Pathophysiology of Ventricular Tachycardia

Definition and Classification

Ventricular tachycardia is defined as three or more consecutive ventricular complexes occurring at a rate greater than 100 beats per minute, according to the American Heart Association 1
Sustained VTach lasts longer than 30 seconds or requires termination due to hemodynamic compromise in less than 30 seconds, as stated by the American College of Cardiology 1
Nonsustained VTach terminates spontaneously in less than 30 seconds, as defined by the European Society of Cardiology 1

Mechanisms of VTach

The reentry mechanism is the most common mechanism in structural heart disease, particularly in post-myocardial infarction scars, as reported by the American Heart Association 2
Triggered activity is a common mechanism in outflow tract VTach, especially RVOT VT, resulting from delayed afterdepolarizations and cyclic adenosine monophosphate elevation, as stated by the European Heart Journal 2
Abnormal automaticity can occur in ventricular tissue, resulting in spontaneous depolarization of ventricular cells at accelerated rates, as reported by the American College of Cardiology 2

Anatomical Substrates

Myocardial scarring is the most common substrate in ischemic heart disease, creating heterogeneous tissue with areas of preserved myocardium within fibrotic scar, as stated by the European Society of Cardiology 3
Dilated cardiomyopathy creates a substrate for VTach through myocardial fibrosis, myocyte disarray, and altered cellular electrophysiology, as reported by the American Heart Association 4

Electrophysiological Characteristics

VTach presents with wide QRS complexes (>120 ms) and AV dissociation, which is diagnostic of VTach, as stated by the American College of Cardiology 5
Fusion complexes represent merging of supraventricular and ventricular impulses, and concordance of precordial QRS complexes suggests VTach, as reported by the European Heart Journal 5

Clinical Significance

VTach can present as hemodynamically stable or unstable, and even brief episodes of VTach in patients with structural heart disease indicate increased risk for sudden cardiac death, as stated by the American Heart Association 1
Idiopathic VTach can occur in the absence of structural heart disease with generally better prognosis, as reported by the European Society of Cardiology 2

Special Considerations

Rapid anterograde conduction during atrial fibrillation over accessory pathways can lead to ventricular fibrillation and sudden cardiac death, as stated by the American College of Cardiology 6
Incessant forms of VTach may result in tachycardia-induced cardiomyopathy, as reported by the European Heart Journal 6

Diagnostic Features

Wide QRS complex tachycardia requires differentiation from supraventricular tachycardia with aberrancy, and ECG algorithms can help distinguish VTach from SVT with aberrancy, as stated by the American Heart Association 5
Electrophysiological testing can confirm the diagnosis and mechanism when ECG is inconclusive, as reported by the European Society of Cardiology 2

Pathophysiology of Ventricular Tachycardia

Primary Pathophysiological Mechanisms

The reentry mechanism in structural heart disease requires anatomical or functional conduction block, slow conduction pathway, and unidirectional block allowing retrograde conduction, according to the American Heart Association 7
Triggered activity is a common mechanism in outflow tract VT, especially right ventricular outflow tract (RVOT) VT, and results from delayed afterdepolarizations (DADs) dependent on intracellular calcium overload and cyclic adenosine monophosphate elevation, as stated by the American College of Cardiology 8
Triggered activity in outflow tract VT is often adenosine-sensitive and facilitated by catecholamines, and may not be easily inducible at baseline electrophysiological testing, requiring rapid burst pacing or isoproterenol stimulation, as noted by the American Heart Association 8

Special Considerations in Different Populations

Arrhythmias are common in children after surgical repair of congenital heart disease, and VT in pediatric patients may result from surgical incisions, coronary manipulation, electrolyte imbalance, or infusion of vasoactive medication, according to the American Academy of Pediatrics 7
Idiopathic VT arising from the right ventricle is the most common form in apparently healthy people, usually has left bundle-branch, inferior-axis morphology, and often presents as non-ischemic exercise-induced and/or repetitive monomorphic VT, as stated by the European Society of Cardiology 8

Coronary Artery Disease and Ventricular Tachycardia

Diagnostic Evaluation

The European Society of Cardiology recommends electrophysiological study for diagnostic evaluation of patients with remote myocardial infarction presenting with symptoms suggestive of ventricular tachyarrhythmias, including palpitations, presyncope, and syncope 9
The diagnostic yield of electrophysiological testing may reach 50% in CAD patients 10

Risk Stratification and Prognosis

Infarct surface area and mass on delayed enhancement cardiac MRI identify patients with substrate for VT better than LVEF alone, with scar size greater than 5% of LV mass showing a sharp increase in event rates 11
The American Heart Association suggests that extent of myocardial scar is a strong independent predictor of mortality and appropriate ICD therapy, even after adjusting for LVEF 11

Management and Treatment

The American College of Cardiology recommends CABG to improve survival in survivors of sudden cardiac death with presumed ischemia-mediated VT, reflecting the direct causal relationship between CAD and life-threatening ventricular arrhythmias 12
The European Heart Journal reports that catheter ablation outcomes differ by etiology, with patients with VT related to post-myocardial scar tend to have better outcomes following catheter ablation than patients with VT due to non-ischemic cardiomyopathy, and the SMASH-VT trial demonstrated that substrate-guided ablation in post-MI patients reduced VT episodes and appropriate ICD shocks 13

Mechanisms and Substrates of Ventricular Tachycardia

Primary Electrophysiological Mechanisms

Reentry is the predominant mechanism for sustained ventricular tachycardia in patients with structural heart disease, requiring an anatomical or functional substrate that creates zones of slow conduction and unidirectional block. 14
Myocardial scar from a prior infarction provides the most common re‑entry substrate, producing heterogeneous tissue with islands of viable myocardium within fibrotic areas that form re‑entrant circuits. 14
Re‑entry circuits commonly circulate around fixed anatomical obstacles such as post‑myocardial‑infarction scar or surgical incisions (e.g., ventriculotomy, ventricular septal defect patches). [14][15]
Triggered activity caused by delayed afterdepolarizations is the main mechanism of right‑ventricular‑outflow‑tract (RVOT) ventricular tachycardia; it depends on intracellular calcium overload and cyclic‑AMP elevation. 15
This triggered activity is adenosine‑sensitive, facilitated by catecholamines, and may terminate with vagal maneuvers. 15
Abnormal automaticity arises when partially depolarized membrane potentials occur, typically during acute myocardial infarction or transient ischemia due to extracellular potassium accumulation. 14
Enhanced normal automaticity can develop in Purkinje fibers or ventricular myocardium when pacemaker cell function is altered. 14

Structural Heart‑Disease Substrates

Post‑myocardial‑infarction scar is the single most common cause of sustained monomorphic ventricular tachycardia. 14
Acute coronary ischemia is the leading precipitant of ventricular fibrillation. 14
Hypertrophic cardiomyopathy creates an electrically unstable substrate; complex ventricular tachyarrhythmias are the most frequent mechanism of sudden cardiac death in this population. [16][17]
In hypertrophic cardiomyopathy, approximately 90 % of adults demonstrate ventricular arrhythmias on 24‑hour Holter monitoring, with nonsustained ventricular tachycardia occurring in about 20‑30 % of patients. [16][17]
Arrhythmogenic right‑ventricular cardiomyopathy/dysplasia generates a patchy‑fibrosis substrate that predisposes to ventricular tachycardia. 14
Congenital lesions such as aortic stenosis, tetralogy of Fallot (especially after RVOT patch repair), D‑transposition of the great arteries, L‑transposition, severe Ebstein anomaly, and single‑ventricle physiology all provide substrates for ventricular tachycardia. 18
In repaired tetralogy of Fallot, macro‑reentrant ventricular tachycardia circuits typically revolve around ventriculotomy or ventricular septal defect patch scars, with a sudden cardiac death incidence of roughly 2 % per decade. 18

Idiopathic Ventricular Tachycardia (Structurally Normal Hearts)

RVOT ventricular tachycardia is the most common idiopathic form, usually presenting with a left‑bundle‑branch‑block, inferior‑axis morphology on the electrocardiogram. 15
Left‑ventricular‑outflow‑tract ventricular tachycardia accounts for a small minority and may arise from endocardial, coronary‑cusp, or epicardial sites. 15
Idiopathic outflow‑tract ventricular tachycardias have an excellent prognosis; symptoms are generally mild and syncope is rare. 15

Genetic and Channelopathy‑Related Substrates

Inherited channelopathies such as Brugada syndrome create a substrate that predisposes to polymorphic ventricular tachycardia and ventricular fibrillation. 19

Common Precipitating Factors

Intense physical exertion can trigger ventricular tachycardia, particularly in hypertrophic cardiomyopathy where it is the most frequent cause of sudden cardiac death among young competitive athletes. [16][17]
Myocardial ischemia initiates a vicious cycle involving diastolic dysfunction, outflow obstruction, and systemic hypotension, thereby facilitating ventricular tachyarrhythmias. [16][17]
Acute ischemia raises extracellular potassium levels, leading to partial membrane depolarization that favors both triggered activity and re‑entry. 14
Supraventricular tachyarrhythmias may precipitate ventricular tachyarrhythmias by reducing stroke volume and coronary perfusion. [16][17]
Premature ventricular contractions can act as triggers that initiate re‑entrant circuits. 14

Dynamic Nature of the Substrate

The ventricular tachycardia substrate is continuously modulated by cardiac metabolism, electrolyte balance, intracellular signaling pathways, and autonomic influences, reflecting a complex interplay between fixed anatomical abnormalities and modifiable triggers. 14