What is the common mechanism for monomorphic VT in ischemic cardiomyopathy seen in EPS?

• A. Reentry around scar tissue (scar-related reentrant VT)
• B. Focal automaticity from Purkinje fibers
• C. Triggered activity
• D. AV nodal reentry tachycardia

Answer: (A)

Monomorphic VT after myocardial infarction typically arises from a reentrant circuit around scar tissue. The infarct scar creates a nonconductive core with surviving myocardial fibers in the border zone, forming slow conduction channels. The impulse travels around the scar through one of these channels, establishing a stable reentrant circuit. That fixed pathway produces a single, consistent QRS morphology during the tachycardia—the hallmark of monomorphic VT. In an EPS, mapping often localizes a critical isthmus within the scar-border zone, and ablation targeting that channel can interrupt the circuit to terminate the VT.

Other mechanisms are less likely in this setting: focal automaticity from Purkinje fibers can cause VT but tends to be less characteristic of the classic scar-related, monomorphic VT seen after ischemic injury; triggered activity depends on afterdepolarizations and typically isn’t the dominant mechanism in post-infarct monomorphic VT; AV nodal reentry tachycardia is a supraventricular mechanism, not a ventricular scar–based VT.