转型VT患者，应处理延长复极的任何药物或电解质紊乱。

虽然所有LVEF（＜0.35）明显下降的患者考虑植入ICD,对于NSVT合并缺血性心脏病而左心室功能障碍不那么严重（LVEF＜0.40）的患者，程控电刺激有用。程控电刺激能诱发心室颤动或持续性VT患者，建议置入ICD。同样，如NSVT见于既往有心肌梗死、晕厥病史而LVEF＞40%的患者，通常建议行电生理检查指导治疗，只要诱发出VT，通常需植入ICD。无症状且LVEF＞40%的患者，NSVT通常不需要特别的抗心律失常治疗，目标是充分治疗基础心脏病。伴或不伴其他主要危险因素的HCM患者,发生NSVT时考虑ICD治疗是合适的。总之，对于有症状的SHD患者，再血管化、充分的药物治疗或控制可逆性因素后NSVT反复发作，应考抗心律失常药物治疗。

[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.

（童鸿）