A 42-year-old woman presents with recurrent palpitations and presyncope triggered by exercise and emotional stress. 12-lead ECG during an episode shows a wide QRS complex with left bundle branch block pattern and inferior axis deviation, with precordial transition at V4. Transthoracic echocardiography is normal. The arrhythmia marked **A** in the diagram is suspected. Which of the following is the MOST distinctive electrophysiologic mechanism underlying this arrhythmia that explains its acute response to intravenous adenosine?
A. Cyclic-AMP-mediated triggered activity from delayed afterdepolarizations in RVOT myocytes, suppressed by adenosine-induced cAMP reduction
B. Reentrant mechanism involving the atrioventricular node and an accessory pathway, terminated by AV nodal block
C. Catecholamine-dependent polymorphic activity arising from abnormal calcium handling in the sarcoplasmic reticulum
D. Abnormal automaticity from scar tissue in the right ventricular free wall following prior myocardial infarction
Explanation
Why option 1 is correct
The arrhythmia marked A — idiopathic RVOT VT — is driven by cyclic-AMP-mediated triggered activity from delayed afterdepolarizations in myocytes of the right ventricular outflow tract, just below the pulmonic valve. This mechanism is exquisitely sensitive to adenosine, which suppresses cAMP and abruptly terminates the arrhythmia — a diagnostic and therapeutic hallmark that distinguishes idiopathic RVOT VT from scar-related reentrant VT. The catecholamine/exercise-dependence and adenosine sensitivity are pathognomonic for this cAMP-mediated triggered activity mechanism (2017 AHA/ACC/HRS Guideline; Harrison 21e Ch 250).
Why each distractor is wrong
Option 2 (AV nodal reentry/accessory pathway): This describes antidromic AVRT in WPW (marked D in the diagram), not idiopathic RVOT VT. While adenosine does block the AV node, the mechanism and clinical context are entirely different — WPW presents with pre-excitation on resting ECG and orthodromic reentry is far more common than antidromic.
Option 3 (scar-related reentrant VT): This describes the mechanism of sustained scar-related VT post-MI (marked C in the diagram). Scar VT is reentrant, NOT adenosine-sensitive, and occurs in structurally abnormal hearts with prior infarction — the opposite of the normal heart and adenosine responsiveness seen in idiopathic RVOT VT.
Option 4 (catecholamine-dependent polymorphic activity from abnormal calcium handling): This describes catecholaminergic polymorphic ventricular tachycardia (CPVT), which arises from abnormal ryanodine receptor or CASQ2 mutations causing sarcoplasmic reticulum calcium leak. CPVT is NOT adenosine-sensitive and presents with bidirectional or polymorphic morphology, not monomorphic LBBB+inferior axis VT.
High-YieldNEET PG
Idiopathic RVOT VT = cAMP-triggered activity + adenosine sensitivity + exercise/catecholamine-dependent + structurally normal heart + LBBB+inferior axis + ~70% of idiopathic VTs in adults.
2017 AHA/ACC/HRS Guideline for Management of Ventricular Arrhythmias; Harrison 21e Ch 250
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