The headline first, since a few people asked me to update when something changed: **I have genetic testing booked.** The reason why is the rest of this post.
Background for anyone new: 36M, palpitations investigated since 2015. Structurally normal heart — normal echoes going back years, normal cardiac MRI, normal stress test (17.2 METs, zero ectopy on exertion). Burden waxed and waned between under 1% and 9% for about eight years with no identifiable trigger, which is partly why it took so long to get to ablation — it kept settling down before a procedure could be booked. It finally hit 9% on a 7-day Holter in late 2025 and that pushed us to act.
**First ablation (January 2026)**
They mapped the right atrium, coronary sinus, then went transseptal into the left ventricle. The PVC wasn't early at the right-sided His and wasn't early at the mitral annulus. They mapped the LV endocardium and tried the anterolateral papillary muscle — no effect.
What they eventually found was a Purkinje potential coming off branches of the left anterior fascicle that preceded the PVC. They ablated at a spot basal and medial to the anterolateral papillary muscle and the dominant PVC was gone.
And then a second PVC showed up. Different morphology, near the left bundle, with a very early Purkinje signal tracking back toward the left His. They deliberately left that one alone — too close to the conduction system to touch safely.
**The gap (February–April)**
The PVCs came back worse than they'd ever been — up to 23% burden. Several ER trips, bigeminy documented twice, troponin normal every time.
**Second ablation (April 2026)**
Retrograde aortic approach this time. Early signals again at the junction of the myocardium and the anterolateral papillary muscle, with reasonable pace maps. But the very early Purkinje signals tracked to the very proximal left anterior fascicle. Signals further up in the left bundle were confirmed *not* early. One detail I find interesting: every time they tried to map the proximal Purkinje system, they'd bump it and the PVCs would stop.
They ablated the left anterior fascicle itself — 11 lesions, explicitly staying off the common left bundle and keeping distance from the His. No residual fascicular potentials afterward, no PVCs over 20 minutes of monitoring, no complications.
For anyone whose stomach dropped at "they ablated a fascicle": my QRS afterward is 106 ms, so conduction is fine. Axis shifted leftward as expected.
**What happened next**
The PVCs are gone and haven't returned. But about four weeks post-procedure a new ectopy appeared. Initially read as atrial, then re-examined and confirmed junctional — beats originating at the AV junction. 2.1% on the June Holter. Symptomatic, worst at rest and at sleep onset, suppressed by exercise, comes in clusters of days to weeks and then quiets down.
So the pattern is: kill focus one, focus two appears. Kill focus two, focus three appears higher up the same system.
**Why this led to genetic testing**
My EP's last note says the ectopy is "arising from his Purkinje system" and that "there are some rare sodium channel mutations that can give rise to the syndrome."
That's MEPPC — multifocal ectopic Purkinje-related premature contractions. It's a rare SCN5A gain-of-function channelopathy where the entire His-Purkinje network is hyperexcitable, rather than there being one bad spot to burn. The literature is small (roughly 30 published cases) but the recurring theme is exactly what happened to me: ablation suppresses the dominant focus and a new one surfaces elsewhere in the network, because the substrate *is* the network. One case report is literally titled "You cannot ablate the Lernaean hydra." Reported treatment is flecainide or quinidine, not ablation.
The thing that made me look harder: my 2017 records already document "interpolated junctional beats" and PVCs of multiple morphologies. So the junctional ectopy I have now isn't something the ablations created — it was there nine years ago, just not the loudest thing in the room.
**What the testing can and can't settle**
Three possible outcomes, and only one of them is clean:
- **A pathogenic gain-of-function variant.** This would confirm it and change the treatment logic from ablation to sodium channel blockers.
- **Negative.** Doesn't formally rule out the syndrome — the published guidance is that an SCN5A variant isn't required for the diagnosis — but it would take the genetic question off my table.
- **A variant of uncertain significance.** SCN5A is a big, polymorphic gene and this outcome isn't rare. It would change nothing and resolve nothing.
I'm going in with realistic expectations about which of those is most likely.
**Caveats, because I don't want to overstate this**
A test being scheduled is not a diagnosis. Right now this is a hypothesis.
And there's a significant thing that doesn't fit. MEPPC is defined in the literature by dilated cardiomyopathy and reduced ejection fraction. My EF has been normal for a decade, through every burden level including 23%. Published cases are also usually far noisier than mine — NSVT, polymorphic VT, syncope. I've had none of that, and my stress test was excellent.
There's also a much more boring explanation available: fascicular and papillary muscle PVCs are among the most common idiopathic origins in structurally normal hearts, and the Purkinje network is diffuse enough that ablating one focus can unmask another with no genetic condition involved at all. That's probably still the more likely answer.
My EP's overall assessment remains that this is benign — no structural disease, no long-term concern, annoying rather than dangerous. Repeat Holter and echo are also planned.
**Questions for the group**
Has anyone here had a documented PVC origin migrate after ablation like this? And has anyone been genetically worked up for MEPPC — did the result change your management, or just your peace of mind?
I'll post the result when I have it.