A 28-year-old woman presents to the emergency department with recurrent syncope during emotional stress. Her 12-lead ECG shows the pattern marked **A** in the diagram — a polymorphic ventricular tachycardia with QRS complexes twisting around the isoelectric baseline, and a prolonged baseline QTc of 520 ms. She has no prior cardiac history, normal electrolytes, and is on no medications. Which of the following is the most likely underlying pathophysiological mechanism responsible for the arrhythmia pattern shown at **A**?

Explanation

## Why "Delayed ventricular repolarization leading to early afterdepolarizations during phase 2/3 of the action potential" is right The pattern marked **A** — polymorphic VT with QRS twisting around the baseline (torsades de pointes) and prolonged QTc >500 ms — is the hallmark of Long QT Syndrome. The pathophysiology is precisely delayed ventricular repolarization (prolonged action potential duration) that creates a substrate for early afterdepolarizations (EADs) during phase 2/3 of the cardiac action potential. These EADs trigger ectopic activity that manifests as the characteristic twisting polymorphic pattern. This mechanism is the fundamental basis of LQTS-related torsades de pointes, as confirmed in Harrison 21e Ch 248. ## Why each distractor is wrong - **Rapid atrial ectopic activity with variable AV conduction and aberrancy**: This describes atrial fibrillation or atrial flutter with aberrant conduction, which produces irregularly irregular (or regular) narrow-complex rhythms, not the polymorphic wide-complex twisting pattern of **A**. The baseline QTc prolongation is also inconsistent with this mechanism. - **Abnormal automaticity in the His bundle with retrograde P waves**: This describes a junctional tachycardia or His bundle tachycardia, which produces regular narrow-complex tachycardia with retrograde P waves — matching pattern **D** in the diagram, not the polymorphic VT of **A**. - **Reentry within the ventricular myocardium due to fixed anatomical scar**: Fixed anatomical reentry (as in post-MI scar or arrhythmogenic cardiomyopathy) produces monomorphic VT with consistent QRS morphology and axis, not the progressively changing amplitude and rotation around the baseline seen in **A**. LQTS is a functional (electrical) disorder, not a structural one. **High-Yield:** Torsades de pointes = polymorphic VT from EADs in LQTS; delayed repolarization (prolonged QT) → EADs during phase 2/3 → triggered activity → twisting QRS complexes. [cite:Harrison 21e Ch 248 — Ventricular Arrhythmias; Long QT Syndrome pathophysiology]