Long RP Tachycardia in a Structurally Normal Heart: Which Circuit?
A 45-year-old woman with a structurally normal heart (EF 60%) has had disabling palpitations for 3 years. During an EP study, a narrow-complex tachycardia at 150 bpm (cycle length 400 ms) is induced with atrial pacing. The surface P waves are negative in II, III, and aVF, and the RP interval (QRS onset to P onset) measures 280 ms. Intracardiac recordings show earliest retrograde atrial activation at the His-bundle region, 10 ms ahead of the coronary sinus ostium. Ventricular overdrive pacing from the RV apex at 340 ms entrains the tachycardia; after pacing stops, the return sequence is V-A-A-V, with two atrial cycles continuing at 400 ms while the ventricles are dissociated. Adenosine 12 mg IV produces transient AV block while atrial activity continues at the same 400 ms cycle length.
1. Interpret these findings and state the most likely mechanism. Explain how each piece of data constrains the differential diagnosis.
Read the worked answer
The findings fit an atrial tachycardia (AT) arising near the anteroseptal/para-Hisian right atrium, not AVNRT or an accessory pathway.
- Long RP (280 ms > PR 120 ms) narrows the differential to atypical (fast-slow) AVNRT, PJRT, or AT. That alone cannot separate them.
- V-A-A-V return sequence is the decisive maneuver. After the last paced ventricular beat there are two atrial signals before the next ventricular signal, meaning the atrium is driving the ventricle. AVNRT and AVRT require ventriculoatrial conduction and give V-A-V (or A-V-A).
- Adenosine producing AV block while atrial activity continues unchanged at 400 ms confirms the atrium is not dependent on the AV node or ventricle. In AVNRT or PJRT the tachycardia terminates.
- Earliest activation at the His region then localizes the focus rather than identifying the mechanism, and is consistent with negative inferior P waves (low-to-high atrial spread from a septal origin).
A His-refractory PVC that fails to reset the atrium would further support this conclusion.
2. Mapping shows a local activation 35 ms before the surface P wave, a QS on the unipolar recording, and pace-mapping that reproduces the clinical P wave with a stimulus-to-P of 25 ms. The site is 8 mm below the His bundle. What are your options, what are the risks, and how do you modify your approach?
Read the worked answer
These meet the standard criteria for a good AT focus (earliest activation, QS unipolar, concordant pace map), but the location is the problem. A para-Hisian site carries roughly a 5-10% risk of complete AV block, and RF there can also injure the artery to the AV node and the membranous septum.
Options, in order of preference at this location:
- Cryoablation - cryomapping at -30 C tests reversibility before a permanent lesion, and the risk of permanent AV block is lower. This is the preferred tool when the His is within about 1 cm.
- RF with a small-tip catheter at low power (20-30 W), beginning at the edge of the target farthest from the His, with continuous watch for junctional acceleration, PR prolongation, or loss of His capture, and immediate cessation if any appear.
- Defer ablation and treat medically if the risk is judged unacceptable or the focus is not reproducibly inducible.
Regardless of choice: consent for pacemaker placement, temporary pacing back-up, and a documented discussion with the patient.