What are the causes of ventricular tachycardia?

Causes of Ventricular Tachycardia

Ventricular tachycardia results from either structural heart disease (most common) or primary electrical disorders, with ischemic heart disease and prior myocardial infarction representing the leading causes in adults. 1, 2

Structural Heart Disease Causes

Ischemic heart disease is the most common substrate for VT, with acute coronary ischemia causing ventricular fibrillation and myocardial scar from prior infarction causing sustained monomorphic VT. 1, 2, 3

Cardiomyopathies

• Nonischemic cardiomyopathy (NICM), including dilated cardiomyopathy, represents a major structural cause. 1
• Hypertrophic cardiomyopathy predisposes to ventricular arrhythmias through myocardial disarray and fibrosis. 1, 3
• Arrhythmogenic right ventricular cardiomyopathy (ARVC) causes VT through progressive fibro-fatty replacement of ventricular myocardium. 1, 3

Other Structural Causes

• Valvular heart disease, particularly mitral valve prolapse, can trigger VT. 1
• Congenital heart disease, especially post-surgical states like repaired tetralogy of Fallot, creates anatomical substrates for VT through slowly conducting anatomical isthmuses. 1, 3, 4
• Heart failure with reduced ejection fraction (LVEF ≤35%) significantly increases VT risk regardless of etiology. 1

Primary Electrical Disorders (Channelopathies)

Inherited ion channelopathies cause VT in structurally normal hearts and require different risk stratification than structural disease. 1, 5

Specific Channelopathies

• Long QT syndrome (LQTS) causes torsades de pointes, particularly with QTc >500 ms, which carries 2-3 times higher risk. 1, 6, 5
• Brugada syndrome presents with polymorphic VT and sudden death, diagnosed by ECG patterns rather than electrophysiological study. 1, 5
• Catecholaminergic polymorphic VT (CPVT) manifests as bidirectional VT, polymorphic VT, or ventricular fibrillation triggered by exercise or emotional stress. 1, 5
• Short QT syndrome and early repolarization syndromes represent additional channelopathy causes. 1

Idiopathic VT (Structurally Normal Hearts)

Up to 10% of VT occurs without identifiable structural disease, carrying better prognosis than structural VT. 7, 5

• Right ventricular outflow tract (RVOT) VT is the most common idiopathic form, presenting as monomorphic VT. 5
• Idiopathic left ventricular tachycardia (ILVT) originates from the left ventricle with characteristic morphology. 5
• Idiopathic propranolol-sensitive VT (IPVT) may be monomorphic or polymorphic and responds to beta-blockade. 5

Metabolic and Electrolyte Disturbances

Electrolyte abnormalities are critical reversible causes that must be routinely considered, particularly in patients on diuretics. 1, 8

Specific Electrolyte Abnormalities

• Hypopotassemia induced by thiazide and loop diuretics contributes to sudden cardiac death in hypertension and heart failure patients, and is an independent risk factor during acute myocardial infarction. 8
• Hypomagnesemia is arrhythmogenic and often coexists with hypopotassemia, though definite causal evidence is lacking. 8
• Hypercalcemia and intracellular calcium changes contribute to VT with acute ischemia, reperfusion, exercise, and digitalis toxicity. 8
• Acute kidney injury and chronic kidney disease predispose to VT through electrolyte disturbances. 1

Medication-Induced and Toxic Causes

Multiple medications and substances directly cause or aggravate VT through various mechanisms. 1

Drug-Induced Causes

• QT-prolonging medications (antiarrhythmics and non-cardiac drugs) cause torsades de pointes, particularly with drug-drug interactions. 1, 6
• Stimulants including cocaine and amphetamines directly provoke VT. 1
• Anabolic steroids and supplements can trigger ventricular arrhythmias. 1
• Alcohol and substance use (including THC) can trigger VT through multiple mechanisms. 9

Proarrhythmic Effects

• Sodium channel blockers (Class I antiarrhythmics) increase mortality in ischemic heart disease patients and should be avoided except in specific circumstances. 1
• Digitalis toxicity causes VT through calcium-mediated mechanisms. 8

Acute Ischemia and Reperfusion

Acute coronary ischemia increases myocardial extracellular potassium, which is a major factor in lethal ventricular arrhythmias after coronary occlusion. 8

• Reperfusion injury causes VT through calcium-mediated mechanisms. 8
• Exercise-induced ischemia can trigger VT in patients with coronary disease. 1

Other Precipitating Factors

Multiple systemic conditions and triggers must be evaluated when assessing VT etiology. 1

• Thyroid disease (both hyper- and hypothyroidism) can precipitate VT. 1
• Emotional stress serves as a trigger, particularly in CPVT and LQTS. 1
• Lung disease may contribute through hypoxia and sympathetic activation. 1

Family History Considerations

Genetic predisposition significantly influences VT risk and guides diagnostic evaluation. 1

• Sudden cardiac death in first-degree relatives raises concern for inherited cardiomyopathies or channelopathies. 1
• Family history of cardiomyopathy (hypertrophic, dilated, ARVC) requires genetic evaluation. 1
• Sudden infant death syndrome (SIDS) or unexplained drowning in family members suggests cardiac channelopathies. 1

Clinical Pitfalls

The absence of structural heart disease on routine imaging does not exclude VT risk, as channelopathies and early cardiomyopathies may not be apparent. 1, 5

Electrophysiological study has no prognostic value for channelopathies (LQTS, CPVT, Brugada, short QT syndrome), where risk stratification relies on ECG, exercise testing, and genetic testing. 1

Ventricular bigeminy with QTc >500 ms represents an imminent risk substrate for torsades de pointes, requiring urgent intervention including discontinuation of QT-prolonging drugs and electrolyte correction. 6