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Ventricular tachycardia in the absence of structural heart disease
  1. Ammar M Killu1,
  2. William G Stevenson2
  1. 1 Department of Cardiovascular Disease, Mayo Clinic, Rochester, Minnesota, USA
  2. 2 Cardiovascular Division, Vanderbilt University Medical Center, Nashville, Tennessee, USA
  1. Correspondence to Dr William G Stevenson, Cardiovascular Division, Vanderbilt University Medical Center, Nashville TN 37232-8802, USA; william.g.stevenson{at}vanderbilt.edu

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Learning objectives

  • Determine the mechanisms of ventricular tachycardia.

  • Recognise the major types of idiopathic ventricular tachycardia.

  • Recognise differences between ventricular tachycardia in patients with inherited arrhythmia syndromes versus those without.

Introduction

The earliest recorded description of ventricular tachycardia (VT) is credited to Sir Thomas Lewis in 19 091. VT is defined as a rhythm originating in the ventricles ≥3 beats duration, with a heart rate of ≥100 beats/minute.2 It is often associated with structural heart disease (SHD), from any disease process affecting ventricular myocardium, including acute or healed myocardial infarction and cardiomyopathies often associated with reduced ventricular ejection fraction and myocardial scar. Less frequently, VT occurs in the absence of SHD. These may be associated with a defined electrophysiological abnormality that is often genetic or may occur with no definable electrical or structural abnormality in which case they are often referred to as idiopathic ventricular arrhythmias (IVT). Detection and characterisation of underlying SHD and recognition of sudden cardiac death (SCD) risk is a critical component of management.

In this article, we review salient features of various types of VTs seen in patients with structurally normal hearts, including some associated with inherited arrhythmia syndromes, and provide an overview of therapy. 

Types of VTs

VT can be classified according to its duration and morphology (figure 1):

Figure 1

Classification of ventricular tachycardia in the absence of structural heart disease.

  • Duration: VT is sustained if it lasts ≥30 s, causes syncope or haemodynamic compromise requiring therapy. 

  • Morphology:

    • Monomorphic VT (MMVT): It has a single QRS morphology, indicating that the sequence of ventricular activation is the same from beat to beat and that a structural substrate or arrhythmia focus is present.

    • Pleomorphic VT:  More than one distinct QRS morphology occurring during same VT episode; it is almost always associated with scar-related VT and is rare in the absence of SHD.

    • Polymorphic VT (PMVT): It has continuously changing QRS morphology, indicating a changing ventricular activation sequence—it occurs due to acute myocardial ischaemia, acquired and congenital long QT syndromes, and in other arrhythmia syndromes. When sustained, it degenerates to ventricular fibrillation (VF).

Mechanisms of VT

VT may arise by one of the three mechanisms (figure 2). Re-entry is due to a circulating wavefront revolving around an anatomical obstacle, usually a region of ventricular scar or region of functional conduction block. Although the arrhythmia substrate is stably present, episodes of VT are usually intermittent, initiated when an excitation wavefront blocks in one direction in the re-entry path and travels in the opposite direction to return to the initial region of block after it has recovered, thus initiating VT. Re-entry is the most common mechanism of sustained MMVT in SHD. Although it appears less commonly in structurally normal hearts, re-entry involving fascicles of the Purkinje system causes verapamil-sensitive fascicular VT. Spiral-wave re-entry takes the form of a circulating curved wavefront that may anchor to a region, causing MMVT, or may meander across the heart giving rise to PMVT or VF. In the absence of SHD, VT often originates from an automatic focus. Triggered activity is due to oscillations in the membrane potential that occur during repolarisation (ie, phase 3, called ‘early afterdepolarisations’, EAD) or immediately following repolarisation (ie, during phase 4, called ‘delayed afterdepolarisations’, DAD). When an afterdepolarisation reaches threshold, a new action potential is generated. If this process repeats, self-sustaining VT may arise. DADs can be produced by factors that increase intracellular calcium, including sympathetic stimulation, digoxin and increasing heart rate. Examples of DAD-mediated VT include idiopathic right ventricular outflow tract (RVOT) VT and catecholaminergic-polymorphic VT (CPVT). EADs are facilitated by prolonged action potential duration and are implicated as an initiating factor in the PMVT, torsades de pointes (TDP). PMVT may be due to the firing of multiple foci or foci initiating re-entry. Automaticity at a slow rate may be normal in the Purkinje system. Abnormal automaticity arises from tissue that is partially depolarised, such as damaged tissue in an infarct border region or perhaps in VTs arising from papillary muscles.

Figure 2

Mechanisms of ventricular arrhythmias. The most common mechanism of ventricular tachycardia is re-entry, especially in patients with structurally abnormal hearts (A). Re-entry is due to a circulating wavefront revolving around an anatomical obstacle, usually a region of scar (as shown), or region of functional conduction block. Other mechanisms include afterdepolarisations (B) and enhanced automaticity (C).

Recognition of VT

Most VT originates from the ventricular myocardium outside the His-Purkinje system giving rise to a QRS morphology typically >140 ms wide. The major electrocardiographic challenge is distinguishing VT from supraventricular tachycardia (SVT) with aberrancy or, less commonly, conduction over an accessory pathway in Wolff-Parkinson-White syndrome. The presence of atrioventricular dissociation with fewer ‘A’s’ than ‘V’s’ usually indicates VT with infrequent exception. A 1:1 atrioventricular (AV) relationship is less helpful as it can be seen either with SVT or VT with 1:1 conduction to the atria. ECG algorithms that aim to help with this distinction incorporate the common principle that a slow initial QRS deflection and unusual QRS axis/vector are more likely to indicate an origin outside of the normal conduction system, and although helpful, none are completely reliable (figure 3).3 4 The QRS morphology of VT is extremely helpful, however, in suggesting the location of the VT exit, which often suggests whether SHD is present. It is important to recall that a wavefront of activation moving away from a positive electrode generates a negative deflection (S-wave) while a wavefront moving toward an electrode produces a positive deflection (R-wave). In general, VT that has a dominant S-wave in V1 is referred to as left bundle branch block (LBBB)-like VT indicating initial depolarisation of the right ventricle (RV) or interventricular septum, beneath the anterior chest wall location of V1, with the wavefront vector moving away from that region. A dominant R-wave in V1 is described as right bundle branch block (RBBB)-like VT and usually indicates a left ventricular (LV) origin. Similarly, a frontal-plane axis directed inferiorly (R wave in II, III, AVF) indicates initial cardiac activation of the cranial aspect of the heart (eg, outflow tract (OFT) region); a superiorly directed frontal-plane axis indicates initial depolarisation of the diaphragmatic aspect of the ventricles.

Figure 3

Illustration explaining the fundamental difference in QRS morphology between sinus rhythm and ventricular tachycardia. In sinus rhythm, the depolarisation wavefront is rapidly conducted through the Purkinje system (yellow arrow), resulting in a narrow QRS complex in the absence of bundle branch block (top). However, rhythms that originate within the ventricular muscle produce a depolarisation wavefront that propagates slowly through the myocardium before engaging the conducting system. This results in a wide QRS with initial slow onset (bottom).

Initial assessment

VT presentations range from asymptomatic arrhythmia noted on routine examination to palpitations (most common), presyncope/syncope and SCD. Other symptoms include chest pain and dyspnoea. Benign non-sustained VT or premature ventricular complexes (PVCs), if frequent, can occasionally cause depressed ventricular dysfunction, presenting similar to tachycardia-induced cardiomyopathy.

Patients presenting with VT require evaluation for SHD, as this is present in over 90% of patients with sustained VT.5 This includes history and physical examination, 12-lead ECG (at rest or with exercise), transthoracic echocardiogram and assessment for CAD if they have an intermediate or greater pretest probability of the disease. Severe symptoms mandate initial in-hospital evaluation for SHD or an arrhythmia syndrome. Benign VT in patients with structurally normal hearts is monomorphic; identification of PMVT should prompt evaluation for ischaemia from coronary artery disease or an inherited arrhythmia syndrome. Further, any ECG abnormality should raise concern for SHD or an arrhythmia syndrome. Although echocardiography is most easily obtained to assess for possible cardiomyopathy, MRI has an increasingly prominent role in the evaluation of ventricular function and scar. In areas of ventricular scar, gadolinium contrast is slow to washout allowing MRI detection of this potential VT substrate.

When SHD is absent, the diagnosis is most likely IVT which has extremely important implications. Most importantly, though there are some exceptions, IVT has an excellent prognosis and sudden death is rare. The rare cases of VF initiated by an idiopathic arrhythmia have been reported in patients who have short-coupled PVCs (arising from the OFT or the Purkinje system)  that interrupt the T-wave and cause very rapid, often PMVT.6 Second, the response to therapy predictably varies with the specific type of IVT. Catheter ablation is curative for many IVTs, providing an alternative to antiarrhythmic drugs.

Non-inherited VT in structurally normal hearts

Idiopathic focal VTs

These arrhythmias originate from a small focus in the ventricles. The mechanism is usually consistent with automaticity, although some may be due to a small re-entry circuit. Indeed, physical or emotional stress can provoke episodes.7 These foci usually cause non-sustained VT or unifocal PVCs, but sustained VT may be seen in approximately 25% of individuals.8 9 As highlighted below, these arrhythmias have stereotypical locations that are indicated by the arrhythmia QRS morphology that predict the likely success of ablation.

Outflow tract VT

The majority of OFT VTs arise from the RVOT, but left ventricular outflow tract (LVOT) variants are common.8 10 Women, aged 30–50 years appear to be the most commonly affected. Triggered activity from DADs is suggested by the observation that adenosine suppresses the arrhythmia, consistent with its antiadrenergic effects (via the inhibitory G-protein).11 Some are terminated by Valsalva manoeuvre (50% in one study),12 likely through release of acetylcholine (decreases cAMP (cyclic AMP) concentrations via muscarinic cholinergic receptors).9 13 Evidence for a somatic mutation increasing sensitivity to sympathetic stimulation of the focus has been reported.14 However, adenosine insensitivity and focal structural abnormalities on cardiac MRI have been reported in some individuals, suggesting that small re-entry circuits or abnormal automaticity may sometimes be a cause.9 15 Like other IVTs, OFT VT is typically induced by sympathetic stimulation (emotional or physical). Often, it emerges during the cool-down phase of exercise, correlating with elevated circulating catecholamines levels.7 In the electrophysiological laboratory, the arrhythmia is induced by burst pacing and isoproterenol or epinephrine infusion is needed to facilitate induction in over 50% of patients.7

RVOT arrhythmias have a typical ECG pattern of LBBB morphology in lead V1 with inferior axis. LVOT arrhythmias can have a similar appearance (figure 4). With foci that are progressively more posterior and leftwards in location (moving from the right aortic valve cusp to the left aortic valve cusp and superior mitral annulus), the R-wave in V1 becomes progressively taller and broader. The OFT is a highly complex anatomical region and predicting the precise location of the VT from the ECG may be difficult and only possible during electrophysiological study where mapping of the pulmonary artery, aortic valve cusps/sinuses of Valsalva, LVOT, coronary venous system and even epicardium may be required (figure 5). It is important to distinguish IVT from other causes of LBBB-morphology VT, such as arrhythmogenic cardiomyopathy or sarcoid with RV scar-related VT (table 1).

Figure 4

Outflow tract ventricular tachycardia. (A) Right ventricular outflow tract tachycardia—characterised by left bundle branch block morphology in lead V1, inferior axis (positive in II, III, aVF). Note also the negative QRS in aVL and aVR (superior leads) as the vector is moving inferiorly away from the positive electrodes of these leads at the left and right arms, respectively. (B) Left ventricular outflow tract tachycardia—early transition in the QRS from lead V1 to V2 is seen.

Figure 5

Outflow tract anatomy. Surgeons view of the heart at the valve annulus level. The coronary sinus has been unroofed, demonstrating the complexity of cardiac anatomy. Specifically, note the spatial relationship and proximity of various sites to the right and left ventricular outflow tracts. AV, aortic valve; AVN, atrioventricular node; LAD, left anterior descending coronary artery; LCx, left circumflex coronary artery; MV, mitral valve; PV, pulmonary valve; RCA, right coronary artery; SOV, sinus of Valsalva; TV, tricuspid valve annulus. Figure courtesy of Dr William Edwards (Mayo Clinic, Rochester, Minnesota).

Table 1

Useful characteristics to assist differentiating idiopathic from scar-related monomorphic RV VT

Therapy is guided by symptoms. Often reassurance as to the benign nature of the arrhythmia is all that is required. If therapy is required, beta-blockers, non-dihydropyridine calcium channel blockers or antiarrhythmic drugs (eg, class Ic drugs such as flecainide or propafenone) diminish symptoms for some patients.13 If pharmacological therapy is not desired or ineffective, catheter ablation is an important treatment option. If the arrhythmia is sufficiently frequent to cause depressed ventricular function, ablation is generally considered even if the arrhythmia is asymptomatic. The efficacy and risks of the ablation procedure are determined by whether the arrhythmia can be precipitated in the laboratory for mapping and whether its origin is accessible for catheter ablation. Detailed assessment of the QRS morphology is helpful in assessing preprocedure risk and anticipated benefit. The LV ‘summit’ (highest point of the left ventricular myocardium) is the most frequent site of idiopathic epicardial LV arrhythmias and represents unique challenges. In such situations, endocardial ablation may be insufficient and detailed mapping within the coronary venous system and/or epicardium, via percutaneous epicardial puncture, may be required.16 17 Ablation eliminates IVT in >80% of patients. Success rates are higher for RVOT than non-RVOT locations.18 Complications are largely related to vascular access and are rarely serious. However, cardiac perforation with tamponade occurs in up to 1% of cases.19 Mapping and ablation in the aortic root and LVOT has the potential for injury to the coronary ostia/arteries and the bundle of His. Therefore, careful anatomic assessment is imperative to minimise risks.

Mitral and tricuspid annular VT

Mitral annular VTs account for fewer than half of IVTs arising from the LV.20 Most arise from the anterior portion of the mitral annulus, close to the aortomitral continuity.21 The QRS morphology is of RBBB, typically with dominant R-waves across the precordial leads that can mimic ventricular pre-excitation. The aetiology is unknown, but foci may be related to remnants of the atrioventricular ring with tissue prone to triggered automaticity.20 21 As VT arising from this location can be related to abnormal substrate and arise due to local re-entry, cardiac MRI (cMRI) is useful to assess for perivalvular scar indicating a myopathic process. Catheter ablation is highly successful for IVTs in these locations—care is required while ablating on the annulus due to proximity to the circumflex coronary artery laterally and the AV node septally.20 21

Peritricuspid annular VTs are infrequent, accounting for <10% of IVTs.22 The VT QRS demonstrates a LBBB pattern, with positive QRS in lead I, V5 and V6. Many arise near the His bundle, where ablation has a risk of heart block (this may account for the lower success rate of ablation compared with those from the lateral tricuspid annulus).

Papillary muscle VT

Idiopathic papillary muscle arrhythmias manifest as a RBBB morphology VT or PVCs, with superior axis if originating from the posterior (inferior) LV papillary muscle and rightward axis if from the lateral papillary muscle (figure 6). Unlike fascicular VTs, which they can resemble, it is usually non-sustained and has a QRS duration >150 ms23. Typically, VT is not inducible with programmed stimulation. However, it is responsive to beta-adrenergic stimulation which suggests either enhanced automaticity or a triggered mechanism. Occasionally, an RV papillary muscle gives rise to an idiopathic arrhythmia that has an LBBB morphology. Adjacent endocavitary structures such as false tendons and the RV moderator band which contain conduction tissue may also be the origin of these VTs.24

Figure 6

Papillary muscle premature ventricular complex (PVC). PVC arising from the inferior papillary muscle is seen. The QRS morphology is typical with a wide right bundle branch block pattern and superior axis.

Papillary muscle arrhythmias can be a challenge to locate and ablate because the focus can be deep within the papillary muscle, although success is achieved for the majority. Intracardiac echocardiography imaging is useful during ablation allowing identification of the papillary muscles, and to view catheter location and tissue contact.25 Papillary muscle arrhythmias can be seen in patients with mitral valve prolapse. Rare patients have SCD that has been associated with fibrosis in the papillary muscles and/or inferobasal LV wall on cMRI that has been suggested to be a potential substrate for dangerous arrhythmia.26 The approach to identifying and treating patients who may be at risk remains controversial.

Fascicular VT

Fascicular VTs involve the Purkinje system—as such, the QRS is relatively narrow, typically <140 ms, and the time from QRS onset to peak (RS interval) is typically <80 ms. (figure 7). Differentiation from SVT with aberrancy may be difficult. The QRS morphology is dependent on which fascicle activates the ventricles during tachycardia. The most common form involves the LV Purkinje system producing RBBB-morphology tachycardia that can have a superiorly or inferiorly directed frontal-plane axis.

Figure 7

Fascicular tachycardia. The QRS is relatively narrow. Precordial concordance is seen. The morphology is that of a left anterior fascicular block, suggesting that activation of the ventricles arises from the left posterior fascicle in this case.

There are two predominant types: interfascicular re-entrant VT accounts for approximately 15% of IVTs from the left ventricle.27–31 It also has been referred to as fascicular tachycardia, idiopathic left VT, Belhassen tachycardia and verapamil-sensitive VT.32–34 The anatomic circuit can involve the left posterior (most common), left anterior or left mid-septal fascicles. Rare cases involve the right bundle branch. The tachycardia cycle length and QRS morphology may vary subtly during VT due to different breakout points at the junction of the Purkinje fibre–myocardial junction. Interfascicular re-entry VT typically presents with sustained VT in young adult males in their third to fifth decade with episodes often precipitated by exertion. SCD is very rare and the prognosis is generally excellent. Although termination by intravenous verapamil is a hallmark of this arrhythmia, chronic oral verapamil or diltiazem therapy has variable success in preventing VT. Therefore, catheter ablation is the major therapy when medications are ineffective or not desired. Ablation targets the distal ramification of the involved fascicles or the adjacent diastolic pathway when this is identifiable. Similar to OFT VT, ablation of fascicular VT has a high acute success rate (>85%), especially when VT is inducible.35 36 When VT is not inducible, empiric anatomic-based ablation may be used targeting the mid to inferior septum midway to two-thirds toward the apex, although up to 20% of patients have recurrences.37

The second form of fascicular VT is relatively uncommon and appears to be due to abnormal automaticity in the Purkinje system. Although classically regarded as a ‘normal heart arrhythmia’, recent studies have demonstrated focal myocardial abnormalities on imaging and association with SHD and myocardial ischaemia.38 The VT may be incessant and can be difficult to suppress with medications. Yet, ablation can be challenging if the arrhythmia cannot be provoked as detailed mapping is required to identify the focus among the complex, branching Purkinje network.

Inherited arrhythmia syndromes

Considering the possibility of an inherited arrhythmia syndrome is extremely important in the evaluation of patients with ventricular arrhythmias in the absence of SHD. The initial evaluation may be the only opportunity to prevent SCD. Recognition of an inherited syndrome should prompt cascade screening of family members. While IVT is almost always monomorphic, most inherited arrhythmia syndromes without SHD cause PMVT or VF (figure 8).

Congenital long-QT syndrome (LQTS)

Symptomatic patients with LQTS may present with syncope and SCD due to PMVT (known as TDP for its characteristic waxing and waning QRS amplitude). Numerous types of congenital LQTS have been described, attributable to 17 gene mutations that result in prolongation of the action potential and, hence, QT interval. However, >90% of cases are due to mutations involving one of three genes that cause LQTS types 1–3. Mutations that decrease repolarising currents from voltage-gated potassium channel account for approximately two-thirds of LQTS, including LQTS1 and LQTS2. Gain-of-function mutation in the SCN5A gene that codes for the cardiac sodium channel causes LQTS3. QT prolongation typically >480 ms is usually present in symptomatic individuals, yet concealed forms with normal QT intervals are well described making identification of asymptomatic carriers difficult.39 Some phenotypes tend to have characteristic precipitating events: swimming for LQT1, sudden startle for LQT2 and sleep for LQT3.

Recently, management has been refined with better definition of the mutations causing the disease and correlations with response to therapies. LQTS1 and LQTS2 respond very well to chronic beta-blocker therapy (typically nadolol or propranolol). Patients who have syncope or cardiac arrest despite beta-blocker therapy or who have other high-risk features are considered for additional therapy and often an implantable cardioverter defibrillator (ICD). Mexiletine and ranolazine, which have sodium-channel blocking effects, may be useful in LQTS3. Surgical cardiac sympathectomy of the lower stellate ganglion and upper thoracic sympathetic chain is useful in selected patients who continue to have symptomatic arrhythmias. Avoidance of QT-prolonging drugs (www.crediblemeds.org) is paramount. Referral to a specialist in genetic arrhythmia syndromes is an important consideration for most patients.

Brugada syndrome

Brugada syndrome (BrS) affects 1 in 5000–10 000 individuals. The typical age of diagnosis is around 40 years and men are affected much more than women (9:1 ratio). Affected individuals are at risk for SCD due to PMVT/VF that typically occurs during sleep. BrS is diagnosed by the presence of ≥2 mm ST-elevation in coved pattern (type 1 pattern) in any lead of V1–V3 (or V1 or V2 positioned an interspace higher than standard). The pattern may emerge only in response to fever or administration of a sodium channel blocker—asymptomatic individuals with this feature appear to be at lower risk of arrhythmia.40 Multiple susceptibility genes for BrS have been described including loss of function mutations in the sodium (SCN5A) or calcium (CACNA1C) channels, but a specific genetic abnormality is identified in fewer than half of patients. Management involves control of fever and avoidance of drugs known to exacerbate arrhythmias (ie, those with sodium-channel blocking properties—a list can be found at brugadadrugs.org). ICDs are recommended for patients with syncope or resuscitation from cardiac arrest. Recurrent episodes of VT/VF can be prevented by chronic therapy with quinidine via blockade of the transient-outward current (Ito, which acts to increase transmural heterogeneity) while isoproterenol can terminate arrhythmia storms.41 42 More recently, epicardial catheter ablation of abnormal areas in the RVOT that display fractionated electrical signals has been shown reduce recurrent PMVT/VF and even reverse the BrS ECG pattern.43

Other repolarisation syndromes

Early repolarisation characterised by J-point elevation >0.1 mV at the terminal phase of the QRS complex is a benign normal variant in the vast majority of people. Rarely, it is associated with SCD, referred to as the Early Repolarisation Syndrome (ERS). In the absence of arrhythmias, patients are termed to have early repolarisation pattern. ERS has an estimated prevalence of 1 in 10 000. Presence in both inferior and lateral ECG leads and a flat, rather than upsloping ST-segment preceding the T-wave may be associated with greater likelihood of disease. Its presence in patients presenting with syncope, resuscitation from cardiac arrest or a family history of SCD raises concern for its diagnosis. However, it remains a diagnosis of exclusion.

Short QT syndrome is a very rare genetic disorder associated with QT <320 ms and predisposition to VF and atrial fibrillation.

Catecholaminergic-polymorphic VT

CPVT is a rare genetic disorder most frequently due to a malfunctioning ryanodine receptor that results in intracellular calcium overload and PMVT from DADs. Patients present with exercise or emotion-induced syncope or cardiac arrest. PMVT or an unusual bidirectional VT can be provoked with exercise testing. Beta-blockers are first-line therapy, followed by flecainide and surgical sympathectomy. ICDs are problematic because ICD shocks elicit sympathetic activation that often reinitiates the arrhythmia and can provoke fatal VT storms.

A summary of idiopathic monomorphic ventricular tachycardia is provided in table 2.

Table 2

Summary features of idiopathic monomorphic VTs and inherited arrhythmia syndromes

Conclusion

Benign forms of VT in the absence of SHD are generally monomorphic, have typical QRS morphologies that aid in recognition and are associated with an excellent prognosis. Catheter ablation is an excellent option for many if treatment is required. VT associated with an inherited channelopathy is more often polymorphic and is associated with SCD despite the absence of SHD. The diagnosis can be difficult and referral to an arrhythmia specialist is often warrantedSupplementary file 1 .

Figure 8

ECG examples of inherited arrhythmia syndromes. (A) Long-QT interval associated torsades des pointes. A junctional escape rhythm is noted with ventricular bigeminy (stars). After the third sequence of bigeminy, the next sequence demonstrates a premature ventricular complex of different morphology that results in polymorphic ventricular tachycardia (which in the context of a long-QT interval is termed torsades des pointes). (B) Type 1 Brugada pattern ECG. Characteristic ST segment elevation with a ‘coved’ pattern is seen in V1 and V2 (arrows). (C) Early repolarisation (arrows) is seen in multiple leads. Inset of each panel magnifies the main finding.

Key messages

  • Ventricular tachycardia (VT) may arise from one of the three mechanisms: re-entry (most common, eg, scar-mediated ventricular tachycardia), triggered activity (eg, right ventricular outflow VT and catecholaminergic-polymorphic VT) and automaticity (eg, idiopathic focal VTs).

  • VT presentations range from asymptomatic arrhythmia to palpitations (most common), presyncope, syncope and sudden cardiac death.

  • Benign forms of VT in the absence of structural heart disease are generally monomorphic, have typical QRS morphologies and are associated with an excellent prognosis.

  • VT associated with an inherited channelopathy is more often polymorphic and is associated with sudden cardiac death.

  • Catheter ablation is an excellent management option for monomorphic VT, if treatment is required.

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View Abstract

Footnotes

  • Contributors AMK–planning, drafting and critical revision of manuscript. WGS–planning and critical revision of manuscript. Both authors are responsible for the overall content of the manuscript.

  • Funding The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.

  • Competing interests WGS has received speaking honoria from Boston Scientific and Abbott Medical and is co-holder of a patent for needle ablation that is consigned to Brigham Hospital.

  • Patient consent Not required.

  • Provenance and peer review Commissioned; externally peer reviewed.

  • Author note References which include a * are considered to be key references.

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