## Most Common Cause of Sustained Monomorphic VT ### Epidemiology of Structural Causes **Prior myocardial infarction (MI) with scar formation** is the single most common cause of sustained monomorphic ventricular tachycardia in adults, accounting for approximately 70–80% of cases presenting with structural heart disease. The scar tissue creates fixed anatomical barriers and zones of slow conduction that serve as the substrate for reentrant circuits. ### Pathophysiological Basis 1. **Scar formation** post-MI creates heterogeneous conduction zones 2. **Reentrant circuits** develop at the border between viable and infarcted myocardium 3. **Reproducible monomorphic morphology** reflects a fixed anatomical substrate 4. **Risk increases** with larger infarcts and reduced ejection fraction ### Comparative Frequency of Structural Causes | Cause | Frequency | Mechanism | |-------|-----------|----------| | **Prior MI with scar** | 70–80% | Reentry at scar border | | Dilated cardiomyopathy | 10–15% | Reentry in fibrotic areas | | Acute myocarditis | 5–10% | Inflammation + edema | | ARVC | 2–5% | Fibro-fatty infiltration | | Idiopathic (no structural disease) | 10% | Triggered activity (RVOT) | ### Key Point: **Sustained monomorphic VT = scar-based reentry until proven otherwise.** The fixed morphology indicates a fixed anatomical substrate, which is pathognomonic for prior MI. ### Clinical Pearl: A patient with prior MI presenting with sustained monomorphic VT has a **fixed reentrant circuit** that can be mapped and ablated. The ECG morphology remains constant across episodes because the circuit anatomy does not change. ### High-Yield: - **Monomorphic** VT in structural disease → **prior MI** (most common) - **Polymorphic** VT or **bidirectional** VT → consider acute myocarditis, catecholaminergic VT, or Brugada syndrome - **Idiopathic monomorphic** VT (normal heart) → RVOT origin [cite:Harrison 21e Ch 226]
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