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.[14][15][16][17] Incidental NSVT is a common finding in routine cardiological investigation (e.g., when investigating non-cardiac disease, before participating in sports, before cancer treatments), as well as during routine monitoring (e.g., during anaesthesia or sedation).[2]
While ischaemic cardiac disease is still the most common aetiology of NSVT, especially in high-income 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.[18]
Structural heart diseases such as hypertrophic cardiomyopathy, idiopathic dilated cardiomyopathy, congenital heart disease, and valvular heart disease are also associated with NSVT.[19][20][21]
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.[22][23]
Electrolyte abnormalities (particularly hypokalaemia and hypo-magnesaemia) 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 first-degree 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.
Sleep disordered breathing (SDB) (e.g., obstructive sleep apnoea, central sleep apnoea, Cheyne-Stokes breathing) is associated with various cardiac arrhythmias.[24] Epidemiological studies show that patients with SDB have a two-fold higher odds of NSVT.[24]
Pathophysiology
Similar to other tachyarrhythmias, NSVT can be due to increased automaticity, triggered activity or re-entry. Patients with compromised myocardium secondary to prior myocardial infarction 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.[1][13] In apparently healthy people, repetitive monomorphic VT most commonly arises from the right ventricular outflow tract.[25] 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.[4]
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.[5]
Non-sustained polymorphic VT:
Ectopic arrhythmia characterised by NSVT with multiple different wide (120 milliseconds or greater) QRS complex morphologies arising from the ventricle.[6]
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