What is the most common cause of sustained ventricular tachycardia (VTach)?

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Most Common Cause of Sustained Ventricular Tachycardia

Coronary artery disease, particularly prior myocardial infarction with resulting myocardial scar, is the most common cause of sustained ventricular tachycardia. 1, 2

Pathophysiology and Mechanism

Sustained ventricular tachycardia (VT) in the setting of structural heart disease is predominantly caused by:

  1. Scar-related reentry:

    • Myocardial scarring from prior infarction creates the substrate for reentrant circuits 3
    • The scar tissue creates areas of slow conduction and unidirectional block that facilitate reentry
    • This typically manifests as monomorphic VT that may degenerate to ventricular fibrillation 3
  2. Disease-specific mechanisms:

    • In coronary artery disease: Scar from prior MI is the predominant mechanism 2, 4
    • In non-ischemic cardiomyopathy: Fibrosis and myocardial disarray create arrhythmogenic substrate 3
    • In hypertrophic cardiomyopathy: Myocardial disarray and fibrosis 3

Epidemiology of Sustained VT by Etiology

  • Coronary artery disease:

    • Most common cause of sustained monomorphic VT 1, 2
    • 73-83% of patients in major ICD trials (AVID, CASH, CIDS) had underlying coronary artery disease 3
  • Non-ischemic dilated cardiomyopathy:

    • Second most common cause of sustained VT 3
    • Often presents with monomorphic VT similar to ischemic cardiomyopathy 3
  • Hypertrophic cardiomyopathy:

    • Most common cause of cardiac arrest in individuals younger than 40 years 3
    • Affects approximately 1 in 500 persons 3
  • Other structural heart diseases:

    • Arrhythmogenic cardiomyopathies
    • Chagas disease
    • Sarcoidosis
    • Repaired congenital heart disease 2

Clinical Presentation and Risk Factors

Sustained VT may present with:

  • Hemodynamic compromise (syncope, near-syncope, heart failure, shock)
  • Palpitations
  • Sudden cardiac arrest

Risk factors for sustained VT in coronary artery disease include:

  • Prior myocardial infarction
  • Reduced left ventricular ejection fraction (≤40%)
  • Ventricular aneurysm
  • Older age at time of infarct repair 3
  • Advanced RV dilation (in repaired Tetralogy of Fallot) 3

Diagnostic Approach

  1. 12-lead ECG: Essential for diagnosis and localization of VT origin 2
  2. Cardiac imaging: To assess structural abnormalities and ejection fraction
  3. Electrophysiologic study: Particularly valuable in:
    • Patients with unexplained syncope and structural heart disease 3
    • Determining mechanism of arrhythmia
    • Guiding ablation procedures 2

Management Considerations

For patients with sustained VT and structural heart disease:

  • ICD therapy is the cornerstone of treatment for prevention of sudden cardiac death 3
  • Catheter ablation can reduce VT episodes and ICD shocks in appropriate candidates 2
  • Antiarrhythmic medications have limited efficacy as standalone therapy 2

Important Caveats

  1. Acute coronary syndrome: Polymorphic VT or VF is more common than monomorphic VT in the acute setting of myocardial infarction 3

  2. Idiopathic VT: Can occur in the absence of structural heart disease and generally has a more benign prognosis 3

  3. Risk stratification: Left ventricular ejection fraction remains the most frequently used parameter to stratify sudden death risk in both ischemic and non-ischemic cardiomyopathy 1

  4. Timing after MI: VT/VF occurring >48 hours after hospital presentation carries a higher mortality risk than early VT/VF (within 48 hours) 3

References

Research

Ventricular tachycardia and sudden cardiac death.

Mayo Clinic proceedings, 2009

Guideline

Guideline Directed Topic Overview

Dr.Oracle Medical Advisory Board & Editors, 2025

Research

Ventricular scars and ventricular tachycardia.

Transactions of the American Clinical and Climatological Association, 2009

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Professional Medical Disclaimer

This information is intended for healthcare professionals. Any medical decision-making should rely on clinical judgment and independently verified information. The content provided herein does not replace professional discretion and should be considered supplementary to established clinical guidelines. Healthcare providers should verify all information against primary literature and current practice standards before application in patient care. Dr.Oracle assumes no liability for clinical decisions based on this content.

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