What are the causes of ventricular tachycardia (VT)?

Causes of Ventricular Tachycardia

Ventricular tachycardia results from three primary mechanisms—reentry (most common in structural heart disease), triggered activity (common in outflow tract VT), and abnormal automaticity—with the underlying substrate ranging from myocardial scar and cardiomyopathy to channelopathies and idiopathic causes in structurally normal hearts. 1, 2

Primary Mechanisms

Reentry (Most Common)

• Reentry is the underlying mechanism for most sustained VT in patients with structural heart disease, requiring an anatomical or functional substrate that creates areas of slow conduction and unidirectional block 1, 2
• Myocardial scar from prior infarction represents the most common substrate, creating heterogeneous tissue with preserved myocardium within fibrotic areas that form reentrant circuits 1, 2, 3
• Reentry circuits typically revolve around fixed anatomical obstacles such as post-MI scar or surgical incisions (ventriculotomy, VSD patches) 1

Triggered Activity

• Triggered activity from delayed afterdepolarizations is the predominant mechanism in right ventricular outflow tract (RVOT) VT, dependent on intracellular calcium overload and cyclic AMP elevation 1, 2
• This mechanism is adenosine-sensitive, facilitated by catecholamines, and may terminate with vagal maneuvers 1
• Early afterdepolarizations during phase 2 or 3 of the action potential cause VT in long QT syndromes, resulting from decreased repolarization reserve 4

Abnormal Automaticity

• Abnormal automaticity arises from partially depolarized membrane potentials, typically occurring during acute MI or transient ischemia when increased extracellular potassium causes partial depolarization 1
• Enhanced normal automaticity can occur in Purkinje fibers or ventricular myocardium with altered pacemaker cell function 1

Structural Heart Disease Substrates

Coronary Artery Disease

• Post-myocardial infarction scar is the single most common cause of sustained monomorphic VT, with infarct surface area and mass on delayed enhancement MRI identifying substrate better than LVEF alone 2, 3
• Acute coronary ischemia is the most common cause of ventricular fibrillation 1, 3
• Scar size greater than 5% of LV mass shows sharp increase in event rates 2

Cardiomyopathies

• Dilated cardiomyopathy creates substrate through myocardial fibrosis, myocyte disarray, and altered cellular electrophysiology 2
• Hypertrophic cardiomyopathy causes VT through electrically unstable myocardial substrate, with complex ventricular tachyarrhythmias being the most common mechanism of sudden cardiac death 1
• In HCM, 90% of adults demonstrate ventricular arrhythmias on 24-hour Holter monitoring, with nonsustained VT occurring in 20-30% 1
• Arrhythmogenic right ventricular cardiomyopathy/dysplasia creates patchy fibrosis substrate 1

Valvular and Congenital Heart Disease

• Congenital aortic stenosis, tetralogy of Fallot (especially with RVOT patch), D-TGA, L-TGA, severe Ebstein anomaly, and single ventricle physiology all create VT substrates 1
• In repaired tetralogy of Fallot, macroreentrant VT circuits revolve around ventriculotomy or VSD patch scars, with sudden cardiac death incidence of 2% per decade 1

Idiopathic VT (Structurally Normal Hearts)

Outflow Tract VT

• RVOT VT is the most common form of VT in apparently healthy people, typically presenting with left bundle-branch, inferior-axis morphology 1
• Left ventricular outflow tract VT accounts for a small percentage, arising from endocardial, coronary cusp, or epicardial origins 1
• These VTs are associated with good prognosis, with symptoms typically mild and syncope rare 1

Genetic/Channelopathies

• Long QT syndrome causes VT through early afterdepolarization-mediated triggered activity from decreased repolarization reserve 4
• Catecholaminergic polymorphic VT results from sarcoplasmic reticulum calcium overload and diastolic calcium leak 4
• Brugada syndrome and other inherited channelopathies create substrate for polymorphic VT/VF 1

Precipitating Factors

Environmental/Physiologic

• Intense physical exertion can trigger VT, particularly in HCM where it is the most common cause of cardiovascular sudden death in young competitive athletes 1
• Myocardial ischemia creates a vicious cycle with diastolic dysfunction, outflow obstruction, and systemic hypotension 1

Metabolic/Electrolyte

• Hypokalemia and hypomagnesemia lower the threshold for triggered activity and reentry 5
• Acute ischemia causes increased extracellular potassium leading to partial membrane depolarization 1

Arrhythmogenic Triggers

• Supraventricular tachyarrhythmias can trigger ventricular tachyarrhythmias through decreased stroke volume and coronary perfusion 1
• Premature ventricular contractions serve as triggers to initiate reentrant circuits 1

Critical Clinical Distinctions

Polymorphic VT indicates acute, often reversible conditions (ischemia, QT prolongation, electrolyte abnormalities) and cannot be treated by catheter ablation 6, 7

Monomorphic VT indicates repetitive activation in the same sequence, either from focal abnormal activity or macro-reentry substrate, and is potentially amenable to catheter ablation 6, 7

The substrate is dynamically influenced by cardiac metabolism, electrolytes, signaling pathways, and autonomic effects, making VT a complex interplay between fixed anatomical substrate and modifiable triggers 1