Routine screening exposed ventricular pre-excitation in an asymptomatic rugby player
A semi-professional rugby player arrived for routine pre-participation screening feeling entirely well. He took no regular medication and had no family history of sudden cardiac death. His physical examination was unremarkable, yet the resting 12-lead ECG immediately raised the question of an accessory pathway rather than a benign athletic variant.
The tracing showed a short PR interval of 80 ms, a slurred delta wave most obvious in II, aVF, and V5-V6, and a broad QRS complex measuring 135 ms. Those features fit Wolff-Parkinson-White pattern and separate it from left bundle branch block, which would not shorten the PR interval or produce the same slurred initial upstroke. Deep S waves in V1-V2 can look like infarction at first glance, but here they reflected pseudo-infarct change from pre-excitation rather than prior myocardial injury.
A predominantly negative V1 suggested a right-sided pathway, although localization by surface ECG remains imprecise. The more important point was not where the pathway sat, but what it could do under stress.
Asymptomatic pre-excitation still demands risk stratification before clearance
In a competitive athlete, incidental pre-excitation is not something to wave away because symptoms are absent on the day of screening. Rapid antegrade conduction over an accessory pathway can become dangerous if atrial fibrillation develops, since the ventricle may then be driven at very high rates without the normal filtering effect of the AV node.
For that reason, clearance to play came after referral to cardiology for risk stratification. The 2019 ESC guidance supports an electrophysiology study in this setting. The anatomy of the ECG alone does not define risk; the pathway’s conduction properties do.
One short PR interval can hide a much larger arrhythmic threat.
Sudden palpitations during training revealed orthodromic AVRT
Three weeks later, while still waiting for specialist review, he developed sudden-onset racing palpitations during training. He remained alert, but mild lightheadedness signaled a hemodynamically tolerated tachycardia rather than complete cardiovascular collapse. The follow-up ECG changed the diagnostic picture in a way that only pre-excitation can.
The rhythm was regular and narrow, with a QRS duration of 71 ms and a rate of 196/min. The delta wave had disappeared because ventricular activation now traveled down the AV node and returned retrogradely through the accessory pathway. A retrograde P wave, separated from the QRS, pointed to orthodromic AVRT rather than typical AVNRT. Flutter waves were absent, and the abrupt onset argued strongly against sinus tachycardia.
The same pathway that widened the baseline ECG had now become the circuit for re-entrant tachycardia.
Vagal manoeuvres came first because the patient was stable
Management followed the basic logic of stable narrow-complex SVT. Vagal manoeuvres, including the modified Valsalva, came first. In this case, the rhythm terminated with the manoeuvre, and sinus rhythm with pre-excitation returned afterward.
If vagal manoeuvres had failed, IV adenosine would have been the next step because orthodromic AVRT depends on the AV node. Blocking the AV node interrupts the loop and stops the tachycardia. DC cardioversion is reserved for the unstable patient, not the alert athlete who can be managed noninvasively at the bedside.
The choice of first treatment matters because the mechanism determines the response.
Pre-excited atrial fibrillation changes the drug list immediately
The follow-up episode also sets up the more dangerous scenario that every clinician managing WPW should keep in mind: pre-excited atrial fibrillation. In that rhythm, AV-nodal blockade can push more conduction toward the accessory pathway and create the substrate for ventricular fibrillation.
For that reason, IV verapamil is contraindicated, and the same caution extends to diltiazem, beta-blockers, adenosine, digoxin, and IV amiodarone. When the patient is unstable, synchronized DC cardioversion is appropriate. When stable, procainamide or ibutilide can be used instead.
This is not a subtle pharmacology point. It is the difference between blocking the bottleneck and opening a faster route to the ventricle.
Catheter ablation removes the substrate for both tachycardia mechanisms
After the tachycardia episode, he was referred to electrophysiology. Symptomatic Wolff-Parkinson-White syndrome is an indication for EP study and catheter ablation, and the 2019 ESC guidelines give that strategy a Class I recommendation. Ablation targets the accessory pathway directly, which means it can prevent both orthodromic AVRT and future pre-excited AF.
That makes the management more definitive than long-term rate control or intermittent antiarrhythmic suppression. A beta-blocker may blunt episodes in some patients, but it does not remove the circuit. Catheter ablation does.
The education point here is practical for sports medicine, emergency medicine, and cardiology alike: a normal-looking narrow tachycardia during symptoms does not rule out WPW. The baseline ECG carries the diagnosis, the pathway determines the risk, and the first dangerous mistake is treating pre-excited AF like an ordinary AV-node-dependent SVT.
Baseline ECG findings defined the diagnosis
Both ECGs came from a single accessory pathway used in two different ways. In sinus rhythm, the atrial impulse reached part of the ventricle early through the pathway, shortening the PR interval and producing the delta wave. During the tachycardia, the impulse traveled down the AV node and back up the pathway, so ventricular activation became narrow and organized even while the rate climbed to 196/min.
The case closes with a reminder that the surface ECG can mislead unless the clinician reads it in context. WPW can mimic bundle branch block or infarction on a resting tracing, then later present as a regular narrow SVT that looks deceptively ordinary. In a young athlete with pre-excitation, that sequence should trigger specialist assessment, counseling about high-risk rhythms, and definitive pathway treatment rather than simple reassurance.