Non-sustained ventricular tachycardias

Highlights
Summary Overview

Basics
Definition Epidemiology Aetiology Pathophysiology Classification

Prevention
Primary Secondary

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

Treatment
Details Step-by-step Guidelines Evidence

Follow Up
Recommendations Complications Prognosis

Resources
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History & exam

Key factors
hx of CAD hx of hypertrophic cardiomyopathy hx of idiopathic dilated cardiomyopathy presence of other risk factors asymptomatic presentation

tachycardia

Other diagnostic factors

palpitations dizziness lightheadedness pre-syncope syncope

History & exam details

Diagnostic tests
1st tests to order
ECG electrolyte panel troponin CK-MB

Tests to consider
24-hour ambulatory ECG monitoring echocardiogram cardiac catheterisation cardiac MRI with gadolinium electrophysiological testing stress testing genetic screening Diagnostic tests details

Treatment details
Ongoing
no cardiac comorbidity: asymptomatic o o with electrolyte abnormality correction of electrolyte abnormality without electrolyte abnormality re-assurance + self-monitoring no cardiac comorbidity: symptomatic o with electrolyte abnormality correction of electrolyte abnormality

 o o o post-MI o o o o o

without electrolyte abnormality beta-blocker or calcium-channel blocker catheter ablation antiarrhythmic

without heart failure early re-perfusion + optimisation of medical therapy lifestyle modification with heart failure early re-perfusion + anti-failure therapy lifestyle modification implantable cardioverter defibrillator (ICD) idiopathic dilated or hypertrophic cardiomyopathy

o o o

risk factors for sudden cardiac death implantable cardioverter defibrillator (ICD) EF 35% implantable cardioverter defibrillator (ICD) EF >35% without risk factors for sudden cardiac death observation and monitoring Treatment details

Summary
An ectopic ventricular rhythm on ECG consisting of 3 or more consecutive, wide (duration 120 milliseconds) QRS complexes with a rate greater than 120 bpm, spontaneously resolving in less than 30 seconds. Usually asymptomatic, although brief palpitations may sometimes be experienced. Symptoms in a patient with known non-sustained ventricular tachycardia (NSVT) are most often attributed to underlying cardiac disease rather than the arrhythmia itself. Defined as a self-terminating event. No specific treatment indicated. Management is directed at any underlying heart condition. Implantable cardioverter defibrillator placement may be used for selected patients who have additional risk factors such as structural heart disease. Prognosis dependent on presence or absence of cardiac disease. Left ventricular function in post-MI patients remains the most important prognostic tool for overall mortality and risk for sudden cardiac death. No increase in mortality demonstrated in those patients without associated cardiac disease.

Definition
Non-sustained ventricular tachycardia (NSVT) is an ectopic ventricular rhythm with wide QRS complex (120 milliseconds or greater), rate faster than 120 bpm, lasting for at least 3 beats that spontaneously resolves in less than 30 seconds. [1] It may occur in the absence of any underlying heart disease. However, it is more commonly associated with ischaemic and non-ischaemic heart disease; known genetic disorders such as long QT syndrome, Brugada's syndrome, and arrhythmogenic right ventricular cardiomyopathy; congenital heart disease; metabolic problems, including drug toxicity; or electrolyte imbalance. [2]

Epidemiology
The estimated incidence of NSVT in the general population (both with and without heart disease) is as high as 4%, although this is most likely an underestimate. The prevalence of NSVT becomes more common as age increases. [6] [7] There do not appear to be any sex-specific differences in the incidence of NSVT. However, men are probably more likely to be affected simply due to a higher incidence of CAD. The advent of thrombolytic therapy has decreased the overall prevalence of NSVT in patients after MI from a range of 12% to 25%, down to 5% to 9%. However, this prevalence varies with left ventricular dysfunction. NSVT has been observed in 12% of patients with ejection fraction (EF) less than 35%, compared with 6% in patients with EF greater than 35%. Using 24-hour ambulatory ECG monitoring, NSVT has been observed in 25% of patients with hypertrophic cardiomyopathy and up to 80% of patients with idiopathic dilated cardiomyopathy. [8] [9] [10]

Aetiology
NSVT is most commonly observed in patients with underlying ischaemic or non-ischaemic cardiac disease; although it may also be observed in apparently healthy people. [11] [12] While ischaemic cardiac disease is still the most common aetiology of NSVT, especially in westernised countries, infectious diseases such as Chagas' disease in Central America and other forms of non-ischaemic cardiomyopathy also contribute to the aetiology of NSVT around the world. [13] Structural heart diseases such as hypertrophic cardiomyopathy, idiopathic dilated cardiomyopathy, congenital heart disease, and valvular heart disease are also associated with NSVT. [14] [15] [16] [17] Abnormalities of multiple cellular proteins such as sodium and potassium channels (the long QT syndrome, Brugada's syndrome), intracellular calcium channels (catecholaminergic polymorphic VT), sarcomere proteins (hypertrophic cardiomyopathy), and cellular architecture proteins (idiopathic dilated cardiomyopathy) have all been associated with NSVT. [18] [19]

Electrolyte abnormalities (particularly hypokalaemia and hypomagnesaemia) often incite and/or contribute to NSVT. In addition, certain drugs have the ability to prolong the QT interval, which can promote NSVT (macrolide antibiotics, chlorpromazine, and haloperidol). While antiarrhythmic drugs, such as digoxin, flecainide, sotalol, and dofetilide, are used to treat atrial arrhythmias, they can produce unwanted ventricular arrhythmias, an effect referred to as pro-arrhythmia. Family history of sudden death before 50 years of age (especially in a firstdegree relative) is associated with an increased risk of both sustained and non-sustained VTs. Stress, either mental or physical, may trigger NSVT in patients with long QT syndrome, catecholamine-sensitive VT, and certain idiopathic VTs arising from the ventricular outflow tracts.

Pathophysiology
Similar to other tachyarrhythmias, NSVT can be due to increased automaticity, triggered activity or re-entry. Patients with compromised myocardium secondary to prior MI or non-ischaemic cardiomyopathy have been identified as having regions of slowed conduction adjacent to damaged myocardium or scar tissue. It is within these areas that re-entrant arrhythmias originate. [20] In apparently healthy people, repetitive monomorphic VT most commonly arises from the right ventricular outflow tract. [21] This is usually a result of delayed after-depolarisations (triggered activity) due to reactivation of sodium and calcium ion channels.

Classification
Variants Exercise-induced NSVT:
Observed in patients during stress testing. [3]

Repetitive monomorphic VT:

Ectopic arrhythmia characterised by short bursts of NSVT with an organised, regular, single-morphology QRS complex Arising most commonly from the right ventricular outflow tract, but may also originate from the left ventricular outflow tract and other ventricular sites. [4]

Non-sustained polymorphic VT:

Ectopic arrhythmia characterised by NSVT with multiple different wide (120 milliseconds or greater) QRS complex morphologies arising from the ventricle. [5]

Primary prevention
Primary prevention is best accomplished by addressing risk factors for conditions that predispose to NSVT such as CAD and depressed left ventricular systolic dysfunction. Hypertension and hyperlipidaemia should be managed aggressively and smoking cessation should be strongly pursued. Additional preventive measures include treatment of systolic dysfunction with medications such as ACE inhibitors/angiotensin receptor blockers, betablockers, and aldosterone antagonists. Patients with diagnosed hypertrophic cardiomyopathy, idiopathic dilated cardiomyopathy, arrhythmogenic right ventricular cardiomyopathy, Brugada's syndrome, and long QT syndrome should avoid strenuous physical exertion, as exercise can provoke NSVT (or other arrhythmias) in these populations. A prophylactic implantable cardioverter defibrillator (ICD) should be considered for patients at risk for sudden cardiac death due to sustained ventricular arrhythmias. Although the presence of NSVT may be a useful risk factor for estimating risk in certain conditions, generally the decision on whether an ICD is implanted is based on multiple considerations such as age, family history, the presence of symptoms such as syncope, and the extent of structural heart disease present.

Secondary prevention
Patient compliance with medications prescribed for treatment of the underlying cardiac disease is essential. Factors that may trigger episodes of arrhythmia should also be avoided (e.g., mental or physical stress, or electrolyte imbalance). It is useful to note that caffeine has not been demonstrated to alter the inducibility or severity of ventricular arrhythmias. [54]

History & examination

Key diagnostic factorshide all
hx of CAD (common)

Causes myocardial oxygen deprivation, which can lead to infarction and scarring. Both areas of acute and chronic ischaemia are sources of delayed and aberrant electrical conduction and promote re-entrant arrhythmias.

hx of hypertrophic cardiomyopathy (common)

Genetic disorder resulting in myocardial cell disorganisation and asymmetrical thickening of the ventricle. Both the phenotypic expression of hypertrophic cardiomyopathy and the risk of ventricular arrhythmia vary among patients.

hx of idiopathic dilated cardiomyopathy (common)

Compromised ventricular function from areas of fibrosis scar formation in the heart increases risk of arrhythmias.

presence of other risk factors (common)

Including left ventricular systolic dysfunction, long QT syndrome, Brugada's syndrome, drug toxicity, Chagas' disease, and other cardiomyopathies.

asymptomatic presentation (common) In the vast majority of cases, NSVT is asymptomatic, most likely due to its brief duration. tachycardia (common)

Not always present at time of clinical examination, as NSVT last <30 seconds. Other diagnostic factorshide all palpitations (uncommon)
Brief palpitations secondary to increased heart rate may be experienced. dizziness (uncommon) Suggests diminished cerebral blood flow. lightheadedness (uncommon) Suggests diminished cerebral blood flow. pre-syncope (uncommon) May be experienced by patients if perfusion to brain is compromised. syncope (uncommon)

Risk

May be experienced by patients if they become hypotensive due to NSVT. factorshide all

Strong CAD

Causes oxygen deprivation, and eventually leads to infarction and ventricular scarring. Delayed electrical conduction can occur as a result. Re-entrant arrhythmias originate within these areas. [20]

left ventricular systolic dysfunction

Strong association between ventricular arrhythmias and systolic dysfunction. Scars formed by ischaemic or non-ischaemic cardiomyopathy are areas of slowed electrical conduction and facilitate re-entrant VTs. [20]

hypertrophic cardiomyopathy

Genetic disorder resulting in myocardial cell disorganisation and asymmetrical thickening of the ventricle. Both the phenotypic expression of hypertrophic cardiomyopathy and the risk of ventricular arrhythmia vary among patients. [22]

idiopathic dilated cardiomyopathy

Prevalence of NSVT in idiopathic dilated cardiomyopathy is as high as 80%. [23] While there are many causes for this condition, up to 40% are familial, most attributed to mutations in cardiac sarcomeric or architectural proteins. [14] [24] [25]

long QT syndrome

Patients with this relatively rare genetic disorder have prolonged QT interval (>440 milliseconds) on ECG and are at increased risk of developing torsades de pointes (a polymorphic VT). Clinical manifestations depend on phenotypic manifestation of the particular underlying genetic defect. At least 12 sub-types of long QT (LQT) syndrome have been identified, most commonly types 1 to 3. Patients with LQT1 (potassium-channel defect) are at increased risk of developing ventricular arrhythmias during periods of physical exertion. LQT2 (potassium-channel defect) is characterised by initiation of ventricular arrhythmias following a startle reflex or a period of heightened emotional stress. Patients with LQT3 (sodium-channel defect) tend to develop arrhythmias during sleep. [18] [19] [23]

Brugada's syndrome

A disorder of myocardial sodium channels, which leads to characteristic J point elevation and downwards-sloping ST-segment elevation in the right pre-cordial leads, and increased risk of sudden death due to polymorphic VT and ventricular fibrillation.

electrolyte imbalance

Electrolyte abnormalities (particularly hypokalaemia, hyperkalaemia, and hypo-magnesaemia) often incite and/or contribute to NSVT.

drug toxicity

Certain drugs can prolong the QT interval, which can promote NSVT. These include macrolide antibiotics, chlorpromazine, and haloperidol. Antiarrhythmic drugs, such as digoxin, flecainide, sotalol, and dofetilide, used to treat atrial arrhythmias can produce unwanted ventricular arrhythmias (pro-arrhythmia).

Chagas' disease and other cardiomyopathies

Especially in developing countries, infectious diseases such as Chagas' disease in Central America and other forms of cardiomyopathy (e.g., arrhythmogenic right ventricular cardiomyopathy) also contribute to the aetiology of NSVT. [13]

Weak catecholaminergic polymorphic VT

Rare genetic condition that can cause syncope and result in sudden death. Mainly affects young children.

FHx of sudden death

Especially in a first-degree relative, FHx of sudden death before 50 years of age should prompt search for potential arrhythmogenic causes. Genetic screening is available for common mutations

associated with hypertrophic cardiomyopathy, long QT syndrome, Brugada's syndrome, and catecholaminergic polymorphic VT.
mental or physical stress

Stress, either mental or physical, may trigger arrhythmias in patients with long QT syndrome type 1, catecholamine-sensitive VT, and certain idiopathic VTs arising from the ventricular outflow tracts. Most likely due to effects of increased sympathetic activation on ventricular myocardium.

Diagnostic tests
1st tests to orderhide all
Test

ECG hypertrophy should be sought. Baseline ECG may demonstrate QT interval prolongation, evidence of Brugada's structural cardiac disease. [28]

Positive findings confirm the diagnosis of NSVT. View image Evidence of ischaemic heart disease and left ventri

syndrome, or arrhythmogenic right ventricular cardiomyopathy. T-wave inversion, although non-specific, may sug

electrolyte panel Electrolyte abnormalities may trigger NSVT in patients with or without cardiac disease.

troponin Clinical suspicion for ischaemia should prompt testing of myocardial bio-marker assays, as they provide useful confirmatory information. CK-MB Clinical suspicion for ischaemia should prompt testing of myocardial bio-marker assays, as they provide useful confirmatory information.

Tests to considerhide all

Test

24-hour ambulatory ECG monitoring Useful in selected patients to determine extent of arrhythmia burden. Also helps to establish whether correlation between NSVT and symptoms is required.

Can also be very useful for identifying presence of idiopathic sustained VTs, particularly those arising from the ou tracts. echocardiogram

Safe and inexpensive tool to evaluate for structural cardiac abnormalities such as valvular heart disease, which i presence of an underlying cardiomyopathy.

advanced stages can cause NSVT and is treatable. Echo is also useful to quantify systolic function and detect th

cardiac catheterisation prevalence of NSVT. [8]Also helpful in determining if patient has ischaemic or non-ischaemic cardiac disease. cardiac MRI with gadolinium Useful in investigating patients with suspected structural cardiac disease. Particularly helpful in establishing the presence of arrhythmogenic right ventricular cardiomyopathy, especially wall motion abnormalities in the right ventricle. electrophysiological testing with no identifiable structural abnormalities on previous testing. Useful in patients after MI including those with inducible VT and ejection fraction <40% and with EF <30% to 35% without inducible VT, especially if QRS is VTs, or where NSVT or frequent PVCs are thought to be a cause of cardiomyopathy. stress testing Often stress testing with imaging (nuclear or echo) is required for more definitive identification of underlying ischaemia. genetic screening Consultation with a cardiologist or medical geneticist may be helpful in determining which patients would benefit from genetic screening. [19]

May be appropriate early test for patients presenting with symptoms of MI, since early re-perfusion decreases ov

Testing may provide important clues for the cause of wide complex tachycardias due to NSVT, especially in patie

prolonged.[26] A useful diagnostic and therapeutic tool for selected patients with symptomatic NSVT, with idiopa

Useful in establishing the presence of CAD in patients who have risk factors for CAD, but may be asymptomatic.

Differential diagnosis
Condition SVT with aberrant conduction Differentiating signs/symptoms Differentiating tests

None

ECG, electrophysiological study: failure to meet criteria for NSVT; abse beats; absence of AV dissociation.

Electrical artifact

None

ECG: evidence of underlying sinus rhythm discernable through electric

artifact).

Last u

Step-by-step diagnostic approach

NSVT is defined as an ectopic ventricular rhythm on ECG consisting of 3 or more consecutive, wide (duration 120 milliseconds or greater) QRS complexes with a heart rate greater than 120 bpm, spontaneously resolving in less than 30 seconds. Once the presence of an NSVT is established, the main goals are to identify any existing cardiac pathology and to risk stratify patients with known cardiac disease for appropriate management and

therapy.
sustained wide QRS tachycardiaCreated by author

Evaluation of non-

NSVT is usually asymptomatic on presentation, and symptoms such as palpitations and syncope overlap greatly with other pathologies and tachyarrhythmias. Therefore, further investigation is required to identify the specific aetiology of NSVT. It is appropriate to begin with a complete history and physical examination followed by ECG. Laboratory studies and echocardiography may also be useful in the initial workup of the patient. More expensive and invasive testing such as MRI and cardiac catheterisation should be ordered in the appropriate clinical setting after initial evaluation has been completed.

History
NSVT has been identified in a wide spectrum of patients, from those with no identifiable cardiac condition to patients with ischaemic and non-ischaemic cardiac disease. Therefore, it is important to assess the patient's risk factors in light of NSVT that would prompt further testing and/or therapy. History that places patients at higher risk:
Non-ischaemic cardiomyopathy with left ventricular ejection fraction (LVEF) <35% and New York Heart Association class II or III symptoms Ischaemic cardiomyopathy with LVEF <35% Ischaemic cardiomyopathy with LVEF <40% with NSVT and inducible ventricular tachycardia (VT) during electrophysiological testing Hypertrophic cardiomyopathy (HCM) with personal history of cardiac arrest or sustained VT, first-degree relative with sudden death, unexplained exertional or recurrent syncope, left ventricular septum thickness greater than 30 mm, or frequent or prolonged NSVT Congenital arrhythmia syndromes such as long QT and Brugada's syndromes. [26]

In addition, the patient should be questioned regarding the use of any potentially arrhythmogenic medication (e.g., macrolide antibiotics, chlorpromazine, haloperidol, digoxin, flecainide, sotalol, and dofetilide). Family history of cardiac disease or sudden cardiac death may be of significance. The physician should also enquire about the presence of any current mental or physical stress that may have triggered the arrhythmia. Patients may complain of syncope as a result of hypotension due to the NSVT or an underlying cardiac condition. Dizziness, lightheadedness, and pre-syncope may occur if cerebral blood flow is compromised.

Physical examination
This should focus on possible signs for occult or worsening cardiac disease in patients with no known cardiac condition or patients with known cardiac disease, respectively. Palpation of peripheral pulses provides information on heart rate, identifying a current tachycardia and in combination with peripheral BP monitoring can suggest the status of the patient's cardiac output. The presence of rales on chest examination or the presence of peripheral oedema may be a sign of elevated left or right atrial pressures associated with cardiac dysfunction.

Similarly, palpation of the heart for left or right ventricular heaves and examination of the neck for elevated jugular venous pressure should be performed. Careful auscultation for pathological cardiac murmurs or abnormal heart sounds (S3 or S4) may assist in prompting further workup for ischaemic and non-ischaemic cardiac disease.

ECG
NSVT is diagnosed based on the following specific ECG findings: a ventricular rhythm with wide (120 milliseconds or greater) QRS complex; and a rate faster than 120 bpm lasting for at least 3 beats that spontaneously resolves in less than 30 seconds. View image A 24-hour ambulatory ECG may be necessary to detect the NSVT, determine the extent of the arrhythmia burden and/or analyse the QT interval (can be identified using a standard 12-lead ECG, although at times temporally dynamic changes in the QT interval require more prolonged monitoring periods such as a 24-hour ambulatory monitor). It is important to differentiate between a wide complex tachycardia originating from the ventricles and one that is supraventricular, as the medical management differs. Evidence supporting the diagnosis of a VT includes:
Baseline ECG tachycardia with morphology similar to that of PVCs Initiation of the tachycardia with a PVC making NSVT more likely.View image AV dissociation during tachycardia with dissociated P waves or capture and fusion beatsView image QRS duration greater than 140 milliseconds with right bundle branch block (RBBB) morphology, or QRS duration greater than 160 milliseconds with left bundle branch block (LBBB) morphology (however, does not apply to patients on antiarrhythmic drugs [27] ) A right superior axis or LBBB morphology with any right axis [20] QRS complexes broadly positive in the inferior leads (1, 3, and aVF), in which case NSVT associated with an idiopathic site from the ventricular outflow tracts should be suspected. If the site is within the right ventricular outflow tract, the QRS complex will have LBBB morphology (negative in V1), and if the site is within the left ventricular outflow tract, it will have RBBB morphology (positive QRS in V1). This is important to identify from a clinical standpoint, as these entities are not associated with sudden cardiac death and are often treated with ablation.

Baseline ECG should also be examined for evidence of known risk factors for NSVT including:

Long QT syndrome: QT interval prolongation

ECG from a patient with long QT syndromeKusumoto FM. ECG interpretation. In: Pathophysiology to clinical application. New York, NY: Springer; 2009. Used with permission

Brugada's syndrome: J point elevation and downwards-sloping ST-segment elevation in the right precordial leads

ECG from a patient with Brugada's syndrome, showing terminal positive R-wave and ST-segment elevation in lead V1Kusumoto FM. ECG interpretation. In: Pathophysiology to clinical application. New York, NY: Springer; 2009. Used with permission

Arrhythmogenic right ventricular cardiomyopathy: interventricular conduction delays (a discrete deflection after the QRS complex called an epsilon wave in lead V1 is specific for this disease)

ECG from a patient with arrhythmogenic right ventricular cardiomyopathyKusumoto FM. ECG interpretation. In: Pathophysiology to clinical application. New York, NY: Springer; 2009. Used with permission

Electrolyte disorders: prolonged QT interval

Presence of Q waves, ST-segment abnormalities, or other signs of CADView image LBBB: may be a sign of structural heart disease, including Chagas' disease or dilated cardiomyopathy T-wave inversion: although non-specific, may be an important marker of underlying structural cardiac disease.

Electrolytes and cardiac bio-markers

Electrolyte abnormalities, especially hypokalaemia, hyperkalaemia, and hypomagnesaemia, can often trigger and/or contribute to NSVT, and therefore any blood electrolyte abnormality must be identified. Clinical suspicion for ischaemia should prompt testing of myocardial bio-marker assays (CK-MB and troponin I), as they provide useful confirmatory information regarding MI.

Echocardiogram, stress test, cardiac catheterisation, or MRI

Investigation for underlying cardiac disease is facilitated by several diagnostic tests.
Stress testing and/or cardiac catheterisation is useful in establishing the presence of CAD in patients who have risk factors for CAD but may be asymptomatic. Often, stress testing with imaging (nuclear or echocardiography) is required for more definitive identification of underlying ischaemia. Cardiac MRI with gadolinium may be useful for identifying myocardial scarring associated with CAD, dilated idiopathic cardiomyopathy, and HCM. It also confirms the presence of fibrofatty infiltrates in the ventricle and measures right ventricular dysfunction in patients with suspected arrhythmogenic right ventricular cardiomyopathy.

Electrophysiological testing
Consultation with an electrophysiologist is essential to determining which patients would benefit from an invasive electrophysiological (EP) test, implantable cardioverter defibrillator placement, and medical treatment optimisation. [20] EP testing can be useful for evaluation (and treatment) in a wide range of patients after MI, including those with inducible VT and ejection fraction (EF) less than 40%, and those with EF less than 30% to 35% without inducible VT, especially if QRS is prolonged. [26] In patients with symptomatic NSVT (dizziness, syncope) that arises from the outflow tract, EP testing and ablation is an important diagnostic and therapeutic tool.

Genetic screening

Genetic screening is available for common mutations associated with long QT syndrome, Brugada's syndrome, and catecholaminergic polymorphic VT, as well as HCM. Consultation with a cardiologist or a medical geneticist may be helpful in determining which patients would benefit the most from genetic screening. [19]
Click to view diagnostic guideline references.

Case history #1

A 65-year-old obese man presents with a crushing substernal chest pain for the past 3 hours and is hospitalised for an acute anterior wall MI. His medical history includes hypertension and hyperlipidaemia. He is also a smoker. Primary angioplasty reveals an occluded right coronary artery, which is successfully stented. He is found to have a left ventricular function of 45% with reduced contractility (hypokinesis) of the inferior wall. On the third day of hospitalisation, telemetry reveals a 5-beat run of wide QRS complexes with a rate of 136 bpm. The patient is asymptomatic during this event.

Case history #2
A previously well 45-year-old man presents to the clinic with a 3-week history of progressive shortness of breath. He is able to perform activities of daily living independently but becomes short of breath with mild-to-moderate exertion. Echocardiogram reveals a reduced left ventricular ejection fraction of 30%. Cardiac catheterisation demonstrates normal coronary arteries. A 24hour ambulatory ECG shows several episodes of NSVT.

Other presentations
NSVT is usually asymptomatic, although brief palpitations may sometimes be experienced. Symptoms in a patient with known NSVT are most often attributed to underlying cardiac disease rather than the arrhythmia itself. NSVT may present on a routine ECG or during a stress test being performed for other reasons.

Treatment Options
Treatment Patient group no cardiac comorbidity: asymptomatic with electrolyte abnormality 1st line Treatmenthide all

correction of electrolyte abnormality

Treatment Patient group no cardiac comorbidity: asymptomatic line Treatmenthide all

Electrolyte abnormalities, most commonly hypokalaemia, hyperkalaemia, and hypomagnesaemia, may trigger NSVT in patients with or without cardiac disease. These disturbances should be corrected as efficiently as possible.

without electrolyte abnormality

1st

re-assurance + self-monitoring

NSVT is by definition a self-terminating event, and therefore usually no specific treatment is indicated. Rather, treatment is directed at any existing heart condition.

no cardiac comorbidity: symptomatic with electrolyte abnormality 1st

correction of electrolyte abnormality

Electrolyte abnormalities, most commonly hypokalaemia, hyperkalaemia, and hypomagnesaemia, may trigger NSVT in patients with or without cardiac disease. These disturbances should be corrected as efficiently as possible.

without electrolyte abnormality

1st

beta-blocker or calcium-channel blocker

On the rare occasion that NSVT produces symptoms in the absence of cardiac disease, medication may be indicated.

Beta-blockers (e.g., metoprolol, atenolol) or calciumchannel blockers (generally used when beta-blockers are contraindicated, e.g., asthma) are usually sufficient to control symptoms. Primary Options metoprolol : 50-200 mg/day orally (immediaterelease) given in 2 divided doses OR atenolol : 25-100 mg orally once daily

Treatment Patient group no cardiac comorbidity: asymptomatic line Treatmenthide all

Secondary Options verapamil : 180-240 mg/day orally (immediaterelease) given in 3-4 divided doses; 180-240 mg orally (extended-release) once daily OR diltiazem : 90-360 mg/day orally (immediate-release) given in 3-4 divided doses; 90-360 mg orally (extended-release) once daily
2nd

catheter ablation

Catheter ablation may be considered early in the treatment course if the arrhythmia proves resistant to beta-blockers or calcium-channel blockers.

3rd

antiarrhythmic

Antiarrhythmic agents such as flecainide or propafenone may be used in patients who fail therapy with beta-blockers and/or calcium-channel blockers who are not candidates for catheter ablation or in whom catheter ablation is ineffective. Primary Options flecainide : 100-200 mg orally (immediate-release) twice daily OR propafenone : 150-300 mg orally (immediate-release) three times daily

post-MI without heart failure 1st

early re-perfusion + optimisation of medical therapy

Early re-perfusion decreases overall prevalence of NSVT following acute MI.[8]

Treatment Patient group no cardiac comorbidity: asymptomatic line Treatmenthide all

Optimisation of medical therapy including betablockers, ACE inhibitors, antiplatelet therapy, and statins, reduces the risk of sudden cardiac death following acute MI. [29] [30] [31] [32] [33] [34] [35] [36]

In addition, omega-3 fatty acids may be considered as adjunctive therapy. [37][38] Electrolyte abnormalities, most commonly hypokalaemia, hyperkalaemia, and hypomagnesaemia, may trigger NSVT in patients with or without cardiac disease. These disturbances should be corrected as efficiently as possible. Primary Options aspirin : 75-300 mg orally once daily -- AND -clopidogrel : 75 mg orally once daily -- AND -perindopril : 4-16 mg orally once daily or lisinopril : 5 mg orally once daily for 48 hours initially, followed by 5-10 mg once daily or enalapril : 2.5 mg orally once daily for 48 hours initially, increase gradually to 10 mg twice daily or ramipril : 2.5 mg orally twice daily initially, increase gradually to 5 mg twice daily -- AND -metoprolol : 100 mg orally (immediate-release) twice daily or atenolol : 100 mg orally once daily -- AND --

Treatment Patient group no cardiac comorbidity: asymptomatic line Treatmenthide all

simvastatin : 5-40 mg orally once daily; increased risk of myopathy with 80 mg/day dose or atorvastatin : 10-80 mg orally once daily plus [?] lifestyle modification

Modifiable risk factors such as obesity and smoking should be addressed with a carefully planned exercise, diet, and weight loss programme to further reduce the incidence of sudden cardiac death. [40] [41] [B Evidence]

with heart failure

1st

early re-perfusion + anti-failure therapy

Early re-perfusion decreases overall prevalence of NSVT following acute MI.[8] Medications such as beta-blockers, ACE inhibitors, aldosterone receptor antagonists, aspirin, and statins reduce overall mortality and incidence of sudden cardiac death in patients with heart failure. [44] [45] [34] [46]Angiotensin-II receptor antagonists can be used as an alternative in patients intolerant of ACE inhibitors.

Diuretics have no effect on mortality and are usually indicated to help relieve symptoms of fluid over-load. Electrolyte abnormalities, most commonly hypokalaemia, hyperkalaemia, and hypomagnesaemia, may trigger NSVT in patients with or without cardiac disease. These disturbances should be corrected as efficiently as possible. Primary Options aspirin : 75-300 mg orally once daily -- AND -perindopril : 2-16 mg orally once daily

Treatment Patient group no cardiac comorbidity: asymptomatic line Treatmenthide all

or lisinopril : 2.5 to 40 mg orally once daily or enalapril : 2.5 to 20 mg orally twice daily or ramipril : 1.25 to 10 mg orally once daily or candesartan : 4-32 mg orally once daily or losartan : 25-100 mg orally once daily or valsartan : 40-160 mg orally twice daily -- AND -carvedilol : 3.125 to 25 mg orally (immediate-release) twice daily or metoprolol : 12.5 to 200 mg orally (extended-release) once daily or bisoprolol : 1.25 to 10 mg orally once daily -- AND -simvastatin : 5-40 mg orally once daily; increased risk of myopathy with 80 mg/day dose or atorvastatin : 10-80 mg orally once daily -- AND -spironolactone : 25-100 mg orally once daily or eplerenone : 25-50 mg orally once daily plus [?] lifestyle modification

Modifiable risk factors such as obesity and smoking

Treatment Patient group no cardiac comorbidity: asymptomatic line Treatmenthide all

should be addressed with a carefully planned exercise, diet, and weight loss programme to further reduce the incidence of sudden cardiac death. [40] [41] [B Evidence] adjunct [?] implantable cardioverter defibrillator (ICD)

ICD placement is recommended for patients after MI with NSVT, ejection fraction (EF) 40% or less and inducible ventricular arrhythmias at electrophysiological testing. [42] ICD is also recommended for patients with class II/III heart failure and EF 40% or less. [47]

ICD placement in patients with heart failure may have greater benefit in those who are likely to survive >2 years based on absence of comorbidities. Comorbid conditions that may attenuate the survival benefit of ICDs include chronic kidney disease, diabetes, peripheral vascular disease, and elevated urea (9.6 to 17.9 mmol/L (27 to 50 mg/dL)).

It is important to note that the decision to implant an ICD is based on cardiac function and symptoms rather than the presence or absence of NSVT. [42]

idiopathic dilated or hypertrophic cardiomyopathy risk factors for sudden cardiac death 1st

implantable cardioverter defibrillator (ICD)

ICD placement should be considered for patients with hypertrophic cardiomyopathy and one of the major risk factors for sudden cardiac death, including sudden cardiac arrest, spontaneous sustained VT, unexplained syncope, FHx of sudden cardiac death in a first-degree relative, ventricular septal wall thickness >30 mm, NSVT on 24-hour ambulatory ECG monitoring, and hypotension in response to

Treatment Patient group no cardiac comorbidity: asymptomatic line Treatmenthide all

exercise. Other risk factors include atrial fibrillation, myocardial ischaemia, left ventricular outflow obstruction, a high-risk mutation, and patients who compete in high-intensity physical exercises.[20]
EF 35% 1st

implantable cardioverter defibrillator (ICD)

ICD placement is recommended for patients with underlying idiopathic cardiomyopathy plus ejection fraction 35% and class II/III heart failure. For patients with EF 35% or less and class I heart failure, ICD placement should be considered. [20]

EF >35% without risk factors for sudden cardiac death

1st

observation and monitoring

Close observation, but no activity restriction is recommended for patients with hypertrophic cardiomyopathy with identified genetic mutations but no overt signs of disease or one of the major risk factors for sudden cardiac death.[48]

Implantable cardioverter defibrillator (ICD) is not indicated for patients with NSVT and idiopathic cardiomyopathy with good left ventricular function.

Ongoing

Treatment approach
NSVT is by definition a self-terminating event, and therefore usually no specific treatment is indicated. Rather, treatment is directed at any existing heart condition. Patients with underlying cardiac disease may need more aggressive therapy due to increased mortality risk. In contrast, no increase in mortality has been demonstrated in those patients without an associated cardiac condition and therefore re-assurance is usually sufficient.

Evaluation of non-sustained wide QRS tachycardiaCreated by author

Modifiable risk factors for CAD should be addressed to prevent MI and left ventricular dysfunction. Necessary medical therapy depending on the underlying condition should be undertaken first before more aggressive treatment such as an implantable device is considered. It should also be noted that, although there are international differences regarding the use of therapies such as implantable cardioverter defibrillators (ICDs), the guideline for the prevention of sudden cardiac death due to ventricular arrhythmias was developed jointly by European and US professional cardiology groups. [20]

Symptomatic NSVT
On the rare occasion that NSVT produces symptoms in the absence of cardiac disease, medication or catheter ablation may be required. Medical treatment options include beta-blockers or calcium-channel blockers (usually used when beta-blockers are contraindicated, e.g., asthma) as first-line therapy. Catheter ablation may be considered early in the treatment course if the arrhythmia proves resistant to these drugs. Antiarrhythmics such as flecainide or propafenone may be used in patients who fail therapy with beta-blockers and/or calcium-channel blockers who are not candidates for catheter ablation or in whom catheter ablation is ineffective.

Electrolyte disturbances
Electrolyte abnormalities, most commonly hypokalaemia, hyperkalaemia, and hypo-magnesaemia, may trigger NSVT in patients with or without cardiac disease. These disturbances should be corrected as efficiently as possible.

Post-MI

Early re-perfusion decreases overall prevalence of NSVT following acute MI. [8] Optimisation of medical therapy including beta-blockers, ACE inhibitors, antiplatelet therapy, and statins, reduces the risk of sudden cardiac death following acute MI. [29] [30] [31] [32] [33] [34] [35][36] In addition, omega-3 fatty acids may be considered as adjunctive therapy. [37] [38] In patients who have symptomatic NSVT following MI, amiodarone may be beneficial in reducing risk of sudden cardiac death. [39] [A Evidence] However, several randomised trials have found that amiodarone is not associated with improved clinical outcomes. In addition, the many adverse effects associated with amiodarone limit its use in many clinical situations; therefore it is generally not used. Modifiable risk factors such as obesity and smoking should also be addressed with a carefully planned exercise, diet, and weight loss programme to further reduce the incidence of sudden cardiac death. [40] [41] [B Evidence] ICD is recommended for patients after MI with NSVT, ejection fraction (EF) 40% or less and inducible ventricular arrhythmias at electrophysiological testing. [42] Routine early use of ICD is not recommended. [43]

Heart failure after MI

Medications such as beta-blockers, ACE inhibitors, and aldosterone receptor antagonists reduce overall mortality and incidence of sudden cardiac death in patients with heart failure.[44] [45] [34] [46] Diuretics have no effect on mortality and are usually indicated to help relieve symptoms of fluid over-load. ICD is recommended for patients with class II/III heart failure and EF 40% or less. [47] ICD placement in patients with heart failure may have greater benefit in those who are likely to survive more than 2 years based on absence of comorbidities. Comorbid conditions that may attenuate the survival benefit of ICDs include chronic kidney disease, diabetes, peripheral vascular disease, and elevated urea (9.6 to 17.9 mmol/L (27 to 50 mg/dL)). It is important to note that the decision to implant an ICD is based on cardiac function and symptoms rather than the presence or absence of NSVT. [42]

Idiopathic or hypertrophic cardiomyopathy

ICD placement is recommended for patients with underlying idiopathic cardiomyopathy plus EF 35% or less and class II/III heart failure. For patients with EF 35% or less and class I heart failure, ICD placement should be considered. [20] ICD is not indicated for patients with NSVT and idiopathic cardiomyopathy with good left ventricular function. ICD placement should also be considered for patients with hypertrophic cardiomyopathy who have one of the major risk factors for sudden cardiac death, including sudden cardiac arrest, spontaneous sustained ventricular tachycardia (VT), unexplained syncope, family history of sudden cardiac death in a first-degree relative, ventricular septal wall thickness greater than 30 mm, NSVT on 24-hour ambulatory ECG monitoring, and hypotension in response to exercise. Other risk factors include atrial fibrillation, myocardial ischaemia, left ventricular outflow tract obstruction, a high-risk mutation, and patients who compete in high-intensity physical exercises. [20] If patients have an identified genetic mutation but there are no overt signs of the disease and no risk factors for sudden cardiac death, close observation is sufficient; activity restrictions are not required. [48]

Monitoring

Patients should routinely visit their physician. If appropriate, medical and/or ICD therapy should be initiated and maintained as clinically indicated based on the underlying cardiac disease. Certain drugs may require specific followup to monitor for effectiveness and/or toxicity (e.g., beta-blockers, calciumchannel blockers, flecainide, and propafenone). A cardiologist should also evaluate the patient for potential treatment options and risk stratification as the natural course of the underlying cardiac disease progresses. Although patients implanted with ICDs can be routinely checked by remote telemetry every 3 months, if the device delivers a shock or the patient experiences tachycardia, immediate follow-up should be arranged.

Patient Instructions
The importance of medication compliance should be stressed. Patients should be advised to contact their physician if they begin to experience palpitations, pre-syncope, syncope, or chest pains. These symptoms may indicate worsening of the underlying cardiac disease or increased frequency of arrhythmia. Side effects of medications used to treat an associated cardiac condition should be reviewed with the patient. Patients should be instructed to alert their physician concerning ICD shocks or evidence of device infection (erythema, tenderness, or drainage from the device site). In addition, patients should be advised to avoid factors that may trigger episodes of arrhythmia such as mental or physical stress and dehydration (may cause electrolyte abnormalities). It is useful to mention that caffeine has not been demonstrated to alter the inducibility or severity of ventricular arrhythmias. [54]

Complications
Complicationhide all

sudden cardiac death see our comprehensive coverage of Cardiac arrest Patients with increased risk include those with left ventricular dysfunction, history of MI, spontaneous sustained ventricular tachycardia (VT), unexplained syncope, FHx of sudden cardiac death, left ventricular thickness >30 mm or abnormal exercise BP. Appropriate treatment of underlying cardiac disease including medical management, early re-perfusion after MI, and implantable cardioverter defibrillator (ICD) may be helpful in decreasing incidence.

cardiomyopathy see our comprehensive coverage of Assessment of cardiomyopathy Tachycardia-induced cardiomyopathy can occur in the setting of frequent or incessant NSVT episodes. This complication may be reversed through medical management with medications and/or catheter ablation. [50] [51] [52] [53] ICD-related infection Most often arises from a bacterial infection along the intravascular portion of the leads or in the generator pocket. Removal of the ICD system and a course of antibiotics are usually required for treatment. ventricular fibrillation see our comprehensive coverage of Cardiac arrest Re-entrant rhythms near scar tissue may result in sustained VT, which can subsequently progress to ventricular fibrillation, which has a high mortality rate.

Prognosis
The significance and prognosis of NSVT in patients is highly dependent on presence and severity of underlying cardiac disease. In patients without evidence of ischaemia or structural heart disease, NSVT has not been found to adversely influence prognosis. [11] [12]Meanwhile, patients with ischaemic or non-ischaemic cardiac disease may require lifelong medical therapy with medications, catheter ablation, and/or implantable cardioverter defibrillator (ICD) placement.

Exercise-induced NSVT
In asymptomatic, apparently healthy people, NSVT observed during exercise was previously thought to be a normal response to exertion, but some studies suggest that it may predict CAD.[3]

NSVT in apparently healthy people

Most commonly, the tachycardia originates from the right ventricular outflow tract and may cause symptoms including palpitations and pre-syncope, but the risk of death is very low. [21][49] Tachycardia-induced cardiomyopathy can occur in the setting of frequent or incessant NSVT episodes. Genetic arrhythmias and occult cardiomyopathy may appear later in life, and longterm follow-up may be indicated.

Ischaemic and non-ischaemic NSVT

In the setting of known cardiac disease, prognosis is based on risk stratification with extent of left ventricular dysfunction playing a pivotal role. Early re-perfusion in the setting of MI decreases the overall prevalence of NSVT, and in high-risk patients who meet accepted criteria, ICD implantation allows for continuous monitoring and long-term therapy, with evidence suggesting decreased risk of mortality. [8] [9] [10]