Causes of Ventricular Tachycardia
Ventricular tachycardia (VT) is primarily caused by structural heart disease, with coronary artery disease and myocardial infarction being the most common underlying etiologies, followed by cardiomyopathies, electrolyte abnormalities, and genetic disorders. 1
Structural Heart Disease Causes
Ischemic Heart Disease
- Coronary artery disease (CAD) - Most common cause of VT in adults
- Prior myocardial infarction (MI) - Scar tissue creates substrate for reentry circuits
- Acute myocardial ischemia - Can trigger VT through abnormal automaticity and injury currents 1
Cardiomyopathies
- Dilated cardiomyopathy - Myocardial fibrosis creates arrhythmogenic substrate
- Hypertrophic cardiomyopathy - Associated with myocardial disarray and fibrosis 1
- Arrhythmogenic right ventricular cardiomyopathy (ARVC) - Fibro-fatty replacement of myocardium
- Infiltrative cardiomyopathies - Sarcoidosis, amyloidosis, hemochromatosis
Non-Structural Causes
Electrolyte Abnormalities
- Hypocalcemia - Prolongs QT interval, destabilizes cardiac cell membranes 2
- Hypokalemia - Increases risk of VT recurrence even after correction 3
- Hypomagnesemia - Often coexists with other electrolyte disorders
- Hyperkalemia - Particularly in advanced kidney disease
Medication-Related
- Antiarrhythmic drugs - Particularly Class IA and IC agents (proarrhythmic effect)
- QT-prolonging medications - Can induce torsades de pointes (polymorphic VT)
- Stimulants - Cocaine, amphetamines, and other sympathomimetics 1
Genetic/Inherited Disorders
- Long QT syndrome - Congenital or acquired
- Brugada syndrome - Characteristic ECG pattern with ST elevation in V1-V3 1
- Catecholaminergic polymorphic VT - Exercise-induced arrhythmia
- Short QT syndrome - Rare but highly arrhythmogenic
Other Causes
- Congenital heart disease - Post-surgical repair creates substrate for reentry
- Myocarditis - Inflammation creates transient arrhythmogenic substrate
- Idiopathic VT - Often originates from right ventricular outflow tract or left ventricular fascicles
- Mechanical triggers - Catheter manipulation, trauma
- Autonomic influences - Increased sympathetic tone
Pathophysiologic Mechanisms
VT occurs through several mechanisms 1:
Reentry - Most common mechanism in structural heart disease
- Requires anatomical obstacle (scar) or functional block
- Creates circuit for self-perpetuating electrical activity
Enhanced automaticity - Abnormal spontaneous depolarization
- Common in acute ischemia and electrolyte disorders
Triggered activity
- Early afterdepolarizations - Associated with QT prolongation
- Late afterdepolarizations - Associated with calcium overload states
High-Risk Features
Certain findings indicate higher risk for life-threatening VT 1:
- Prior cardiac arrest or sustained VT
- Family history of sudden cardiac death
- Unexplained syncope
- Severe left ventricular hypertrophy (≥30mm)
- Abnormal blood pressure response to exercise
- Nonsustained VT on monitoring
Clinical Pearls
- VT should be considered in any wide-complex tachycardia until proven otherwise
- Transient causes (electrolyte abnormalities, drug effects) should be corrected but don't eliminate risk of recurrence in patients with structural heart disease 1, 3
- Polymorphic VT may have different causes than monomorphic VT, with medication effects and electrolyte disorders being more common 4
- In young patients without obvious heart disease, consider genetic channelopathies and congenital anomalies 1
Remember that identifying and treating the underlying cause is essential for effective management of VT and prevention of sudden cardiac death.