Targeted ablation of the distal Purkinje-myocardium interface for premature ventricular complex-induced cardiomyopathy by delayed Purkinje conduction-induced re-excitation: a case report.

BACKGROUND

In structurally normal hearts, premature ventricular complexes (PVCs) are primarily driven by enhanced automaticity or afterdepolarization-dependent triggered activity. Traditionally, re-entrant excitation has only been associated with cardiac conditions involving scar formation, such as post-myocardial infarction or cardiac sarcoidosis.

CASE SUMMARY

We present a case of an asymptomatic 28-year-old patient with a high burden of monomorphic PVCs originating near the posteromedial papillary muscle. Left ventricular (LV) dilatation with reduced systolic function (ejection fraction 45%) was diagnosed as PVC-induced cardiomyopathy, given the absence of fibrosis and coronary artery disease. During an electrophysiological study, a 2-cm region was identified where abnormal Purkinje potentials (P1), exhibiting markedly reduced conduction velocity (0.88 mm/ms), consistently followed the rapid conduction via the left posterior fascicle (LPF). Local activation time velocity vectors of P1 pinpointed the earliest abnormal Purkinje activation at the proximal LPF. The impulse excited the distal one-third of the interventricular septum before conducting retrogradely to the LPF. Radiofrequency ablation targeted at the Purkinje-myocardial pivot point successfully eliminated the PVCs, restoring LV systolic function at follow-up.

DISCUSSION

Even in the absence of structural heart disease, delayed anterograde Purkinje conduction can facilitate monomorphic PVCs via re-excitation. This highlights the potential for targeted ablation at the distal Purkinje network as an effective treatment strategy.