History and exam
Key diagnostic factors
common
history of coronary artery disease
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.
history of 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.
history of idiopathic dilated cardiomyopathy
Compromised ventricular function from areas of fibrosis scar formation in the heart increases risk of arrhythmias.
presence of other risk factors
Including left ventricular systolic dysfunction, long QT syndrome, Brugada's syndrome, drug toxicity, Chagas' disease, and other cardiomyopathies.
asymptomatic presentation
In the vast majority of cases, NSVT is asymptomatic, most likely due to its brief duration.
tachycardia
Not always present at time of clinical examination, as NSVT last <30 seconds.
Other diagnostic factors
uncommon
palpitations
Brief palpitations secondary to increased heart rate may be experienced.
dizziness
Suggests diminished cerebral blood flow.
lightheadedness
Suggests diminished cerebral blood flow.
pre-syncope
May be experienced by patients if perfusion to brain is compromised.
syncope
May be experienced by patients if they become hypotensive due to NSVT. Recent syncope due to a suspected cardiac cause is a high-risk symptom that may require inpatient investigation.[2]
Risk factors
strong
coronary artery disease
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.[1]
left ventricular systolic dysfunction
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.[26]
idiopathic dilated cardiomyopathy
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.[22][23][27]
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.[18]
sleep-disordered breathing
Sleep-disordered breathing (SDB), including obstructive sleep apnoea (OSA), central sleep apnoea (CSA), and Cheyne-Stokes breathing, is associated with a two-fold higher odds of NSVT.[24] In patients with heart failure, OSA and CSA predict sleep-specific lethal ventricular tachyarrhythmias (VTA).[24] Screening and diagnostic testing for SDB and nocturnal hypoxia should be considered for patients with VTA.[24] Small trials suggest that treating OSA is associated with reduced VTA, particularly in heart failure patients; however, larger trials are required to assess whether treating OSA is beneficial.[24]
weak
catecholaminergic polymorphic VT
Rare genetic condition that can cause syncope and result in sudden death. Mainly affects young children.
family history of sudden death
Especially in a first-degree relative, family history 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.
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