Sustained ventricular tachycardias

Highlights
Summary Overview

Basics
Definition Epidemiology Aetiology Pathophysiology Classification

Prevention
Primary Screening Secondary

Diagnosis
History & examination Tests Differential Step-by-step Criteria Guidelines Case history

Treatment
Details Step-by-step Emerging Guidelines Evidence

Follow Up
Recommendations Complications Prognosis

Resources
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History & exam

Key factors
CAD presence of other risk factors

tachycardia hypotension

Other diagnostic factors

asymptomatic weak pulse syncope presyncope airway compromise impaired consciousness light-headedness dizziness diminished responsiveness chest discomfort dyspnoea History & exam details

Diagnostic tests
1st tests to order
ECG electrolytes troponin I CK-MB

Tests to consider
transthoracic echocardiogram cardiac catheterisation cardiac MRI electrophysiological (EP) study genetic screening Diagnostic tests details

Treatment details
Presumptive
haemodynamically unstable VT with a pulse synchronised cardioversion according to ACLS protocol + treatment of reversible cause (if present) anti-arrhythmic medication

torsades de pointes IV magnesium sulphate + withdraw offending drugs + correct electrolyte abnormalities isoprenaline infusion temporary or permanent pacing

Acute
haemodynamically stable non-idiopathic sustained VT anti-arrhythmic medications + treatment of reversible cause (if present) synchronised cardioversion anti-arrhythmic medications haemodynamically stable idiopathic sustained VT IV anti-arrhythmic medications synchronised cardioversion

Ongoing
non-idiopathic: at high risk for VT or Hx sustained VT/cardiac arrest without identifiable reversible cause o idiopathic VT o o specialist referral for ongoing anti-arrhythmic Tx mild-to-moderate symptoms (rare palpitations that do not interfere with daily activities) beta-blockers or calcium-channel blockers or catheter ablation moderate-to-severe symptoms (syncope, presyncope, or frequent, disabling palpitations) catheter ablation failure of beta-blockers, calcium-channel blockers, or catheter ablation, or non-candidates for catheter ablation o class I or class III anti-arrhythmic medications Treatment details implantable cardioverter defibrillator (ICD) anti-arrhythmic medication anti-arrhythmic monotherapy structural heart disease with recurrent episodes of VT catheter ablation

Summary
A ventricular rhythm faster than 100 bpm lasting at least 30 seconds or requiring termination due to haemodynamic instability. ECG findings include wide QRS complex (duration >120 milliseconds) at a rate greater than 100 bpm.

Patients may have a normal cardiac output or may be haemodynamically compromised during episodes of ventricular tachycardia (VT). Presence or absence of symptoms does not differentiate VT from supraventricular tachycardia (SVT).

Torsades de pointes (TdP): polymorphic VT with a characteristic twisting morphology occurring in the setting of QT interval prolongation.

Sustained VT is usually observed in ischaemic cardiomyopathy, but idiopathic VT may also be observed in patients without structural heart disease.

Among patients with prior MI or non-ischaemic cardiomyopathy, VT is usually due to re-entry involving regions of slowed conduction adjacent to scar.

Due to the unpredictable and life-threatening nature of most aetiologies of sustained VT, prophylactic implantable cardioverter defibrillator implantation is recommended in high-risk patients.

Definition
Sustained ventricular tachycardia (VT) is a ventricular rhythm faster than 100 bpm lasting at least 30 seconds or requiring termination earlier due to haemodynamic instability. View image VT is defined as a wide complex tachycardia (QRS 120 milliseconds or greater) that originates from one of the ventricles, and is not due to aberrant conduction (e.g., from bundle branch block), at a rate of 100 bpm or greater. 'Idiopathic' VT occurs in the absence of structural heart disease (e.g., prior MI, active ischaemia, cardiomyopathy, valvular disease, or other disorders of the myocardium), known genetic disorder (e.g., long QT syndrome, Brugada syndrome, arrhythmogenic right ventricular cardiomyopathy), drug toxicity, or electrolyte imbalance. VT can be described as monomorphic or polymorphic. Torsades de pointes is a polymorphic VT with a characteristic twisting morphology occurring in the setting of QT interval prolongation. View imageSustained VT usually results in hypotension and symptoms of weakness, syncope, or palpitations; however, the arrhythmia may be present in patients who are asymptomatic and normotensive.

Epidemiology
Approximately 300,000 to 450,000 sudden deaths occur annually in the US, and another 400,000 occur annually in western Europe. Overall, sudden death accounts for approximately 1 out of every 6 deaths due to natural causes. Furthermore, approximately 90% of sudden deaths are cardiac in origin, and the vast majority are due to ventricular tachycardia (VT) or ventricular fibrillation (VF). Population studies have estimated the incidence of fatal ventricular arrhythmias in the general population to be 54 per 100,000 people; this risk increases with age, with the presence of risk factors for CAD,

and with the presence of structural heart disease, such as left ventricular dysfunction or scar from prior MI. Some studies suggest that women have a lower incidence of sudden cardiac death compared to men and are less likely to have spontaneous or inducible VT. However, women have longer QT intervals than men and are more likely to manifest torsades de pointes (whether drug-induced or due to congenital long QT syndrome) than men. [1]

Aetiology
Ventricular tachycardia (VT) is usually observed in the setting of ischaemic heart disease and cardiomyopathy, although it may also be observed in patients without structural heart disease (idiopathic VT). Ischaemia and coronary artery disease (CAD) are the most common aetiologies of VT around the world, especially among North Americans and Europeans. Across the developing world, infectious and other forms of non-ischaemic cardiomyopathy may also play a significant role in the aetiology of ventricular arrhythmias (e.g., Chagas disease in Central America). [2] Other forms of structural heart disease, hypertrophic cardiomyopathy, arrhythmogenic right ventricular cardiomyopathy, and anomalous coronary arteries are also associated with ventricular arrhythmias. At the cellular level, congenital or acquired abnormalities in cardiac sodium channels (congenital long QT syndrome, Brugada syndrome), potassium channels (long QT syndrome, short QT syndrome), and calcium channels (catecholaminergic polymorphic VT) have been implicated as causes of VT and sudden death. Mutations in cardiac anchoring proteins may also lead to the long QT syndrome. [3] [4] Environmental and/or physiological stressors can unmask sub-clinical abnormalities that predispose to sudden cardiac death. Pharmacogenetic variants exist that result in prolongation of the QT interval with administration of certain drugs (an up-to-date list of drugs is available through research centres [Arizona Center for Education and Research on Therapeutics] (external link)); catecholamine-sensitive VT may only arise during periods of heightened mental or physical stress. It is estimated that 5% to 10% of sudden cardiac deaths occur in the absence of cardiomyopathy or CAD. [5]

Pathophysiology
Among patients with prior MI or non-ischaemic cardiomyopathy, regions of slowed conduction (usually adjacent to damaged myocardium or scar) are the substrate for re-entrant arrhythmias. Ventricular tachycardia (VT) may also arise from triggered activity due to early after-depolarisations (EADs) leading to torsades de pointes, a polymorphic ventricular tachycardia seen in the setting of a prolonged QT interval, or delayed afterdepolarisations (DADs), which are seen in idiopathic right ventricular outflow tract VT or catecholaminergic

polymorphic VT. [6]EADs occur during phase 2 or 3 of the action potential, whereas DADs occur during phase 4. When an EAD or DAD reaches a 'threshold' potential, it can result in triggering of another action potential. Enhanced automaticity of the ventricular tissue may also produce a relatively slow VT called accelerated idioventricular rhythm, which generally follows a benign course. This arrhythmia is frequently observed in the setting of acute ischaemia or early after reperfusion. [5]

Classification
Ventricular tachycardia (VT) Presence of a wide complex tachycardia (QRS 120 milliseconds or greater) at a rate of 100 bpm or greater. Sustained VT A ventricular rhythm faster than 100 bpm lasting at least 30 seconds or requiring termination due to haemodynamic instability. View image Non-sustained VT A ventricular rhythm faster than 100 bpm lasting for at least 3 consecutive beats but terminating spontaneously in less than 30 seconds, and not resulting in significant haemodynamic instability. Polymorphic VT Tachyarrhythmia with multiple different wide QRS complex (>120 milliseconds) morphologies arising from one of the ventricles. Monomorphic VT Tachyarrhythmia with an organised, single-morphology QRS complex arising from one of the ventricles. Haemodynamically stable VT VT associated with a normal BP and no symptoms due to haemodynamic compromise. Haemodynamically unstable VT VT associated with hypotension, signs of diminished cerebral perfusion (e.g., confusion, dizziness, syncope), or signs of diminished coronary perfusion (e.g., angina, dyspnoea). Idiopathic VT VT occurring in the absence of structural heart disease (e.g., ischaemia, prior infarction, cardiomyopathy, valvular disease or other disorders of the

myocardium), known genetic disorder (e.g., long QT syndrome, Brugada syndrome, arrhythmogenic right ventricular cardiomyopathy), drug toxicity, or electrolyte imbalance. View image Torsades de pointes (TdP) A form of polymorphic VT with a characteristic twisting morphology occurring in the setting of QT interval prolongation. TdP is initiated by an early afterdepolarisation (EAD) and perpetuated by re-entry.View image Catecholaminergic polymorphic VT Patients with this condition demonstrate cellular abnormalities of calcium handling, especially during periods of sympathetic stimulation. Increased intracellular calcium predisposes the patients to develop VT. Outflow tract VT This form of 'idiopathic' VT typically arises from the right ventricular outflow tract, but may also arise from the left ventricular outflow tract region (including the sinuses of Valsalva), and results from cyclic AMP-mediated triggered activity; therefore this form of VT is uniquely sensitive to adenosine. Fascicular VT A common form of idiopathic VT arising from the left ventricle, involving the Purkinje fibres, that is characteristically sensitive to verapamil.

Primary prevention
Primary prevention of ventricular arrhythmia is best accomplished by treating risk factors for CAD and left ventricular systolic dysfunction, including smoking cessation and management of HTN and hyperlipidaemia. Additional preventative measures include medical treatment of systolic dysfunction with medications such as ACE inhibitors/angiotensin receptor blockers, beta-blockers, and aldosterone antagonists. In patients with hypertrophic cardiomyopathy, arrhythmogenic right ventricular cardiomyopathy, and the long QT syndrome, strenuous physical exertion should be avoided as exercise can provoke arrhythmias in these populations. In addition, owing to the unpredictable and life-threatening nature of sustained ventricular tachycardias (VTs), primary prevention is critical in high-risk patients and can be accomplished through implantation of a prophylactic implantable cardioverter defibrillator (ICD).

Screening
Screening for potential causes of ventricular arrhythmias should focus on populations at increased risk of developing the disorder and will allow institution of primary prevention. The highest-risk patients include those with LV dysfunction (ischaemic or non-ischaemic cardiomyopathy), heart failure symptoms, congenital

arrhythmia syndromes (e.g., long QT syndrome, short QT syndrome, Brugada syndrome, catecholaminergic polymorphic ventricular tachycardia [VT]), hypertrophic cardiomyopathy, and arrhythmogenic right ventricular cardiomyopathy (ARVC). Invasive electrophysiological (EP) testing may be useful in borderline cases. An implantable cardioverter defibrillator (ICD) is the most important preventative/therapeutic intervention performed for patients at high risk of developing a sustained ventricular arrhythmia.

Secondary prevention
In general, compliance with prescribed anti-arrhythmic medications should help to lessen the burden of ventricular arrhythmias. Patients with ischaemic VT should explore the feasibility of revascularising their ischaemic myocardium.

History & examination

Key diagnostic factorshide all
CAD (common)

Ventricular fibrillation (VF) is common during active ischaemia; chronic coronary disease leads to scar formation, which increases risk of ventricular tachycardia (VT).

presence of other risk factors (common)

Other risk factors include left ventricular systolic dysfunction, hypertrophic cardiomyopathy (HCM), long QT syndrome, Brugada syndrome, arrhythmogenic right ventricular cardiomyopathy (ARVC), and FHx of sudden death.

tachycardia (common) Essential to the diagnosis by definition. hypotension (common)

Degree of hypotension will depend on the rate and duration of the tachycardia and will be an indication of reduced cardiac output.

Other diagnostic factorshide all

weak pulse (common)

Palpation of the carotid or femoral pulse provides useful information regarding the heart rate (frequency of the pulse in bpm) and cardiac output (force of the pulse), which, if reduced, may be revealed by a weak pulse.

syncope (common)

Frequently observed in patients with VT, due to cerebral hypoperfusion from hypotension; however this is non-specific.

presyncope (common) Frequently progresses to syncope. airway compromise (common) This may include stridor and/or apparent obstruction to breaths delivered during rescue breathing. impaired consciousness (common)

Unconsciousness is a sign of diminished cerebral perfusion in a haemodynamically unstable patient. An alert patient with a normal BP would be considered haemodynamically stable.

light-headedness (common) Sign of diminished cerebral perfusion in a haemodynamically unstable patient. dizziness (common) Sign of diminished cerebral perfusion in a haemodynamically unstable patient. diminished responsiveness (common) Sign of diminished cerebral perfusion in a haemodynamically unstable patient. chest discomfort (common) Symptom of inadequate coronary perfusion. dyspnoea (common)

Symptom of inadequate coronary perfusion, often with resultant left ventricular dysfunction or mitral regurgitation.

asymptomatic (uncommon)

VT does not always cause symptoms.

Risk factorshide all

Strong CAD

CAD creates ischaemia in myocardial tissue. In the long term, MI leads to ventricular scarring, with areas of delayed electrical conduction along the border zone of the scar, as well as within the scar, that are the substrate for re-entrant circuits.

acute MI

Acute ischaemia facilitates arrhythmias due to 3 electrophysiological mechanisms: re-entry, triggered activity, and automaticity.

left ventricular systolic dysfunction

Systolic dysfunction, regardless of the cause, is strongly associated with ventricular arrhythmias. Scars in the ventricle create areas of slowed electrical conduction and set up the substrate necessary for re-entrant ventricular tachycardia (VT)/ventricular fibrillation (VF). These scars can be created by prior MI (ischaemic cardiomyopathy) or abnormal myocardial fibrosis (non-ischaemic cardiomyopathy). [5]

hypertrophic cardiomyopathy (HCM)

HCM, a genetic condition characterised by cellular disarray of the myocardium that results in asymmetrical thickening of the ventricle, has been linked to increased risk of developing ventricular arrhythmias. The phenotypic expression of this disorder is highly variable, and the risk of ventricular arrhythmia varies among individuals. While the science of risk-stratifying patients with HCM remains an evolving field, the following clinical risk factors are considered high risk and merit consideration of prophylactic therapy: 1) personal hx of sudden cardiac death or sustained VT; 2) FHx of sudden cardiac death in a first-degree relative; 3) a ventricular septal wall thickness >30 mm; 4) unexplained syncope; 5) frequent or prolonged non-sustained VT discovered on a Holter monitor; and 6) an abnormal BP response (i.e., fall in BP on exercise treadmill test). [5] [7] [8]

long QT syndrome

Long QT syndrome represents a genetic disorder that manifests as a prolongation of the corrected QT interval on the ECG. The clinical prognosis varies according to the phenotypic manifestation of the genetic defect. Multiple subtypes of long QT syndrome have been described; patients are at increased risk of experiencing a particular form of polymorphic VT known as torsades de pointes (TdP). Typically, patients with long QT syndrome type 1 (LQT1) are at increased risk of developing TdP during periods of physical exertion. Long QT syndrome type 2 (LQT2) is often characterised by initiation of TdP following a startle reflex or a period of heightened emotional stress. Patients with long QT syndrome type 3 (LQT3) tend to develop arrhythmias during sleep. [9] Beta-blocker medications have been shown to reduce the arrhythmia burden in LQTS, except with LQT3 patients. Implantable cardioverter defibrillators are recommended for patients with high-risk features. [4] [10]

short QT syndrome

Syndrome manifested by a short QT interval and an increased risk of sudden death due to polymorphic VT.

Brugada syndrome

Brugada syndrome is a disorder of myocardial sodium channels, which leads to a characteristic Jpoint elevation and downwards-sloping ST segment elevation in the right precordial leads due to regional inhomogeneities in ventricular repolarisation, and results in an increased risk of sudden death due to polymorphic VT and VF. A mutation in the SCN5A (sodium channel) gene has been implicated in a minority of patients. Drug challenges with various anti-arrhythmic medications (procainamide, flecainide, or ajmaline) can be helpful to diagnose borderline cases of Brugada syndrome; positive response to the drug challenge results in increased ST elevation of the right precordial leads. [11]

ventricular pre-excitation

ECG abnormality notable for a slurring of the R wave due to an abnormal AV conduction pathway, which activates the ventricular myocardium before the normal electrical impulse conducts down the AV node/His-Purkinje system. Pre-excitation is most commonly seen in patients with an accessory pathway due to Wolff-Parkinson-White syndrome (WPW). Patients with WPW that are capable of rapid conduction down the accessory pathway (i.e., from atria to ventricles) are at risk of having atrial fibrillation with rapid conduction to the ventricles degenerating into ventricular fibrillation.

arrhythmogenic right ventricular cardiomyopathy (ARVC)

ARVC is a genetic disorder characterised by heart failure, ventricular arrhythmias, and sudden death. In this disease, various regions of the right (and less commonly left) ventricular muscle are replaced by deposition of fat and fibrotic tissue. The disease may be transmitted in an autosomaldominant fashion and in some families is related to mutations in the genes encoding desmosomal proteins (plakoglobin, desmoplakin, and plakophilin). Early symptoms include syncope and

palpitations (especially during periods of heavy exertion); as the disease progresses, symptoms of right ventricular failure become more prominent. In advanced presentations, patients may develop biventricular failure. Patients with ARVC frequently manifest interventricular conduction delays on ECG; the finding of an epsilon wave in lead V1 is a specific sign for the disease. A Holter monitor typically reveals left bundle branch block-morphology premature ventricular contractions, or nonsustained ventricular tachycardia. Echocardiogram and/or right ventricular angiography may reveal right ventricular dilation, regional dyskinesis, and/or reduced systolic function. Cardiac MRI may reveal fibro-fatty infiltration of the right ventricular myocardium.[3] [12]
electrolyte imbalance

Electrolyte abnormalities (particularly hypokalaemia and hypomagnesaemia) may incite and/or contribute to VT.

drug toxicity

Pharmacogenetic variants exist that result in prolongation of the QT interval with administration of certain drugs, including macrolide antibiotics, chlorpromazine, haloperidol, and domperidone. An up-to-date list of drugs is available through research centres. [Arizona Center for Education and Research on Therapeutics] (external link)

Chagas disease, and other cardiomyopathies

Across the developing world, infectious and other forms of non-ischaemic cardiomyopathy may also play a significant role in the aetiology of ventricular arrhythmias (e.g., Chagas disease in Central America). [2]

Weak Family history of sudden death

A family history of sudden death should alert the physician to seek potential arrhythmogenic causes. Genetic screening is available for common mutations associated with long QT syndrome, Brugada syndrome, and catecholaminergic polymorphic VT.

mental or physical stress

Catecholamine-sensitive VT may only arise during periods of heightened mental or physical stress.

Diagnostic tests
1st tests to orderhide all
Test

ECG Required to establish diagnosis of ventricular tachycardia (VT). Clinician should look for AV dissociation, fusion/capture beats, and other criteria for ventricular tachycardia. The absence of extreme axis deviation does not imply a supraventricular origin of the tachycardia. [5]

electrolytes Serves as baseline measurement and may reveal contributory factors to arrhythmia.

troponin I Ischaemia is a reversible cause of ventricular tachycardia and should be sought promptly to allow for revascularisation. CK-MB Ischaemia is a reversible cause of VT and should be sought promptly to allow for revascularisation.

Tests to considerhide all

Test

transthoracic echocardiogram Non-invasive test that can quickly reveal contributory and complicating mechanical and structural problems.

cardiac catheterisation setting of acute MI.

May be an appropriate early test for patients, especially those presenting with VT/ventricular fibrillation (VF) in th

cardiac MRI Particularly useful in establishing the presence of arrhythmogenic right ventricular cardiomyopathy.

electrophysiological (EP) study EP testing is also used for risk stratification among patients with non-sustained VT and less severe degrees of prophylactic implantable cardioverter defibrillator (ICD). [5]

cardiomyopathy. May be helpful in such cases in determining whether or not a given patient would benefit from a

genetic screening Determines underlying genetic factors associated with a number of important conditions.

Differential diagnosis
Condition Supraventricular tachycardia (SVT) with aberrancy Differentiating signs/symptoms Differentiating tests

None.

ECG; electrophysiological (EP) study: failure to meet c tachycardia (VT); absence of fusion or capture beats; dissociation.

SVT with pre-excitation

None.

ECG, EP study: failure to meet criteria for VT; absenc beats; absence of AV dissociation.

Electrical artefact

None.

Evidence of underlying sinus rhythm on ECG discerni noise (motion artefact).

Evidence of arrhythmia isolated to specific leads on 12

Sepsis or fever

Raised temperature, malaise, rigors, symptoms of underlying infection.

ECG shows underlying sinus rhythm.

Appropriate cultures may show presence of infecting a

Panic/hyperventilation

Anxiety or panic, fear of imminent death, paraesthesiae, chest pain, numbness, faintness, dizziness, sweating.

ECG shows underlying sinus rhythm.

Hospital Anxiety and Depression Scale (HADS) anxie

Hyperthyroidism

Tremor, anxiety, weight loss but good appetite, diarrhoea, eyelid retraction and lid lag, fatigue, heat intolerance, goitre.

ECG shows underlying sinus rhythm or atrial fibrillatio Raised T4/T3 and low TSH levels.

Acute haemorrhage

Low BP, abdominal pain with haematemesis and/or melaena, haemorrhage from other sites, hx of likely cause of blood loss: for example, trauma

ECG shows underlying sinus tachycardia.

US or CT may show internal bleeding source and/or c

or post-operative. Phaeochromocytoma

Headache, sweating, palpitations, fluctuating HTN, anxiety, nausea, vomiting, weight loss, heat intolerance, tremors, chest and abdominal pain.

ECG shows underlying sinus tachycardia.

Increased plasma and 24-hour urine epinephrine (adr (noradrenaline)/metanephrine levels.

Glucagon stimulation test positive. Clonidine suppression test positive.

CT, MRI, or m-iodobenzylguanidine (MIBG) scans sho gland.

Pericarditis

Tachycardia and friction rub; jugular venous distension and pulsus paradoxus indicate pericardial effusion causing tamponade.

ECG shows diffuse concave-up ST-elevation, associa

CXR may show enlarged cardiac silhouette (globular h effusion present.

Echocardiogram may show pericardial effusion.

Caffeine, alcohol, amphetamine use

Hx of recent use or high intake.

ECG shows underlying sinus tachycardia.

Tremor, agitation, signs of intoxication.

Step-by-step diagnostic approach

The presenting symptoms and signs of ventricular tachycardia (VT) and supraventricular tachycardias (SVTs) share considerable overlap. With the exception of signs of AV dissociation (e.g., cannon A waves) that are diagnostic of VT, few clinical findings can definitively identify the source of a wide complex tachycardia.

History
A history of acute or prior MI, or depressed left ventricular systolic dysfunction, strongly favours a diagnosis of VT, but the converse is not necessarily true. Most symptoms associated with ventricular tachycardia are non-specific in that they may also be present in patients with other conditions, including supraventricular tachycardia. For example, palpitations, dyspnoea, chest discomfort, and nausea/diaphoresis are common in patients with VT, but not pathognomonic. In addition, hypotension does not help to identify the origin of their arrhythmia; many instances of well-tolerated VT and of poorly tolerated SVT have been described. The patient may have a history of syncope or presyncope. A family history of sudden death, especially if at an early age, should alert the physician to seek potential arrhythmogenic causes. Particularly if sudden death did not occur in the setting of underlying coronary artery disease, the physician must pay even more careful attention to screen for primary electrical abnormalities such as long QT syndrome and Brugada syndrome. In addition, imaging modalities including echocardiography and cardiac MRI should be considered, to evaluate for evidence of conditions such as hypertrophic cardiomyopathy and arrhythmogenic right ventricular cardiomyopathy. Patients at high risk for VT include those with:
Ischaemic cardiomyopathy (left ventricular ejection fraction [LVEF] 35%) and mild-to-moderate congestive heart failure symptoms (New York Heart Association class II or III symptoms) Ischaemic cardiomyopathy (LVEF 40%) with non-sustained VT and inducible sustained VT during electrophysiological (EP) testing Non-ischaemic cardiomyopathy (LVEF 35% and New York Heart Association class II or III symptoms) Hypertrophic cardiomyopathy with personal history of sudden death or sustained VT, first-degree relative with sudden death, unexplained exertional or recurrent syncope, massive LVH (left ventricular septum thickness >30 mm), or frequent or prolonged non-sustained VT, or abnormal BP response to exercise Congenital arrhythmia syndromes, including symptomatic patients with long QT syndrome, Brugada syndrome, and catecholaminergic polymorphic VT.

Physical examination

The physical examination in a patient with suspected VT should include an assessment of the patient's level of consciousness, airway stability, breathing, and circulatory support. This will help determine, once VT is confirmed, whether to cardiovert the patient immediately or to attempt pharmacological therapy first. Signs of airway compromise may include stridor and/or apparent obstruction to breaths delivered during rescue breathing. Palpation of the carotid or femoral pulse may be necessary to determine the heart rate if the patient is relatively hypotensive (e.g., systolic BP <90 mmHg), and can also provide a crude estimate of the cardiac output (by noting the force of the pulse) if a BP measurement cannot be immediately obtained. Patients with a weak pulse and hypotension are classified as haemodynamically unstable, as are patients with signs of diminished cerebral perfusion (e.g., lightheadedness, dizziness, diminished responsiveness, or unconsciousness) or diminished coronary perfusion (e.g., chest discomfort, dyspnoea). Again, this does not help distinguish VT from SVT.

ECG
The ECG is crucial to the diagnosis of a ventricular tachycardia. VT is defined by the presence of a wide complex tachycardia (QRS 120 milliseconds or greater) at a rate of 100 bpm or greater. However, it is important to recognise that not all wide complex tachycardias are due to VT. When evaluating the patient with a wide complex tachycardia it is essential to distinguish VT from SVT that conducts with aberrancy or with pre-excitation, as these conditions are managed very differently. When available, review of the patient's baseline ECG provides important clues to determining the origin of a wide complex arrhythmia. Evidence supporting a diagnosis of an SVT includes:
Pre-existing pre-excitation of a similar morphology to the wide complex arrhythmia; and/or Baseline bundle branch block that resembles the wide complex tachycardia. [13]

A stepwise approach has been proposed that utilises a 4-step approach to regular wide complex tachycardias to differentiate VT from SVT with aberrancy. [14] These steps are:
1. Absence of an RS complex in any precordial lead confirms diagnosis of VT

2. If RS complex is present in step 1, measure the QRS onset to nadir of S wave: a. R-to-S interval of >100 milliseconds confirms diagnosis of VT 3. If R-to-S interval is <100 milliseconds: examine ECG for atrioventricular (AV) dissociation. If present, diagnosis is VT.

o o

4. If no AV dissociation, examine QRS complex in V1 and V6: a. with right bundle branch block QRS morphology: i. in lead V1: monophasic R, QR, or RS favours VT ii. in lead V6: R/S ratio of <1 favours VT; QS, QR, or monophasic R favours VT b. with left bundle branch block QRS morphology: i. in either lead V1 or V2: R >30 milliseconds, R-to-S (nadir) interval of >60 milliseconds or a notched S wave favours VT

o step.

ii. in lead V6: QR or QS favours VT c. Note: both V1/V2 and V6 criteria need to favour VT for the diagnosis to be made using this

If none of the steps above favours VT, a diagnosis of SVT is made. AV dissociation can manifest as dissociated P waves (usually best seen in V1) or the presence of capture beats and fusion beats. Fusion beats are changes to the QRS complex that arise when the native rhythm competes or fuses with a cycle of VT. The fusion beat demonstrates a distinct morphology from that of the other QRS complexes in an otherwise monomorphic VT and is intermediate between the wide complexes and the patient's baseline QRS morphology. A capture beat is an ECG phenomenon characterised by a narrow QRS complex that occurs during a run of VT; the capture beat results from a sinus beat temporarily penetrating the VT circuit. The capture beat occurs at an earlier RR interval than would otherwise be expected by the VT cycle length. When evaluating a patient with an undiagnosed wide complex tachycardia, the presence of capture or fusion beats proves that the arrhythmia is VT and not SVT with aberrancy. Evidence that suggests the arrhythmia is more likely to be from the ventricle includes:

Ventricular premature contractions of similar morphology to the tachycardia present on the baseline ECG. [13]

ECG evidence of previous MI also favours a diagnosis of VT. A new algorithm using only lead aVR for differentiating VT from SVT has been reported, with superior accuracy. [15] Lead aVR was analysed for:
1. Presence of an initial R wave 2. Width of an initial r or q wave >40 milliseconds 3. Notching on the initial downstroke of a predominantly negative QRS complex 4. Ventricular activation-velocity ratio (vi/vt), where v is the vertical excursion recorded during the initial (vi) and terminal (vt) 40 milliseconds of the QRS complex.

The finding of any of the above results in a diagnosis of VT. Other ECG evidence supporting a diagnosis of VT includes:
QRS duration: >140 milliseconds with right bundle branch block morphology, or QRS duration >160 milliseconds with left bundle branch block morphology (these criteria do not apply to patients treated with antiarrhythmic drugs) The presence of a right superior axis or left bundle branch block morphology and any right axis. The absence of extreme axis deviation does not imply a supraventricular origin of the tachycardia. [5]

The baseline ECG should also be examined carefully for evidence of:
QT interval prolongation View image Brugada syndrome: a disorder characterised by cardiac conduction abnormalities, which leads to a characteristic J-point elevation and downwards-sloping ST segment elevation in the right pre-cordial lead that can lead to sudden death due to polymorphic ventricular tachycardia. Mutations in 8 genes are known to cause Brugada syndrome. A sodium channel mutation (SCN5A) has been the most commonly reported mutation, but still accounts for a minority of patients with Brugada syndrome Arrhythmogenic right ventricular cardiomyopathy (ARVC): a genetic disorder characterised by ventricular tachycardia, sudden death, and progressive heart failure. In this disease, various regions of the right (and occasionally the left) ventricular muscle are replaced by deposition of fat and fibrotic tissue. Patients with ARVC frequently manifest right ventricular conduction delay on ECG; the finding of an epsilon wave in lead V1 is a specific, although not sensitive, sign for the disease. An epsilon wave represents late activation of a region of the ventricular myocardium, with delay being due to the presence of fatty infiltration and fibrosis.

Although it is tempting to imagine that the rate of the tachycardia suggests whether or not it is from the ventricle, the tachycardia rate is not helpful in diagnosing the location of the tachycardia. Likewise, the regularity of the tachycardia generally is not helpful to classify its origin, although gross irregularity suggests the possibility of atrial fibrillation with aberrancy or preexcitation.

Electrolytes and cardiac enzymes

Electrolyte abnormalities (particularly hypokalaemia and hypomagnesaemia) may incite and/or contribute to VT. When time and the patient's condition permit, blood electrolytes should be investigated and any abnormalities of these electrolytes should be corrected. In situations where ischaemia or infarction is the suspected mechanism of the VT, myocardial biomarker assays (creatine kinase and troponin) provide useful confirmatory information.

Echocardiogram, stress test, cardiac catheterisation, or MRI

Given the widely varying prognosis and management strategies for idiopathic VT and VT associated with structural heart disease, it is crucial to establish the presence or absence of structural heart disease in a patient presenting with VT. Echocardiogram is an efficient way to determine the presence or absence of structural heart disease in addition to quantifying systolic function. In patients suspected of having arrhythmogenic right ventricular cardiomyopathy, cardiac MRI is indicated to evaluate for the presence of fibro-fatty infiltration of the right ventricle and for right ventricular dysfunction. Stress testing and/or cardiac catheterisation should be considered to establish the presence of CAD, to exclude the possibility of asymptomatic ischaemia, especially among patients with risk factors for CAD.

Electrophysiological (EP) testing

The determination of which patients would benefit from an invasive EP study is made in consultation with an electrophysiologist. [5] It may be required to distinguish VT from SVT with aberrancy in cases where the surface ECG cannot establish a diagnosis. The EP study may also be used to establish the mechanism of VT in patients with structurally normal hearts. In addition, EP

studies are used for risk stratification among patients with non-sustained VT and less severe degrees of cardiomyopathy, and may be helpful in such cases in determining whether or not a given patient would benefit from a prophylactic implantable cardioverter defibrillator (ICD).

Genetic screening
Genetic screening is available for common mutations associated with long QT syndrome, Brugada syndrome, and catecholaminergic polymorphic VT. Consultation with an electrophysiologist and/or a medical geneticist is useful when deciding which patients should undergo genetic screening. [4] Guidelines have been published regarding the indication for genetic testing with respect to channelopathies and cardiomyopathies. [16]
Click to view diagnostic guideline references.

Diagnostic criteria

Pulseless ventricular tachycardia (VT)

Haemodynamically unstable: patient unconscious with hypotension and undetectable pulse.

VT with a cardiac output

Haemodynamically stable/well: an alert patient with a normal BP. Haemodynamically unstable/unwell: patient with weak pulse and hypotension, signs of diminished cerebral perfusion (light-headedness, dizziness, diminished responsiveness, or unconsciousness) or diminished coronary perfusion (chest discomfort, dyspnoea).

Case history #1
A 65-year-old man has a history of prior anterior wall MI that occurred 2 years ago, complicated by severe left ventricular systolic dysfunction. While walking to the shops, he suddenly notes palpitations, diaphoresis, dizziness, and a sense of overwhelming malaise. One minute later, he turned grey, lost consciousness, and collapsed onto the floor. An ECG revealed sustained monomorphic ventricular tachycardia at 150 bpm. View image Cardiopulmonary resuscitation was initiated and the patient was cardioverted to sinus rhythm with a 200-J biphasic shock delivered from an external defibrillator. The patient regained consciousness. There was no antecedent chest discomfort and cardiac enzymes were negative after the event. Serum electrolytes were also normal. He received an implantable cardioverter/defibrillator the next day.

Case history #2
A 30-year-old woman presented to her general practitioner complaining of recurrent palpitations during exercise. She had previously been healthy and was on no medications. She described a long history of 'skipped heart beats'. Her doctor arranged a treadmill exercise test, which demonstrated good effort tolerance and no evidence of ischaemia. During early recovery she developed sustained ventricular tachycardia with a left bundle branch block, inferior axis morphology. View image A cardiac MRI was performed that demonstrated normal biventricular function without evidence of myocardial scar or fatty infiltration. Electrophysiological testing was notable for inducible adenosine-sensitive ventricular tachycardia (with identical morphology to the clinical tachycardia) that was successfully ablated in the right ventricular outflow tract.

Other presentations
Ventricular arrhythmias may present with a diverse spectrum of symptoms, including palpitations, chest pain, and/or syncope, or may be asymptomatic. The type of symptom associated with the arrhythmia depends on its duration, its rate, and whether or not it is associated with abnormal perfusion to the heart or brain. Short-lived arrhythmias frequently are asymptomatic or manifest as brief palpitations, whereas longer and more rapid arrhythmias are frequently associated with presyncope or syncope. Sudden cardiac death is the most severe manifestation of ventricular arrhythmias; victims of sudden cardiac arrest rarely survive without cardiopulmonary resuscitation and prompt electrical defibrillation.

Treatment Options

Treatment Patient group haemodynamically unstable VT with a pulse line 1st Treatmenthide all

synchronised cardioversion according to ACLS protocol + treatment of reversible cause (if present)

Cardioversion is essential for the acute treatment of haemodynamically unstable VT (symptomatic or severely hypotensive VT).

Synchronised cardioversion should be considered before attempting anti-arrhythmic drug therapy in patients who are suffering from syncope, presyncope, frequent palpitations, or hypotension (particularly those with symptoms of diminished cerebral perfusion), even if they have apparently stable haemodynamics.

Cardioversion may be repeated as needed until rhythm is controlled. In patients with an identifiable reversible cause of ventricular tachycardia (e.g., ischaemia, MI, toxicity, drug overdose) management will also involve treatment of the reversible cause.

adjunct [?]

anti-arrhythmic medication

Medical therapy provides an important adjunctive therapy to emergency cardiovascular care, based on the ACLS protocol. Amiodarone and/or lidocaine are considered useful anti-arrhythmic drugs in these circumstances.[17] [18] Primary Options amiodarone : 300 mg intravenous push Secondary Options lidocaine : 1 to 1.5 mg/kg intravenously as a single dose

torsades de pointes

1st

IV magnesium sulphate + withdraw offending drugs + correct electrolyte abnormalities

Torsades de pointes, a special type of ventricular tachycardia characterised by a twisting

Treatment Patient group haemodynamically unstable VT with a pulse line 1st Treatmenthide all

synchronised cardioversion according to ACLS protocol + treatment of reversible cause (if present)

Cardioversion is essential for the acute treatment of haemodynamically unstable VT (symptomatic or severely hypotensive VT).

Synchronised cardioversion should be considered before attempting anti-arrhythmic drug therapy in patients who are suffering from syncope, presyncope, frequent palpitations, or hypotension (particularly those with symptoms of diminished cerebral perfusion), even if they have apparently stable haemodynamics.

Cardioversion may be repeated as needed until rhythm is controlled. In patients with an identifiable reversible cause of ventricular tachycardia (e.g., ischaemia, MI, toxicity, drug overdose) management will also involve treatment of the reversible cause.

adjunct [?]

anti-arrhythmic medication

Medical therapy provides an important adjunctive therapy to emergency cardiovascular care, based on the ACLS protocol. Amiodarone and/or lidocaine are considered useful anti-arrhythmic drugs in these circumstances.[17] [18] Primary Options amiodarone : 300 mg intravenous push Secondary Options lidocaine : 1 to 1.5 mg/kg intravenously as a single dose

torsades de pointes

1st

IV magnesium sulphate + withdraw offending drugs + correct electrolyte abnormalities

Torsades de pointes, a special type of ventricular tachycardia characterised by a twisting

Treatment Patient group haemodynamically unstable VT with a pulse line 1st Treatmenthide all

synchronised cardioversion according to ACLS protocol + treatment of reversible cause (if present)

Cardioversion is essential for the acute treatment of haemodynamically unstable VT (symptomatic or severely hypotensive VT).

Synchronised cardioversion should be considered before attempting anti-arrhythmic drug therapy in patients who are suffering from syncope, presyncope, frequent palpitations, or hypotension (particularly those with symptoms of diminished cerebral perfusion), even if they have apparently stable haemodynamics.

Cardioversion may be repeated as needed until rhythm is controlled. In patients with an identifiable reversible cause of ventricular tachycardia (e.g., ischaemia, MI, toxicity, drug overdose) management will also involve treatment of the reversible cause.

adjunct [?]

anti-arrhythmic medication

Medical therapy provides an important adjunctive therapy to emergency cardiovascular care, based on the ACLS protocol. Amiodarone and/or lidocaine are considered useful anti-arrhythmic drugs in these circumstances.[17] [18] Primary Options amiodarone : 300 mg intravenous push Secondary Options lidocaine : 1 to 1.5 mg/kg intravenously as a single dose

torsades de pointes

1st

IV magnesium sulphate + withdraw offending drugs + correct electrolyte abnormalities

Torsades de pointes, a special type of ventricular tachycardia characterised by a twisting

Treatment Patient group haemodynamically unstable VT with a pulse line 1st Treatmenthide all

synchronised cardioversion according to ACLS protocol + treatment of reversible cause (if present)

Cardioversion is essential for the acute treatment of haemodynamically unstable VT (symptomatic or severely hypotensive VT).

Synchronised cardioversion should be considered before attempting anti-arrhythmic drug therapy in patients who are suffering from syncope, presyncope, frequent palpitations, or hypotension (particularly those with symptoms of diminished cerebral perfusion), even if they have apparently stable haemodynamics.

Cardioversion may be repeated as needed until rhythm is controlled. In patients with an identifiable reversible cause of ventricular tachycardia (e.g., ischaemia, MI, toxicity, drug overdose) management will also involve treatment of the reversible cause.

adjunct [?]

anti-arrhythmic medication

Medical therapy provides an important adjunctive therapy to emergency cardiovascular care, based on the ACLS protocol. Amiodarone and/or lidocaine are considered useful anti-arrhythmic drugs in these circumstances.[17] [18] Primary Options amiodarone : 300 mg intravenous push Secondary Options lidocaine : 1 to 1.5 mg/kg intravenously as a single dose

torsades de pointes

1st

IV magnesium sulphate + withdraw offending drugs + correct electrolyte abnormalities

Torsades de pointes, a special type of ventricular tachycardia characterised by a twisting

Treatment Patient group haemodynamically unstable VT with a pulse line 1st Treatmenthide all

synchronised cardioversion according to ACLS protocol + treatment of reversible cause (if present)

Cardioversion is essential for the acute treatment of haemodynamically unstable VT (symptomatic or severely hypotensive VT).

Synchronised cardioversion should be considered before attempting anti-arrhythmic drug therapy in patients who are suffering from syncope, presyncope, frequent palpitations, or hypotension (particularly those with symptoms of diminished cerebral perfusion), even if they have apparently stable haemodynamics.

Cardioversion may be repeated as needed until rhythm is controlled. In patients with an identifiable reversible cause of ventricular tachycardia (e.g., ischaemia, MI, toxicity, drug overdose) management will also involve treatment of the reversible cause.

adjunct [?]

anti-arrhythmic medication

Medical therapy provides an important adjunctive therapy to emergency cardiovascular care, based on the ACLS protocol. Amiodarone and/or lidocaine are considered useful anti-arrhythmic drugs in these circumstances.[17] [18] Primary Options amiodarone : 300 mg intravenous push Secondary Options lidocaine : 1 to 1.5 mg/kg intravenously as a single dose

torsades de pointes

1st

IV magnesium sulphate + withdraw offending drugs + correct electrolyte abnormalities

Torsades de pointes, a special type of ventricular tachycardia characterised by a twisting

Treatment Patient group haemodynamically unstable VT with a pulse line 1st Treatmenthide all

synchronised cardioversion according to ACLS protocol + treatment of reversible cause (if present)

Cardioversion is essential for the acute treatment of haemodynamically unstable VT (symptomatic or severely hypotensive VT).

Synchronised cardioversion should be considered before attempting anti-arrhythmic drug therapy in patients who are suffering from syncope, presyncope, frequent palpitations, or hypotension (particularly those with symptoms of diminished cerebral perfusion), even if they have apparently stable haemodynamics.

Cardioversion may be repeated as needed until rhythm is controlled. In patients with an identifiable reversible cause of ventricular tachycardia (e.g., ischaemia, MI, toxicity, drug overdose) management will also involve treatment of the reversible cause.

adjunct [?]

anti-arrhythmic medication

Medical therapy provides an important adjunctive therapy to emergency cardiovascular care, based on the ACLS protocol. Amiodarone and/or lidocaine are considered useful anti-arrhythmic drugs in these circumstances.[17] [18] Primary Options amiodarone : 300 mg intravenous push Secondary Options lidocaine : 1 to 1.5 mg/kg intravenously as a single dose

torsades de pointes

1st

IV magnesium sulphate + withdraw offending drugs + correct electrolyte abnormalities

Torsades de pointes, a special type of ventricular tachycardia characterised by a twisting

Treatment Patient group haemodynamically unstable VT with a pulse line 1st Treatmenthide all

synchronised cardioversion according to ACLS protocol + treatment of reversible cause (if present)

Cardioversion is essential for the acute treatment of haemodynamically unstable VT (symptomatic or severely hypotensive VT).

Synchronised cardioversion should be considered before attempting anti-arrhythmic drug therapy in patients who are suffering from syncope, presyncope, frequent palpitations, or hypotension (particularly those with symptoms of diminished cerebral perfusion), even if they have apparently stable haemodynamics.

Cardioversion may be repeated as needed until rhythm is controlled. In patients with an identifiable reversible cause of ventricular tachycardia (e.g., ischaemia, MI, toxicity, drug overdose) management will also involve treatment of the reversible cause.

adjunct [?]

anti-arrhythmic medication

Medical therapy provides an important adjunctive therapy to emergency cardiovascular care, based on the ACLS protocol. Amiodarone and/or lidocaine are considered useful anti-arrhythmic drugs in these circumstances.[17] [18] Primary Options amiodarone : 300 mg intravenous push Secondary Options lidocaine : 1 to 1.5 mg/kg intravenously as a single dose

torsades de pointes

1st

IV magnesium sulphate + withdraw offending drugs + correct electrolyte abnormalities

Torsades de pointes, a special type of ventricular tachycardia characterised by a twisting

Treatment Patient group haemodynamically unstable VT with a pulse line 1st Treatmenthide all

synchronised cardioversion according to ACLS protocol + treatment of reversible cause (if present)

Cardioversion is essential for the acute treatment of haemodynamically unstable VT (symptomatic or severely hypotensive VT).

Synchronised cardioversion should be considered before attempting anti-arrhythmic drug therapy in patients who are suffering from syncope, presyncope, frequent palpitations, or hypotension (particularly those with symptoms of diminished cerebral perfusion), even if they have apparently stable haemodynamics.

Cardioversion may be repeated as needed until rhythm is controlled. In patients with an identifiable reversible cause of ventricular tachycardia (e.g., ischaemia, MI, toxicity, drug overdose) management will also involve treatment of the reversible cause.

adjunct [?]

anti-arrhythmic medication

Medical therapy provides an important adjunctive therapy to emergency cardiovascular care, based on the ACLS protocol. Amiodarone and/or lidocaine are considered useful anti-arrhythmic drugs in these circumstances.[17] [18] Primary Options amiodarone : 300 mg intravenous push Secondary Options lidocaine : 1 to 1.5 mg/kg intravenously as a single dose

torsades de pointes

1st

IV magnesium sulphate + withdraw offending drugs + correct electrolyte abnormalities

Torsades de pointes, a special type of ventricular tachycardia characterised by a twisting

Treatment Patient group haemodynamically unstable VT with a pulse line 1st Treatmenthide all

synchronised cardioversion according to ACLS protocol + treatment of reversible cause (if present)

Cardioversion is essential for the acute treatment of haemodynamically unstable VT (symptomatic or severely hypotensive VT).

Synchronised cardioversion should be considered before attempting anti-arrhythmic drug therapy in patients who are suffering from syncope, presyncope, frequent palpitations, or hypotension (particularly those with symptoms of diminished cerebral perfusion), even if they have apparently stable haemodynamics.

Cardioversion may be repeated as needed until rhythm is controlled. In patients with an identifiable reversible cause of ventricular tachycardia (e.g., ischaemia, MI, toxicity, drug overdose) management will also involve treatment of the reversible cause.

adjunct [?]

anti-arrhythmic medication

Medical therapy provides an important adjunctive therapy to emergency cardiovascular care, based on the ACLS protocol. Amiodarone and/or lidocaine are considered useful anti-arrhythmic drugs in these circumstances.[17] [18] Primary Options amiodarone : 300 mg intravenous push Secondary Options lidocaine : 1 to 1.5 mg/kg intravenously as a single dose

torsades de pointes

1st

IV magnesium sulphate + withdraw offending drugs + correct electrolyte abnormalities

Torsades de pointes, a special type of ventricular tachycardia characterised by a twisting

Treatment Patient group non-idiopathic: at high risk for VT or Hx sustained VT/cardiac arrest without identifiable reversible cause line 1st Treatmenthide all

implantable cardioverter defibrillator (ICD)

The group of patients discussed here as nonidiopathic include those with identifiable reversible causes for VT as well as those in whom there are no identifiable causes. Idiopathic VT (although defined as occurring in the absence of structural heart disease, known genetic disorder, drug toxicity, or electrolyte imbalance) is identifiable by electrophysiological testing and response to certain medications. Therefore, in the case of ventricular tachycardias, idiopathic VT refers to a specific subtype of tachycardias that are defined and identifiable. This is different from tachycardias with no identifiable cause, in which the patient would have no signs of a definitive cause for the VT or signs of an idiopathic VT.

Patients at high risk for VT include those with: ischaemic cardiomyopathy (left ventricular ejection faction [LVEF] 35%, or 40% with non-sustained VT and inducible VT during electrophysiological [EP] testing); non-ischaemic cardiomyopathy (LVEF 35% and New York Heart Association class II or III symptoms); hypertrophic cardiomyopathy with one or more of the following: 1) personal hx of sudden cardiac death or sustained VT; 2) FHx of sudden cardiac death in a first-degree relative; 3) a ventricular septal wall thickness >30 mm; 4) unexplained syncope; 5) frequent or prolonged nonsustained VT discovered on a Holter monitor; and 6) an abnormal BP response (i.e., fall in BP on exercise treadmill test); previous VT/ventricular fibrillation (VF); or congenital arrhythmia syndromes, including long QT syndrome and Brugada syndrome with high-risk features.

ICD therapy provides a continuous monitor for the cardiac rhythm and the capability of terminating VT by overdrive pacing and/or cardioversion

Treatment Patient group non-idiopathic: at high risk for VT or Hx sustained VT/cardiac arrest without identifiable reversible cause line 1st Treatmenthide all

implantable cardioverter defibrillator (ICD)

The group of patients discussed here as nonidiopathic include those with identifiable reversible causes for VT as well as those in whom there are no identifiable causes. Idiopathic VT (although defined as occurring in the absence of structural heart disease, known genetic disorder, drug toxicity, or electrolyte imbalance) is identifiable by electrophysiological testing and response to certain medications. Therefore, in the case of ventricular tachycardias, idiopathic VT refers to a specific subtype of tachycardias that are defined and identifiable. This is different from tachycardias with no identifiable cause, in which the patient would have no signs of a definitive cause for the VT or signs of an idiopathic VT.

Patients at high risk for VT include those with: ischaemic cardiomyopathy (left ventricular ejection faction [LVEF] 35%, or 40% with non-sustained VT and inducible VT during electrophysiological [EP] testing); non-ischaemic cardiomyopathy (LVEF 35% and New York Heart Association class II or III symptoms); hypertrophic cardiomyopathy with one or more of the following: 1) personal hx of sudden cardiac death or sustained VT; 2) FHx of sudden cardiac death in a first-degree relative; 3) a ventricular septal wall thickness >30 mm; 4) unexplained syncope; 5) frequent or prolonged nonsustained VT discovered on a Holter monitor; and 6) an abnormal BP response (i.e., fall in BP on exercise treadmill test); previous VT/ventricular fibrillation (VF); or congenital arrhythmia syndromes, including long QT syndrome and Brugada syndrome with high-risk features.

ICD therapy provides a continuous monitor for the cardiac rhythm and the capability of terminating VT by overdrive pacing and/or cardioversion

Treatment Patient group non-idiopathic: at high risk for VT or Hx sustained VT/cardiac arrest without identifiable reversible cause line 1st Treatmenthide all

implantable cardioverter defibrillator (ICD)

The group of patients discussed here as nonidiopathic include those with identifiable reversible causes for VT as well as those in whom there are no identifiable causes. Idiopathic VT (although defined as occurring in the absence of structural heart disease, known genetic disorder, drug toxicity, or electrolyte imbalance) is identifiable by electrophysiological testing and response to certain medications. Therefore, in the case of ventricular tachycardias, idiopathic VT refers to a specific subtype of tachycardias that are defined and identifiable. This is different from tachycardias with no identifiable cause, in which the patient would have no signs of a definitive cause for the VT or signs of an idiopathic VT.

Patients at high risk for VT include those with: ischaemic cardiomyopathy (left ventricular ejection faction [LVEF] 35%, or 40% with non-sustained VT and inducible VT during electrophysiological [EP] testing); non-ischaemic cardiomyopathy (LVEF 35% and New York Heart Association class II or III symptoms); hypertrophic cardiomyopathy with one or more of the following: 1) personal hx of sudden cardiac death or sustained VT; 2) FHx of sudden cardiac death in a first-degree relative; 3) a ventricular septal wall thickness >30 mm; 4) unexplained syncope; 5) frequent or prolonged nonsustained VT discovered on a Holter monitor; and 6) an abnormal BP response (i.e., fall in BP on exercise treadmill test); previous VT/ventricular fibrillation (VF); or congenital arrhythmia syndromes, including long QT syndrome and Brugada syndrome with high-risk features.

ICD therapy provides a continuous monitor for the cardiac rhythm and the capability of terminating VT by overdrive pacing and/or cardioversion

Treatment Patient group non-idiopathic: at high risk for VT or Hx sustained VT/cardiac arrest without identifiable reversible cause line 1st Treatmenthide all

implantable cardioverter defibrillator (ICD)

The group of patients discussed here as nonidiopathic include those with identifiable reversible causes for VT as well as those in whom there are no identifiable causes. Idiopathic VT (although defined as occurring in the absence of structural heart disease, known genetic disorder, drug toxicity, or electrolyte imbalance) is identifiable by electrophysiological testing and response to certain medications. Therefore, in the case of ventricular tachycardias, idiopathic VT refers to a specific subtype of tachycardias that are defined and identifiable. This is different from tachycardias with no identifiable cause, in which the patient would have no signs of a definitive cause for the VT or signs of an idiopathic VT.

Patients at high risk for VT include those with: ischaemic cardiomyopathy (left ventricular ejection faction [LVEF] 35%, or 40% with non-sustained VT and inducible VT during electrophysiological [EP] testing); non-ischaemic cardiomyopathy (LVEF 35% and New York Heart Association class II or III symptoms); hypertrophic cardiomyopathy with one or more of the following: 1) personal hx of sudden cardiac death or sustained VT; 2) FHx of sudden cardiac death in a first-degree relative; 3) a ventricular septal wall thickness >30 mm; 4) unexplained syncope; 5) frequent or prolonged nonsustained VT discovered on a Holter monitor; and 6) an abnormal BP response (i.e., fall in BP on exercise treadmill test); previous VT/ventricular fibrillation (VF); or congenital arrhythmia syndromes, including long QT syndrome and Brugada syndrome with high-risk features.

ICD therapy provides a continuous monitor for the cardiac rhythm and the capability of terminating VT by overdrive pacing and/or cardioversion

Treatment Patient group non-idiopathic: at high risk for VT or Hx sustained VT/cardiac arrest without identifiable reversible cause line 1st Treatmenthide all

implantable cardioverter defibrillator (ICD)

The group of patients discussed here as nonidiopathic include those with identifiable reversible causes for VT as well as those in whom there are no identifiable causes. Idiopathic VT (although defined as occurring in the absence of structural heart disease, known genetic disorder, drug toxicity, or electrolyte imbalance) is identifiable by electrophysiological testing and response to certain medications. Therefore, in the case of ventricular tachycardias, idiopathic VT refers to a specific subtype of tachycardias that are defined and identifiable. This is different from tachycardias with no identifiable cause, in which the patient would have no signs of a definitive cause for the VT or signs of an idiopathic VT.

Patients at high risk for VT include those with: ischaemic cardiomyopathy (left ventricular ejection faction [LVEF] 35%, or 40% with non-sustained VT and inducible VT during electrophysiological [EP] testing); non-ischaemic cardiomyopathy (LVEF 35% and New York Heart Association class II or III symptoms); hypertrophic cardiomyopathy with one or more of the following: 1) personal hx of sudden cardiac death or sustained VT; 2) FHx of sudden cardiac death in a first-degree relative; 3) a ventricular septal wall thickness >30 mm; 4) unexplained syncope; 5) frequent or prolonged nonsustained VT discovered on a Holter monitor; and 6) an abnormal BP response (i.e., fall in BP on exercise treadmill test); previous VT/ventricular fibrillation (VF); or congenital arrhythmia syndromes, including long QT syndrome and Brugada syndrome with high-risk features.

ICD therapy provides a continuous monitor for the cardiac rhythm and the capability of terminating VT by overdrive pacing and/or cardioversion

Treatment Patient group non-idiopathic: at high risk for VT or Hx sustained VT/cardiac arrest without identifiable reversible cause line 1st Treatmenthide all

implantable cardioverter defibrillator (ICD)

The group of patients discussed here as nonidiopathic include those with identifiable reversible causes for VT as well as those in whom there are no identifiable causes. Idiopathic VT (although defined as occurring in the absence of structural heart disease, known genetic disorder, drug toxicity, or electrolyte imbalance) is identifiable by electrophysiological testing and response to certain medications. Therefore, in the case of ventricular tachycardias, idiopathic VT refers to a specific subtype of tachycardias that are defined and identifiable. This is different from tachycardias with no identifiable cause, in which the patient would have no signs of a definitive cause for the VT or signs of an idiopathic VT.

Patients at high risk for VT include those with: ischaemic cardiomyopathy (left ventricular ejection faction [LVEF] 35%, or 40% with non-sustained VT and inducible VT during electrophysiological [EP] testing); non-ischaemic cardiomyopathy (LVEF 35% and New York Heart Association class II or III symptoms); hypertrophic cardiomyopathy with one or more of the following: 1) personal hx of sudden cardiac death or sustained VT; 2) FHx of sudden cardiac death in a first-degree relative; 3) a ventricular septal wall thickness >30 mm; 4) unexplained syncope; 5) frequent or prolonged nonsustained VT discovered on a Holter monitor; and 6) an abnormal BP response (i.e., fall in BP on exercise treadmill test); previous VT/ventricular fibrillation (VF); or congenital arrhythmia syndromes, including long QT syndrome and Brugada syndrome with high-risk features.

ICD therapy provides a continuous monitor for the cardiac rhythm and the capability of terminating VT by overdrive pacing and/or cardioversion

Treatment Patient group non-idiopathic: at high risk for VT or Hx sustained VT/cardiac arrest without identifiable reversible cause line 1st Treatmenthide all

implantable cardioverter defibrillator (ICD)

The group of patients discussed here as nonidiopathic include those with identifiable reversible causes for VT as well as those in whom there are no identifiable causes. Idiopathic VT (although defined as occurring in the absence of structural heart disease, known genetic disorder, drug toxicity, or electrolyte imbalance) is identifiable by electrophysiological testing and response to certain medications. Therefore, in the case of ventricular tachycardias, idiopathic VT refers to a specific subtype of tachycardias that are defined and identifiable. This is different from tachycardias with no identifiable cause, in which the patient would have no signs of a definitive cause for the VT or signs of an idiopathic VT.

Patients at high risk for VT include those with: ischaemic cardiomyopathy (left ventricular ejection faction [LVEF] 35%, or 40% with non-sustained VT and inducible VT during electrophysiological [EP] testing); non-ischaemic cardiomyopathy (LVEF 35% and New York Heart Association class II or III symptoms); hypertrophic cardiomyopathy with one or more of the following: 1) personal hx of sudden cardiac death or sustained VT; 2) FHx of sudden cardiac death in a first-degree relative; 3) a ventricular septal wall thickness >30 mm; 4) unexplained syncope; 5) frequent or prolonged nonsustained VT discovered on a Holter monitor; and 6) an abnormal BP response (i.e., fall in BP on exercise treadmill test); previous VT/ventricular fibrillation (VF); or congenital arrhythmia syndromes, including long QT syndrome and Brugada syndrome with high-risk features.

ICD therapy provides a continuous monitor for the cardiac rhythm and the capability of terminating VT by overdrive pacing and/or cardioversion

Treatment Patient group non-idiopathic: at high risk for VT or Hx sustained VT/cardiac arrest without identifiable reversible cause line 1st Treatmenthide all

implantable cardioverter defibrillator (ICD)

The group of patients discussed here as nonidiopathic include those with identifiable reversible causes for VT as well as those in whom there are no identifiable causes. Idiopathic VT (although defined as occurring in the absence of structural heart disease, known genetic disorder, drug toxicity, or electrolyte imbalance) is identifiable by electrophysiological testing and response to certain medications. Therefore, in the case of ventricular tachycardias, idiopathic VT refers to a specific subtype of tachycardias that are defined and identifiable. This is different from tachycardias with no identifiable cause, in which the patient would have no signs of a definitive cause for the VT or signs of an idiopathic VT.

Patients at high risk for VT include those with: ischaemic cardiomyopathy (left ventricular ejection faction [LVEF] 35%, or 40% with non-sustained VT and inducible VT during electrophysiological [EP] testing); non-ischaemic cardiomyopathy (LVEF 35% and New York Heart Association class II or III symptoms); hypertrophic cardiomyopathy with one or more of the following: 1) personal hx of sudden cardiac death or sustained VT; 2) FHx of sudden cardiac death in a first-degree relative; 3) a ventricular septal wall thickness >30 mm; 4) unexplained syncope; 5) frequent or prolonged nonsustained VT discovered on a Holter monitor; and 6) an abnormal BP response (i.e., fall in BP on exercise treadmill test); previous VT/ventricular fibrillation (VF); or congenital arrhythmia syndromes, including long QT syndrome and Brugada syndrome with high-risk features.

ICD therapy provides a continuous monitor for the cardiac rhythm and the capability of terminating VT by overdrive pacing and/or cardioversion

Treatment approach
Avoidance of behavioural factors associated with CAD and left ventricular dysfunction is useful to prevent the most common causes of ventricular arrhythmia. Likewise, aggressive management of conditions that predispose to CAD and MI (e.g., HTN, hyperlipidaemia, diabetes mellitus) would be expected to reduce the subsequent risk of ventricular tachycardia (VT). In special cases such as hypertrophic cardiomyopathy (HCM), arrhythmogenic right ventricular cardiomyopathy (ARVC), and long QT syndrome type 1, patients should be counselled to avoid physical exertion. It is important to distinguish ventricular arrhythmia patients with underlying structural heart disease from those with idiopathic VT, which is associated with a good prognosis rarely progressing to cardiac arrest. Idiopathic VT (although defined as occurring in the absence of structural heart disease, known genetic disorder, drug toxicity, or electrolyte imbalance) is identifiable by electrophysiological testing. Therefore, in the case of ventricular tachycardias, idiopathic VT refers to a specific sub-type of tachycardias that are can be defined by arrhythmia mechanism. This is different from tachycardias with no identifiable cause, in which the patient would have no signs of a definitive cause for the VT or signs of an idiopathic VT.

Treatment for identifiable reversible cause of VT such as ischaemia, MI, toxicity, drug overdose
In patients with a reversible cause of VT such as active ischaemia, recent MI, or drug toxicity or overdose, management includes treatment of the underlying cause of the VT in addition to the arrhythmia itself. Until the reversible cause of VT has been corrected, an ICD should not be considered.

Haemodynamically unstable sustained VT

Detailed discussion on CPR and defibrillation, in the advanced cardiac life support (ACLS) algorithm for the management of haemodynamically unstable VT in the setting of cardiac arrest such as pulseless VT and VF, is beyond the scope of this monograph but can be found elsewhere. [17] [18] [2010

American Heart Association guidelines for cardiopulmonary resuscitation and emergency cardiovascular care] (external link) Cardioversion is essential for the acute treatment of patients with haemodynamically unstable VT (symptomatic or severely hypotensive VT). Left untreated, these conditions frequently culminate in death; rapid recognition and initiation of appropriate treatment may provide the only hope for the patient's survival. Synchronised cardioversion should be considered before attempting antiarrhythmic drug therapy in patients who are suffering from syncope, presyncope, or hypotension. The anti-arrhythmic medications amiodarone and lidocaine can be used as adjunctive therapy.

Torsades de pointes
Torsades de pointes, a specific type of VT characterised by a twisting appearance around the baseline, occurs in the setting of QT prolongation due to either the congenital or the acquired forms of the long QT syndrome. Torsades de pointes should be treated as any other form of VT according to the ACLS protocol. If the patient is haemodynamically unstable, immediate cardioversion should be performed. There should be special recognition of the fact that hypokalaemia and hypomagnesaemia are frequently associated with torsades de pointes, and empiric administration of magnesium should be considered. Offending drugs should be withdrawn and electrolyte deficiencies should be treated aggressively. An up-to-date list of drugs is available through research centres. [Arizona Center for Education and Research on Therapeutics] (external link) IV magnesium sulphate should be administered. Additionally, overdrive pacing and isoprenaline infusion may be useful adjunctively in this arrhythmia as they reduce the QT interval. [17] [18]

Haemodynamically stable sustained VT (nonidiopathic)

Anti-arrhythmic medications are useful in the acute management of VT that is asymptomatic and associated with a normal BP. Before initiating antiarrhythmic drug therapy for a VT, it is important to be confident in the diagnosis and to make sure that the patient is not experiencing supraventricular tachycardia (SVT) with aberrant conduction. Several antiarrhythmic drugs may be considered in the acute management of stable VT.

The American Heart Association recommends amiodarone bolus as a first choice of medication, and it is preferred in the setting of left ventricular dysfunction.[A Evidence] Lidocaine by infusion may also be considered, especially among patients with history or signs of ischaemia. Procainamide is also another option, but this drug may be pro-arrhythmic and should be used with caution in the setting of baseline QT prolongation. [17] [18] Patients not responsive to initial anti-arrhythmic therapy:
Synchronised electrical cardioversion is another important treatment for haemodynamically tolerated sustained VT. Among patients who fail an initial attempt at synchronised cardioversion, anti-arrhythmic medications such as amiodarone or lidocaine may be administered prior to additional attempts at cardioversion. Synchronised cardioversion should be considered before attempting anti-arrhythmic drug therapy in patients who are suffering from syncope, presyncope, frequent palpitations, or hypotension (particularly those with symptoms of diminished cerebral perfusion), even if they have apparently stable haemodynamic parameters.

Initial management of haemodynamically stable idiopathic VT

There are several distinct entities of ventricular tachycardia that occur in the absence of structural heart disease. Idiopathic VT occurs in the absence of structural heart disease (e.g., ischaemia, prior infarction, cardiomyopathy, and valvular or other disorders of the myocardium), known genetic disorder (e.g., long QT syndrome, Brugada syndrome, ARVC), drug toxicity, or electrolyte imbalance. They are, however, identifiable through electrophysiological testing and response to certain medications. Idiopathic VT requires specific treatment, and consultation with an electrophysiologist is recommended. Specific types of idiopathic VT characteristically respond to specific medications, a feature that is useful for diagnostic as well as therapeutic purposes. Idiopathic outflow tract VT (which typically arises from the right ventricular outflow tract, but which may occasionally arise from the left ventricular outflow tract) demonstrates one of several characteristic ECG morphologies. This arrhythmia results cyclic-AMP-mediated triggered activity which results in delayed after depolarisations and can therefore be terminated with a bolus of adenosine. Outflow tract tachycardia may also respond to beta-adrenergic blockade, calcium channel blockers, or to vagal manoeuvres.

Fascicular VT, a common form of idiopathic VT due to a re-entrant circuit involving either the left anterior or left posterior fascicle, characteristically responds to verapamil, but the drug should be only be used with extreme caution due to the risk of hypotension. Cases of idiopathic VT refractory to adenosine or verapamil can be treated with other anti-arrhythmic medications (lidocaine, amiodarone); if the arrhythmia persists, synchronised electrical cardioversion should be considered. [17] [18] Earlier use of cardioversion may be warranted in patients who are highly symptomatic (particularly with symptoms of diminished cerebral perfusion) despite apparently stable haemodynamics. Among patients who fail an initial attempt at synchronised cardioversion, additional anti-arrhythmic medications such as amiodarone or lidocaine may be administered prior to additional attempts at cardioversion.

Subsequent management of haemodynamically stable idiopathic VT

For patients with idiopathic ventricular tachycardia and mild-to-moderate symptoms (rare palpitations that do not interfere with daily activities), betablockers or calcium-channel blockers usually provide sufficient treatment. Catheter ablation is also reasonable as first-line therapy in patients with mildto-moderate symptoms who prefer not to take medications. [19] It is a matter of patient preference in deciding between medications and ablation in this setting. In patients with moderate-to-severe symptoms (syncope, presyncope, or frequent, disabling palpitations) catheter ablation of VT should be considered as first-line therapy. Catheter ablation is also indicated in patients in whom beta-blockers and/or calcium-channel blockers are ineffective or poorly tolerated. [19] Anti-arrhythmic agents, including class I drugs (mexiletine, flecainide, and propafenone) and class III agents (amiodarone and sotalol), may be used in patients who fail therapy with beta-blockers and/or calcium-channel blockers and who are not candidates for catheter ablation due to medical co-morbidity or reluctance to undergo the procedure, or in whom catheter ablation is ineffective. [20] In patients with idiopathic VT, implantable cardioverter defibrillator (ICD) therapy is not recommended as a first-line treatment. Medication choice is usually based on individual patient/physician preference. In some cases, a beta-blocker or calcium-channel blocker will suffice, whereas in other cases catheter ablation of the arrhythmia is curative. [20] [C Evidence]

Medications such as flecainide, sotalol, and amiodarone may be employed as second-line therapy for patients with idiopathic VT who have refractory symptoms and who fail therapy with beta-blockers or catheter ablation.

Patients at high risk for VT or with history of sustained VT/cardiac arrest without identifiable reversible cause: implantable cardioverter defibrillator (ICD)
ICD implantation is the recommended initial treatment/preventative measure for patients at high risk of developing a malignant ventricular arrhythmia, for:
High-risk patients who have not yet experienced a sustained arrhythmia (primary prevention)[21] [22] [A Evidence] Patients who have survived an episode of sustained VT or ventricular fibrillation (VF) and who have no identifiable reversible cause for VT/cardiac arrest. [23] [24] [25] [A Evidence]

Patients at high risk for VT include those with:

Ischaemic cardiomyopathy (left ventricular ejection fraction [LVEF] 35%) and mild-to-moderate congestive heart failure symptoms (New York Heart Association class II or III symptoms) Ischaemic cardiomyopathy with LVEF 30% Ischaemic cardiomyopathy (LVEF 40%) with non-sustained VT and inducible sustained VT during electrophysiological (EP) testing Non-ischaemic cardiomyopathy (LVEF 35% and New York Heart Association class II or III symptoms) Hypertrophic cardiomyopathy with personal history of sudden death or sustained VT, first-degree relative with sudden death, unexplained exertional or recurrent syncope, massive LVH (left ventricular septum thickness >30 mm), or frequent or prolonged non-sustained VT or abnormal BP response to exercise Congenital arrhythmia syndromes, including symptomatic patients with long QT syndrome, Brugada syndrome and catecholaminergic polymorphic VT.

ICDs are highly effective in terminating sustained ventricular arrhythmias. These devices provide a continuous monitor for the cardiac rhythm and the capability of terminating VT by overdrive pacing and/or cardioversion/defibrillation. Multiple clinical trials have shown the ICDs to be more effective than anti-arrhythmic medications in reducing total mortality for cardiac arrest survivors. It should be emphasised that these trials excluded

patients with reversible causes of cardiac arrest, including toxic/metabolic abnormalities, trauma, and acute ischaemia. ICD implantation is not indicated in such cases when correction of the disorder is considered feasible and likely to substantially reduce the risk of recurrence. Although an invasive procedure, ICD implantation is associated with a procedural mortality of only 0.02%. The long-term risks of ICD therapy include device malfunction, infection, and/or inappropriate shocks. ICD shocks are painful and if frequent may impair the patient's quality of life. [23] [24] [25] [26] All currently available ICDs are capable of responding to arrhythmias in a tiered fashion. They are capable of anti-bradycardia pacing, anti-tachycardia pacing for ventricular tachycardia, low-energy cardioversion for VT, and highenergy defibrillation for VF. ICDs detect arrhythmias primarily on the basis of heart rate. Thus, they will not intervene in the case of VT below the programmed rate and may inappropriately intervene in the case of supraventricular arrhythmias with a rapid ventricular response.

Adjunctive therapies in high-risk patients already implanted with an ICD or for whom ICD therapy is not an option
Anti-arrhythmic drugs may be useful as adjunctive therapies for high-risk patients already implanted with an ICD or for whom ICD therapy is not an option. [5] However, it should be emphasised that with the notable exception of beta-blockers, randomised trials have shown that currently available oral anti-arrhythmic drugs do not prolong life when used chronically in the treatment of life-threatening ventricular arrhythmias and sudden death.[A Evidence] Anti-arrhythmic medications may not be appropriate for patients with structural heart disease because they have negative inotropic properties and may increase the risk of VT. It is important to be aware that amiodarone can increase defibrillation thresholds and potentially impair ICD function. [27] Catheter ablation may also be used as a palliative measure in patients with structural heart disease experiencing recurrent episodes of VT. Catheter ablation has also been shown to decrease appropriate ICD therapies, including ICD shocks. [19] [28] [29]

Emerging treatments
Remote magnetic navigation (RMN)

RMN is an emerging robotic navigation technique used in the mapping and ablation of arrhythmias. One study found RMN to be an effective and safe method for the ablation of ventricular tachycardia with low recurrence and complication rates. However, more studies are necessary. [31]

Monitoring
Patients with ventricular tachycardia (VT) should be evaluated by an electrophysiologist. An assessment of their underlying cardiac status should be undertaken and medical therapy and/or implantable cardioverter defibrillator (ICD) therapy should be initiated as clinically indicated. Patients implanted with an ICD require routine device checks, and need to be re-evaluated promptly if symptoms of the tachycardia recur, or if the device delivers a shock. Many routine device checks can be performed via remote telemetry; these checks are usually performed every 3 months.

Patient Instructions
Patients should report episodes of syncope, presyncope, chest pain, or palpitations to their physicians, as these symptoms may indicate recurrent VT. Patients on long-term anti-arrhythmic medications may require specific follow-up to monitor for efficacy and/or toxicity. Patients should be educated about specific adverse effects associated with their anti-arrhythmic medications, such as symptoms of thyroid dysfunction among patients taking amiodarone. Patients implanted with an ICD should report to their physician any shocks from the device or evidence of device infection (erythema, tenderness, or pus).

Complications
Complicationhide all

Implantable cardioverter defibrillator (ICD) system malfunction (device or leads) May require urgent device replacement or modification of one or more components of the ICD system. However, if the failure rate is sufficiently low and is less than the risk of ICD replacement, optimal management of devices that are prone to failure may consist of close observation of the patient rather than prophylactic device replacement. Ventricular fibrillation (VF) see our comprehensive coverage of Cardiac arrest Patients who develop sustained ventricular tachycardia (VT) in the context of left ventricular systolic dysfunction often have re-entrant rhythms around myocardial scars. Such re-entrant circuits can degenerate to VF and are associated with a high mortality rate.

Sudden cardiac death VT is a common cause of sudden cardiac death. ICD-related infection Often results from bacteraemia. Infection may occur along the intravascular portion of the leads or in the generator pocket. Treatment usually requires complete removal of the ICD system and a prolonged course of antibiotics. Cardiomyopathy see our comprehensive coverage of Hypertrophic cardiomyopathy Frequent or incessant idiopathic ventricular premature complexes (VPCs) or non-sustained VT have been associated with a reversible, tachycardia-induced cardiomyopathy that regresses following therapy with medications or catheter ablation. [32] Amiodarone-induced thyroid dysfunction Amiodarone can cause adverse effects, including thyroid dysfunction (both hypo- and hyperthyroidism).

Prognosis
Idiopathic ventricular tachycardia (VT)
Idiopathic VT generally carries a favourable prognosis. In most patients, idiopathic VT is not a progressive condition. The most common symptoms associated with idiopathic VT are palpitations and presyncope; true syncope is uncommon (10% to 20%). Patients presenting with apparent idiopathic VT arising from the right ventricle should undergo a careful evaluation for occult arrhythmogenic right ventricular cardiomyopathy (ARVC), as ventricular premature complexes (VPC) and VT are frequent early manifestations of this disorder. Frequent or incessant idiopathic VPCs or non-sustained VT have been associated with a reversible, tachycardia-induced cardiomyopathy that regresses following therapy with medications or catheter ablation. [32]

Non-idiopathic VT
In contrast to idiopathic VT, patients who develop sustained VT in the context of left ventricular systolic dysfunction often have re-entrant rhythms around myocardial scars. Such re-entrant circuits can degenerate to ventricular fibrillation (VF) and are associated with a high mortality rate. Implantable cardioverter defibrillator (ICD) implantation provides continuous monitoring of their cardiac rhythm and the capability to terminate VT through overdrive pacing and/or defibrillation. Owing to the unpredictable and rapid onset of

sustained VT, and its serious consequence if left untreated, prophylactic ICD therapy has become the most important treatment to reduce mortality among high-risk patients. [5]