Etiology

NSVT is most commonly observed in patients with underlying ischemic or nonischemic cardiac disease; although it may also be observed in apparently healthy people.[14][15][16][17]​ Incidental NSVT is a common finding in routine cardiologic investigation (e.g., when investigating noncardiac disease, before participating in sports, before cancer treatments), as well as during routine monitoring (e.g., during anesthesia or sedation).[2]​​

While ischemic cardiac disease is still the most common etiology of NSVT, especially in high-income countries, infectious diseases such as Chagas disease in Central America and other forms of nonischemic cardiomyopathy also contribute to the etiology 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 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 hypokalemia and hypomagnesemia) 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 proarrhythmia.

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 nonsustained 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 apnea, central sleep apnea, Cheyne-Stokes breathing) is associated with various cardiac arrhythmias.[24]​ Epidemiologic 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 nonischemic 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 afterdepolarizations (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 characterized by short bursts of NSVT with an organized, 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]

Nonsustained polymorphic VT:

  • Ectopic arrhythmia characterized by NSVT with multiple different wide (≥120 milliseconds) QRS complex morphologies arising from the ventricle.[6]

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