Unforeseen beneficial effect of successful PVC ablation: Achieving migraine attack control without medication

Abstract

Successful catheter ablation of frequent PVCs in a patient with PVC-induced cardiomyopathy resulted in a marked improvement in left ventricular ejection fraction (LVEF), accompanied by complete resolution of migraine with aura attacks. This case illustrates both cardiac and neurological benefits of PVC burden reduction through ablation.

Keywords: catheter ablation; migraine; patent foramen ovale; premature ventricular contractions; tachycardiomyopathy.

FIGURE 1

(A) Selective coronary angiography performed on the patient shows a lesion causing 50%–60% stenosis in the mid portion of the LAD. Additionally, multiple monomorphic PVCs are observed in the rhythm trace during cineangiographic recording (red arrows). (B) After the intracoronary administration of 200 mcg glyceryl trinitrate and an adequate waiting period, the cineangiographic recording shows that the degree of stenosis of the atherosclerotic lesion in the LAD did not decrease (blue arrow).

FIGURE 2

12‐lead pre‐procedural ECG showing PVCs suggestive of a left coronary cusp (LCC) origin. The ectopic QRS complexes demonstrate an inferior axis (positive in II, III, and aVF) and are negative in lead I, consistent with a left‐sided outflow tract origin. Lead V1 shows a tall, notched R wave (RBBB‐like morphology), and the precordial R‐wave transition is early (at V2), with positive concordance through V1–V6. These features distinguish LCC PVCs from those arising in the right ventricular outflow tract (RVOT) or right coronary cusp (RCC), which typically show an LBBB morphology in V1 and later transition. The described morphology aligns with established criteria for LCC origin.

FIGURE 3

(A, B) Electroanatomic mapping aspects; (A). Coronal aspect (B) Inferior aspect. (C) While the ablation catheter was on the hinge point, signals collected from the surface and intracardiac EGMs were observed, and successful ablation was performed in the region that has the earliest activation (approximately −80 ms from the targeted PVC). Asc Ao, Ascending Aorta; LCC, Left coronary cusp; NCC, Non‐coronary cusp; RCC, Right coronary cusp.

FIGURE 4

(A) Polar map of Tc‐99 m sestamibi myocardial perfusion scintigraphy performed pre‐ablation: LVEF was measured at 25%, and no ischemia was noted in the LAD territory. (B) Polar map of Tc‐99 m sestamibi myocardial perfusion scintigraphy performed post‐ablation: LVEF was calculated to be 65%.

FIGURE 5

Cardiac Multigated Acquisition Scan (MUGA) was performed 6 weeks after ablation.

FIGURE 6

At six‐month follow‐up, 24‐h Holter monitoring revealed a PVC burden of <0.1%, reflecting durable suppression of ectopic activity following successful catheter ablation.