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16 y/o soccer player with palpitations

Referred by a colleague. This 16 y/o young man is a professional soccer player who experienced palpitations and dizziness during sports over the past 3 months. Holter recordings revealed the following:

This is a 25mm/s strip, as you can see in the top right corner. The tracing shows tachycardia of 180bpm, wide QRS complexes. AV dissociation is not evident, there seem to be P waves visible that are associated to the QRS complexes (notch at the bottom of the S waves in lead 1).

Later in the tracing the following happens:

The wide complex tachycardia (WCT) transitions to narrow complex tachycardia (NCT). This rules out VT and suggests acceleration dependent bundle branch block (BBB) causing the wide QRS tachycardia. Also, the CL does not change, heart rate stays the same (R-R 260ms to 270ms). This rules out an accessory pathway (AP) on the same side as the BBB being involved in the tachycardia. If CL would shorten (i.e. tachycardia accelerates) with loss of BBB, this would suggest AV reentry tachycardia with an AP ipsilateral to the BBB --> as the BBB resolves conduction velocity increases within the circuit, thus speeding up tachycardia.

Now, looking at the NCT part of the tracing there are P waves present, just before the QRS complexes (best noticed in lead 1). The R-P interval thus is longer than the P-R interval (i.e. long RP tachycardia). This favors atrial tachycardia (AT) or atypical AV nodal reentry tachycardia (aAVNRT) over atrio-ventricular tachycardia (AVRT).

A little later in the tracing you spot the end of the tachycardia:

The CL gets longer (309ms to 395ms) over several beats and terminates with a possible P wave at the end (small negative notch at the end of the T wave in leads 1-3). After a sinus node recovery time of 1,55 seconds sinus rhythm sets in (last beat of the tracing).

Slowing of CL followed by termination of the tachycardia might suggest some form of atrial tachycardia. However, in reentry tachycardias where the AV node (AVN) is part of the circuit, some degree of AVN conduction slowing caused by vagal inputs may precede termination of tachycardia. Also, termination on an atrial event (P wave) rules out atrial tachycardia.

Taking into account all of the above (no increase in HR with loss of BBB; NCT with quite regular CL; long RP tachycardia; termination on an atrial impulse) we clearly favor atypical AVNRT.

Statistically, AVRT (atrio-ventricular reentry tachycardia) via an accessory pathway would be most likely in an adolescent. There appears no clear preexcitation on the sinus beat. However, one could suspect a concealed AP (i.e. AP with retrograde conduction only).

Second most common would be AVNRT (atrio-ventricular nodal reentry tachycardia). In AVNRT loss of bundle branch block would not accelerate tachycardia (AVNRT circuit does not involve the right or left bundle branches).

Typical Slow/Fast AVNRT circuit simplified

We scheduled the patient for electrophysiologic (EP) study. NCT was easily inducible using isoproterenol and ventricular pacing. The tachy showed long RP characteristics and we were able to prove atypical AVNRT (fast/slow). Ablation of the slow pathway was successful. No further tachycardias inducible.

Fast/Slow AVNRT circuit simplified

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