Ventricular arrhythmias and sudden cardiac death

Key points

• Arrhythmias of ventricular origin carry the greatest risk of sudden death.

• The presence of structural heart disease is the most important risk factor in the development of malignant ventricular arrhythmias.

• Ventricular arrhythmias causing cardiac arrest within 48 hours of myocardial infarction carry the same prognosis as that of a similar sized infarct without cardiac arrest.

• Acute management focuses on resuscitation, chemical or electrical cardioversion, electrolyte restoration, and overdrive pacing.

• Implantable cardioverter defibrillators and electrophysiology catheter-based ablations now offer improved survival and quality of life, respectively.

There are 50–100 unexpected, sudden cardiac deaths (SCDs) per 100 000 population per year in Europe and USA, categorized by symptom onset to cardiac arrest time of <1 h.¹ Despite the decline in coronary artery disease mortality and advancements in resuscitation services, survival from these events remains low. Unfortunately, they often occur outside the hospital environment and are associated with a survival rate of <10%. The majority occur in adults over 35 yr of age and at least half of these events can be attributed to ventricular arrhythmias, although the true incidence is unknown due to inevitable degeneration to asystole if unwitnessed.

These arrhythmias may be the presenting complaint in the emergency department and may feature throughout the perioperative period, including at preoperative assessment, during surgery and in the recovery phase, for example in intensive care. They may also be the direct target of therapy in the case of electrophysiological catheter ablation and implantable cardioverter defibrillators (ICDs). They are more frequent and carry greater risks in patients with structural heart disease, but younger patients with ion-channel abnormalities can also be susceptible.² This review classifies the causes and significance of ventricular arrhythmias based on the presence or absence of structural heart disease and provides a simple system to aid confident distinction from supraventricular arrhythmias. Treatment goals focus on acute management, including pharmacological agents and electrical cardioversion and also the long-term role of ICDs and ablation therapies.

Pathophysiology of ventricular arrhythmias

Arrhythmia morphology

Ventricular ectopic beats

Ventricular ectopic beats increase in incidence and frequency with age, with <1% incidence in children under 11 yr to over 60% in subjects over 75 yr. While often benign in nature, hypertension with left ventricular (LV) hypertrophy risks morbidity and sudden death. The mortality risk varies with the extent of underlying disease. However, contrary to previous preoperative risk scores, in the absence of structural heart disease, even frequent and complex ectopics may be completely benign.

Ventricular tachycardia

Ventricular tachycardia (VT)³ is defined as a heart rate >100 beats min⁻¹ with three or more consecutive beats originating from the ventricles, independent of atrial or atrioventricular (AV) nodal conduction. QRS is >120 ms on ECG. They may be non-sustained (<30 s) or sustained (>30 s). Classification can be via clinical presentation, ECG, or disease entity, the latter of which is demonstrated in Table 1. Monomorphic VT has a single QRS morphology, suggesting a stable structural focus, for example, scar. Polymorphic VT presents with continuously changing QRS configuration from a more global activation sequence such as hypoxaemia, metabolic abnormalities, catecholamines, and acute myocardial ischaemia. Torsades de pointes is a rare, polymorphic VT, associated with congenital or drug-induced long QT syndrome. It is covered at length in a previous CEACCP article and is not discussed further.⁴

Table 1

Classification of ventricular arrhythmias by disease entity

Monomorphic

Structural heart disease Coronary artery disease Dilated cardiomyopathy Hypertrophic cardiomyopathy Valvular heart disease Congenital heart disease Infiltrative heart disease (e.g. sarcoidosis, amyloidosis, haemochromatosis) No structural heart disease RV outflow tract VT (fibro-fatty replacement of muscle) LV outflow tract VT Idiopathic LV septal VT (fascicular VT)

Polymorphic

Normal corrected QT interval Acute ischaemia or scar Catecholaminergic polymorphic (CPVT) Brugada syndrome Long corrected QT interval (>440 ms men, >460 ms women) Congenital Acquired (i) Drugs (ii) Electrolyte abnormalities (iii) Neurological injury (iv) Starvation Short corrected QT interval

Ventricular fibrillation

Ventricular fibrillation (VF) is a life-threatening, chaotic rhythm, with marked variability in cycle length and morphology up to 300 beats min⁻¹, with loss of cardiac output. The underlying mechanism for the origins of VF is poorly understood, but prolonged monomorphic VT is a known risk factor, contributed by ischaemia, free radical production, and intracellular calcium release. It can also be precipitated by iatrogenic pacing of the myocardium during the refractory period of cardiomyocytes, which corresponds to the upstroke of the T wave on ECG.

Arrhythmogenic substrate

Coronary artery disease

Two arrhythmogenic mechanisms are described in patients with coronary disease: Scarring increases the proportion of non-conducting tissue, for example, fibroblasts, to conducting myocytes. This changes the velocity and uniformity of action potentials passing through the scarred muscle. Slow conduction and fibrous anatomical barriers generate multiple circuits, risking re-entry of action potentials into repolarizing muscle.

• acute myocardial ischaemia, resulting in polymorphic VT, which degenerates to VF;

• myocardial scarring due to ischaemic cardiomyopathy where the main arrhythmogenic events is a re-entry monomorphic VT.

Despite acute coronary artery occlusion being the main trigger for arrhythmogenic events, family history plays an important role in outcome independent of traditional risk factors, with polymorphisms discovered in multiple stages of the atheroma to plaque cascade. Importantly, in survivors of cardiac arrest due to VF with associated acute ST segment elevation myocardial infarction (STEMI), acute prognosis is not significantly different from that associated with an infarct of similar size without arrest and constitutes part of the MI process. However, the formation of scar after 48 h becomes an arrhythmogenic substrate and risks clinically significant, secondary VT or VF.

Cardiac risk factors for SCD

Hypertension and the consequence of LV hypertrophy are recognized arrhythmogenic substrates, as is left bundle branch block. The Framingham Study, which began in 1948, has looked into risk factors for cardiovascular disease over a long period of time and has shown that cigarette smoking, obesity, and diabetes also increase the risk of SCD. While modest exercise is protective, vigorous exercise in unfit individuals carries a burden of risk as do the social and economic stresses that influence acute coronary events.¹

Cardiomyopathy

In 15–20% of patients with structural heart disease, cardiomyopathies are responsible for arrhythmogenic SCD, especially when associated with LV systolic dysfunction. More importantly, however, severe ventricular impairment is also associated with a higher percentage of non-arrhythmogenic sudden death, due to pump failure.

Absence of structural heart disease

This arrhythmia group commonly carries a benign prognosis. The majority originate from the RV or LV outflow tracts and anterior/posterior fascicles (fascicular VT). The incidence of tachycardia-related cardiomyopathy and SCD is extremely low. However, there are a rare heterogeneous group of arrhythmogenic syndromes, which are strongly related to life-threatening ventricular arrhythmias and SCD, especially in the young population. Inherited gene mutations are responsible for primary electrophysiological abnormalities and disruption of cardiac cell ion channel function (channelopathies).⁵ Examples include: Brugada syndrome warrants further explanation as it has a particularly high risk of SCD with a structurally normal heart. The loss of sodium channel function during phase 1 causes an imbalance between sodium and calcium influx, and different stages of repolarization between endocardium and epicardium. This generates a vulnerable period for an extrasystole during the phase 2 plateau, which can trigger a re-entry tachycardia. Diagnosis depends upon both characteristic coved ST elevation in V1–V3 leads, followed by a negative T wave and clinical criteria (any one): The ECG signs in isolation are of questionable significance. There are three ECG subtypes for the one condition. Type 1 is the classic shape and is shown in Figure 1. Type 2 has a more saddle-shaped ST elevation and type 3 can be either shape but <2 mm ST elevation.

• Long QT (>440 ms in men, >460 ms in women) is a heterogeneous group of at least 13 forms, where the prolonged repolarization period risks Torsades de pointes VT. It is predominantly a potassium-channel abnormality.

• Brugada syndrome is a sodium-channel gene abnormality, with normal QT interval.

• Catecholaminergic polymorphic VT, which occurs during exertion or emotional trauma, is a ryanodine receptor gene abnormality.

• Short QT, a rarer, heterogeneous group, where the QT is typically <300 ms is typically a calcium-channel abnormality, with abnormally short repolarization.

• documented VF or polymorphic VT,

• family history of SCD at <45 yr old,

• coved-type ECG in family members,

• syncope,

• nocturnal, agonal respiration.

Fig 1

Twelve-lead ECG type 1 pattern in Brugada syndrome (images via http://lifeinthefastlane.com/ecg-library/ventricular-tachycardia/).

Diagnosis of VT

Eighty per cent of broad complex tachycardias are ventricular. The positive predictive value in patients with coronary artery disease, heart failure, angina, and age >35 yr is over 95%. However, supraventricular tachycardia (SVT) can be responsible. The distinction between ventricular and supraventricular is important as misdiagnosis risks inaccurate therapeutic decisions, which could be potentially fatal. However, this distinction can be difficult and the debate should not impinge on delivering safe and effective therapy. If there is doubt, one should assume the rhythm is VT.

Broad complex SVT can arise from: With aberrancy, conduction is still via the His–Purkinje system but with a fascicular abnormality, that is, left or right bundle branch block. The right bundle normally repolarizes more slowly than the left, thus even in health, the timing of a supraventricular beat may depolarize one bundle, while the other is still refractory. An example of pre-excitation would be that seen in Wolf–Parkinson–White syndrome.

• aberrancy (bundle branch block),

• antegrade conduction through an accessory pathway (pre-excitation).

Clinical information

Stable VT may be asymptomatic or present with palpitations only. Faster rhythms impact more negatively on cardiac output, producing presyncopal symptoms like dizziness and light headedness, syncope (loss of consciousness with spontaneous recovery) to sudden cardiac arrest, or SCD if not resuscitated.

Physical examination may demonstrate signs of AV dissociation, specific to VT. These signs include varying pulse volume with beat-to-beat variability of systolic arterial pressure, alternating intensity of the first heart sound and irregular cannon A waves. These large pressure waves are transmitted up the internal jugular veins when the right atrium contracts against a closed AV valve. Tachycardia termination by vagal stimulation, for example, Valsalva manoeuvre, suggests supraventricular origin but may occasionally influence VT.

Electrocardiography

With VT, there is often positive or negative concordance in the chest leads, with entirely positive (R) or entirely negative (QS) waves in leads V1–V6, thus concordance has no RS complexes. Criteria favouring VT can also be found in SVT with aberrancy. The supraventricular impulse is transmitted to the ventricle via an abnormal connection but with discordance in the chest leads and RS complexes present. Very broad complexes (>160 ms) increase the likelihood of VT.

The Brugada diagram is an algorithm that aids VT diagnosis from ECG (Fig. 2):

• The absence of an RS wave in all of V₁–V₆ precordial leads diagnoses VT immediately and is nearly 100% specific. An example would be VT arising from the ventricular apex as the wave propagates in the opposite direction to normal depolarization. A positive R wave in aVR is seen.

• If any RS wave is present, and over 100 ms (interval from start of R to nadir of S), VT is diagnosed.

• If the RS wave is shorter than 100 ms, but there is clear evidence of AV dissociation (slower p waves, not linked to QRS), then VT is diagnosed. AV dissociation is difficult to see when the heart rate exceeds 150 beats min⁻¹.

• Finally, if an RS is present in any precordial lead, <100 ms, with no obvious AV dissociation, then morphology criteria using only V_1–2 and V₆ are used for final clarification. QRS morphology criteria are summarized in Table 2.^6,7 They separate the rhythm based on right or left bundle branch type appearance.

Table 2

Morphology criteria for VT vs SVT

Fig 2

Brugada diagram to distinguish supraventricular from ventricular tachycardia.

Suggesting VT, capture beats occur when an occasional, normal sino-atrial node impulse is conducted through to the ventricle. Fusion beats occur when ventricular muscle is depolarized simultaneously by both a normal, supraventricular and abnormal, ventricular beat, which produces a QRS duration length between the two (Fig. 3). They are the collision of wave fronts from two different directions, forming a hybrid beat. Capture and fusion beats are often absent with higher rate VT.

Fig 3

Capture and fusion beats.

Consider the ECG in Figure 4. There is a wide complex, monomorphic tachycardia (135 beats min⁻¹), with QRS of 185 ms. Concordance is not present in all leads as there appear to be both positive (e.g. V1–2) and negative (e.g. V5–6) complexes. Using the Brugada algorithm, RS complexes appear in V1–4, but not all precordial leads, thus the origin of the arrhythmia could still be supraventricular. However, aVR is positive and RS complexes are >100 ms, thus the diagnosis of VT can be made with confidence. Negative complexes in V6 and positive in V1 suggests an origin from the lateral LV, because of the direction of impulse travel. For completeness, there may well be p waves (e.g. V1 nadir), but they are not obvious, thus no AV dissociation is reliably seen. The pattern is an RBBB-type because of positivity in V1–2, and there is a QS wave in V6. All of these tests add weight to the diagnosis of VT. V1 has an R wave notch, which does not feature in any classification; this demonstrates the limitations of any template system of discrimination.

Fig 4

ECG of a broad complex tachycardia.

Investigations

In the preoperative patient with ventricular ectopics or in VT, excluding structural heart disease is the primary focus.⁸ History of syncope, heart failure, or arrhythmias up to 2 months after myocardial infarction are all high-risk characteristics. Electrolyte abnormalities and use of illicit drugs should be identified and addressed.

Important investigations include:

• Twelve-lead ECG: looking for underlying disease like Q waves, bundle branch block, and ventricular hypertrophy and also signs of arrhythmogenic syndromes. Long-term ECG monitoring via implantable loop recorder is useful in monitoring symptoms and correlating them to arrhythmias, but as they provide no therapies, patients with structural heart disease are better protected and monitored by insertion of an ICD instead.

• Exercise testing: identifies silent ischaemia in coronary artery disease but also exercise-induced arrhythmias like catecholaminergic polymorphic VT. Frequent ventricular ectopic beats during exercise risk serious cardiovascular events in patients with structural heart disease, although not specifically SCD.¹ They are difficult to treat, with β-blockers being the only class of drug proven to be efficacious.

• Echocardiography: first-line investigation for evaluation of LV and RV function and wall thickness, regional wall motion abnormalities, valvular disease and congenital abnormalities.

• Cardiac magnetic resonance imaging:⁹ shows higher diagnostic accuracy than echocardiography in identifying and quantifying myocardial scar burden which has been directly linked to SCD; demonstrates accurate and reproducible measurements of LV ejection fraction and volumes; offers qualitative assessment of RV structure and function.

• Coronary angiography: should be performed in all individuals with risk factors for coronary artery disease and inducible ischaemia on non-invasive testing.

• Cardiac CT scanning: non-invasive imaging of congenital coronary malformations or those in whom MRI is contraindicated. Calcification of normal vessels can also be quantified as a ‘coronary artery calcium score’.

• Electrophysiological studies: to induce VT are useful in patients with coronary artery disease to guide diagnostic evaluation and after VT ablation to assess its efficacy. They are also useful as an accessory tool in patients with syncope of unknown cause and structural heart disease to document or exclude ventricular arrhythmias.

Electrophysiological studies

In the laboratory, electrophysiological mapping may be able to detect the source of the ventricular arrhythmia, which can be subsequently ablated using radiofrequency. Mapping, via femoral access, often under local anaesthesia, can provide anatomical reconstruction, which is then correlated to the arrhythmia. Stimulation of the ventricle can evaluate inducibility of VT in at-risk patients, characterize VT pattern and assist treatment choices. Mapping catheter electrodes are usually positioned in the high right atrium, ventricle, coronary sinus (alongside mitral annulus), and His bundles (alongside tricuspid annulus). ECG, echocardiography, and MRI (if no ICD) are vital to predict region of interrogation and avoid unnecessary procedure length. Thus, a lateral infarct suggests circumflex territory and lateral LV source. The RV can be accessed via the femoral vein, the LV either across the interatrial septum or retrograde passage via the aorta, through the aortic valve. The VT QRS morphology will determine the origin of the arrhythmia, thus RBBB pattern suggests the LV as source and vice versa. The His bundle interrogation should exclude the impulses arising from a supraventricular source. Occasionally, especially with structurally normal heart VT, increased automaticity with sympathomimetic drugs, for example, isoprenaline, may be required to generate the arrhythmia.

Management of VT and prevention of sudden death

Resuscitation

In the case of a cardiac arrest, the algorithm of advanced life support is applied. The latest resuscitation algorithm for tachycardia in adults is shown in Figure 5. Haemodynamically unstable VT presents with syncope, hypotension (typically systolic pressure below 90 mm Hg), pulmonary oedema, angina, confusion, and cardiac arrest. End-organ hypoperfusion mandates prompt termination of the arrhythmia, by synchronized DC cardioversion, which is both quicker and more effective than by chemical means. Under general anaesthesia or conscious sedation, a 120–150J synchronized biphasic shock is used, which is increased in increments to a maximum of three attempts. Reversible causes like hypoxaemia, electrolyte abnormalities (in particular hypokalaemia <4 mmol litre⁻¹, hypomagnesaemia, hypocalcaemia), and drug toxicity should be corrected. The Resuscitation Council advise senior help early, rather than the use of multiple pharmacological agents. In the context of acute ischaemia and primarily STEMI, immediate revascularization is indicated.

Fig 5

Resuscitation Council Algorithm for adult tachycardia (with pulse). Reproduced with the kind permission of the Resuscitation Council (UK).

Pharmacological therapy

Historically, the main treatment of acute ventricular arrhythmias has been pharmacological, but questions exist regarding safety and efficacy of drugs. The Vaughan–Williams classification is a useful template, although many drugs have actions across classes and others do not fit into the classification at all. Magnesium (1–2 g slow i.v.) and potassium (aim K⁺ >4 mmol litre⁻¹) are the safest first-line therapy in all cases and can favourably influence the electrophysiological substrate in the onset of arrhythmias. The Resuscitation Council guidelines recommend expert advice for all irregular rhythms, where the arrhythmia origin may be unclear.

Class I sodium-channel antagonists

Pure class I drugs have a limited role to play in VT and are useful only in structurally normal hearts for symptomatic improvement. Flecainide has been shown to increase mortality post-MI. It has a limited role, as does propafenone in idiopathic VT only. Lidocaine may be used in stable, sustained, monomorphic VT in acute MI but increases mortality if used for prophylaxis against VF. It has a rapid onset of action but is more likely to cause hypotension than amiodarone, where the onset of action is slower.

Class II β-blockers

In the context of STEMI, β-blockers are first-line therapy.¹ They are the most successful agents in prevention of ventricular arrhythmias and arrhythmic SCD in a wide spectrum of cardiac diseases with or without underlying structural heart disease. The anti-arrhythmic efficacy stems from competitive adrenergic receptor blockade, which reduces sympathetic triggers, slows the sinus rate, and may inhibit calcium release from the ryanodine receptor. Importantly, however, they are contraindicated in Brugada syndrome as they aggravate ion current imbalances that occur during the early part of the action potential, creating a vulnerable period for an extra-systole. Unopposed vagal tone is the biggest risk factor for arrhythmias (most occur at night), thus sympatholytics and bradycardia are dangerous. In fact, pure β-agonists, for example, isoprenaline, are used for resistant VT in this group of patients.

Class III potassium-channel antagonists

Amiodarone and sotalol have been shown to reduce arrhythmogenic SCD but not all-cause mortality. Class III drugs block potassium repolarization currents and thus increase the threshold for re-entry. In haemodynamically stable patients, with low troponin–myocardial infarction or non-ischaemic VT, there is Class C evidence for the use of either procainamide or amiodarone to terminate confirmed or suspected VT. Procainamide has both class I and III actions and has a favourable side-effect profile but is no longer regularly available in the UK.

Class IV calcium channel blockers

Class IV calcium channel blockers, for example, verapamil, should never be used to terminate broad complex tachycardia of unknown origin as they may precipitate VF. They have a select role to play in confirmed fascicular VT.

Other agents

The role of adenosine continues to remain controversial. The 2010 ILCOR guidelines state that adenosine may aid in diagnosing VT but will not terminate it. Adenosine is considered safe only if an SVT can be confidently excluded using tools discussed, or if SVT with bundle branch block has been previously confirmed. Otherwise, it too may precipitate VF. Amiodarone and adenosine are the only drugs recommended to be used without expert consultation in all broad complex tachycardia groups.

It is important to recognize that ventricular arrhythmias are often the final common pathway in the unstable heart. Drugs with most success long term are not those above, which act directly on conducting muscle. Instead, it is drugs like ACE inhibitors, lipid-lowering agents, and aldosterone antagonists, for example, spironolactone, that influence the course of ischaemia, fibrosis, and biochemical derangement before the arrhythmogenic substrate is set.

Implantable cardioverter defibrillator

The ICD is a battery-powered invasive device with four functions: While implanted in much the same way as a permanent pacemaker, general anaesthesia is usually recommended as VF is induced at the end of the procedure to test function and response time.

• Sensing: the device compares atrial and ventricular rates to assign arrhythmia causation.

• Pacing: anti-bradycardia and overdrive anti-tachycardia pacing (ATP).

• Cardioversion: synchronized electrical current to terminate cardiac output-compatible arrhythmias.

• Defibrillation: to terminate VF.

There is compelling evidence to support their use in the presence of ischaemic heart disease, with impaired LV ejection fraction, supported by NICE guidelines, updated in 2014.

ICDs are also recommended as options for treating people with previous serious ventricular arrhythmia, that is, people who, without a treatable cause: They are also recommended for treating people who: Direct comparison of ICDs with anti-arrhythmic drugs has shown a clear reduction in SCD in carefully selected patients with a high-risk profile.¹⁰ Importantly, anti-arrhythmic drugs such as β-blockers, amiodarone, sotalol, and mexiletine still have a role in primary and secondary prevention. They reduce the arrhythmogenic burden and consequently the number of ICD shocks delivered.

• - have survived a cardiac arrest caused by either VT or VF, or

• - have spontaneous sustained VT causing syncope or significant haemodynamic compromise, or

• - have sustained VT without syncope or cardiac arrest, and also have an associated reduction in LV ejection fraction of 35% or less but their symptoms are no worse than class III of the New York Heart Association (NYHA) functional classification of heart failure.

• - have a familial cardiac condition with a high risk of sudden death, such as long QT syndrome, hypertrophic cardiomyopathy, Brugada syndrome, or arrhythmogenic right ventricular dysplasia, or

• - have undergone surgical repair of congenital heart disease (http://www.nice.org.uk/guidance/ta314/resources/guidance-implantable-cardioverter-defibrillators-and-cardiac-resynchronisation-therapy-for-arrhythmias-and-heart-failure-review-of-ta95-and-ta120-pdf).

Anti-tachycardia pacing

ATP through a temporary pacing wire can overdrive and terminate arrhythmias successfully and more importantly is the first technique an implanted ICD is programmed to perform in the presence of wide complex tachycardia. A slow, monomorphic VT can be detected then accelerated by the device to a short-lived burst of faster ventricular pacing, which on cessation terminates the VT, without the need for general anaesthesia. If unsuccessful, a subsequent burst of fast pacing followed by a low-voltage shock may also work. High energy shocks are very effective but are both painful and are a considerable drain to the ICD battery. ATP is unlikely to work during fast, haemodynamically unstable VT and risks degeneration to VF.

ICDs and surgery

As the indications for ICDs increase, so does the number encountered in patients presenting for surgery. While a detailed management plan for patients with implanted electronic cardiac devices¹¹ is outside the scope of this review, some important principles apply:

• Electromagnetic interference may inappropriately trigger the device. This includes electrocautery (monopolar much greater than bipolar), nerve stimulators, evoked potential monitors, electroconvulsive therapy, radiofrequency ablation, and MRI. Succinylcholine fasciculations, shivering, and large tidal volumes should not interfere with ICD sensing.

• All ICDs can be deactivated with a magnet. This turns off the shock therapy and anti-tachycardia modes but has no effect on pacing and anti-bradycardia modes. Removal of the magnet should restore full device function. However, reactivation to pre-magnet settings is not guaranteed, thus a full ICD check should be completed after operation.

• Formal ICD deactivation by a cardiac technician may be required if surgery is near the box site (e.g. cardiothoracics), remembering that deactivation of the device leaves patients vulnerable to malignant arrhythmias. It is helpful to know the model type, as the interrogation consoles are manufacturer-specific.

• External defibrillator pads are recommended in all ICD patients and the device must be reactivated at the end of surgery.

• Anaesthetic management should focus on reducing arrhythmias. Cardiostable, non-histamine-releasing drugs are recommended. Electrolyte disturbances, particularly potassium and magnesium, should be corrected and meticulous attention should be applied to Seldinger-type insertion of intra-vascular lines.

Ablation of ventricular arrhythmias

Evidence for catheter ablation of VT is mostly from patients with ischaemic heart disease. It is not a simple procedure and few patients are able to tolerate VT for sufficient time to allow all the necessary mapping required to identify all possible re-entry sites. Ablation energies can be applied using radiofrequency, cryotherapy, low energy direct current, or laser.

Success rate varies between 50% and 80% with reported complication rate up to 10% depending on the urgency of the procedure. Evidence exists for both prior and post-ICD implantation with successful reduction in arrhythmic burden and ICD therapies. No direct comparison between ablation and anti-arrhythmic drugs has been performed to date. Despite successful arrhythmia treatment, it is unclear if VT catheter ablation has an effect in SCD and mortality.

A small proportion of patients with RV and LV outflow tract VT have otherwise structurally normal hearts and this procedure importantly may offer a permanent cure.

The success of ablation procedures is expanding into more experimental techniques, including transthoracic pericardial access, transcoronary chemical ablation, and also spinal cord modulation to suppress VT.

Anaesthesia for ablation procedures is covered in a previous CEACCP article.¹²

Conclusion

The most important determinant in assessing the clinical significance of ventricular ectopic beats or tachycardia is the presence or absence of structural heart disease. Benign arrhythmias are more likely in patients under 35 yr old, except in those with hereditary channelopathies. Confidence in excluding the diagnosis of SVT with aberrancy is complex and may require expert help. Treatment of acute VT is via resuscitation, electrical or chemical cardioversion, and then assessing the need for further preventive therapy. ICDs and electrophysiology catheter-based ablations now offer improved survival and quality of life, respectively. Deactivating the defibrillation and anti-tachycardia function of an ICD can be achieved with a magnet. This leaves the patient vulnerable to arrhythmias; thus, the use of external defibrillation pads is mandatory.

Declaration of interest

None declared.

MCQs

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