Can Coronary Artery Disease (CAD) cause Ventricular Tachycardia (VTach)?

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Last updated: November 26, 2025View editorial policy

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Can Coronary Artery Disease Cause Ventricular Tachycardia?

Yes, coronary artery disease is a major cause of ventricular tachycardia, with myocardial scar from prior infarction being the most common substrate for sustained monomorphic VTach in patients with structural heart disease. 1

Primary Mechanisms by Which CAD Causes VTach

Reentry is the dominant mechanism in CAD-related VTach, particularly in post-myocardial infarction scars, where heterogeneous tissue creates areas of preserved myocardium within fibrotic scar tissue 2. This anatomical substrate requires three key elements: anatomical or functional conduction block, a slow conduction pathway, and unidirectional block allowing retrograde conduction 2.

The myocardial scarring from prior infarction creates the most common substrate for sustained monomorphic VT in structural heart disease 1. These scars demonstrate heterogeneous tissue with areas of preserved myocardium interspersed within fibrotic regions, providing the anatomical basis for reentrant circuits 2.

Clinical Context and Risk Stratification

Acute vs. Chronic CAD: The mechanism and timing differ significantly between acute coronary ischemia and chronic infarction 3. Acute coronary ischemia is the most common cause of ventricular fibrillation, while chronic myocardial scar is the primary substrate for sustained monomorphic VT 1.

Post-MI patients face highest risk at presentation, with risk declining over hours and days 4. However, VT occurring more than 48 hours after MI in the absence of ongoing ischemia may warrant ICD implantation 4.

Diagnostic Confirmation in CAD Patients

When evaluating patients with suspected CAD-related VTach:

  • Electrophysiological study is recommended for diagnostic evaluation of patients with remote myocardial infarction presenting with symptoms suggestive of ventricular tachyarrhythmias, including palpitations, presyncope, and syncope 5
  • The diagnostic yield may reach 50% in CAD patients undergoing electrophysiological testing 5
  • Infarct surface area and mass on delayed enhancement cardiac MRI identify patients with substrate for VT better than LVEF alone 5

Specific Characteristics of CAD-Related VTach

Focal mechanisms account for up to 9% of VTs in CAD patients with prior MI, though reentry remains predominant 6. These focal VTs demonstrate significantly shorter pre-systolic intervals (36 ± 17 ms vs. 117 ± 67 ms for reentrant VT) and cannot be entrained 6.

Successful ablation sites for focal VT in CAD patients are predominantly in the basal half of the left ventricle (75%), whereas only 60% of macro-reentrant VTs are basal 6.

Management Implications

Survivors of sudden cardiac death with presumed ischemia-mediated VT have a Class I indication for CABG to improve survival 5. This reflects the direct causal relationship between CAD and life-threatening ventricular arrhythmias.

Catheter ablation outcomes differ by etiology: 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 5. The SMASH-VT trial demonstrated that substrate-guided ablation in post-MI patients reduced VT episodes from 33% to 12% and appropriate ICD shocks from 31% to 9% 5.

Risk Factors and Prognostic Markers

Extent of myocardial scar is a strong independent predictor of mortality and appropriate ICD therapy, even after adjusting for LVEF 5. Scar size greater than 5% of LV mass shows a sharp increase in event rates 5.

The peri-infarct zone (areas of heterogeneous scar) is a particularly strong predictor of VT inducibility and adverse outcomes 5. This zone represents the critical substrate where slow conduction and functional block enable reentrant circuits 2.

Common Pitfalls

Do not assume all VTach in CAD patients is reentrant—focal mechanisms exist in approximately 9% of cases and require different ablation strategies 6. The distinction is critical because ablation site characteristics differ substantially between mechanisms.

Do not rely solely on LVEF for risk stratification—scar burden and characteristics on cardiac MRI provide superior prediction of VT risk 5. Patients with extensive scar may warrant ICD therapy even with preserved ejection fraction.

References

Research

Ventricular tachycardia and sudden cardiac death.

Mayo Clinic proceedings, 2009

Guideline

Pathophysiology of Ventricular Tachycardia

Praxis Medical Insights: Practical Summaries of Clinical Guidelines, 2025

Research

Ventricular arrhythmias in ischemic heart disease.

Annals of internal medicine, 1991

Guideline

Concerning Ventricular Tachycardia

Praxis Medical Insights: Practical Summaries of Clinical Guidelines, 2025

Guideline

Guideline Directed Topic Overview

Dr.Oracle Medical Advisory Board & Editors, 2025

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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