Thank you all for your response! This was one of the most interesting cases I have ever seen…
The story about this patient started 24 years ago, when he had his first episode of palpitations. At that time he was found to be hemodynamically unstable with irregular WCT rate of 270 bpm/min. I have no ECG tracing of that event but by his medical documentation he was urgently defibrillated and pre-excitation was recorded during sinus rhythm. The cardiologist pronounced that WCT as AF+WPW and hospitalized this patient. The EP study was performed and they noted two accessory pathways: left lateral and right postero-septal. However during that time, the patient refused ablation and signed against medical advice that he wants to be discharged. So, he left home with Amiodarone prescribed (which he didn’t use).
Over the next 20 years he was fine (!), but the problems started again few years ago. He started to have palpitations approximately once per a month and was forced to use Amiodarone every time. The last month it got even worse: he had symptoms almost on daily base, so he finally decided to get some help. He called EMS and the ECG #1 was recorded.
Image 1. WCT recorded pre-hospital
This is WCT, rate about 160/min. There is a RAD in limb leads, but it means nothing in context of difference between ventricular tachycrdia (VT) and supraventricular tachycardia (SVT) with aberration. VT can have any axis and it is dangerous to use only this criterion. There is monophasic R wave in leads V1 and leads V2 leaning toward VT, but the morphological findings in leads V5 and V6 suggest SVT. However, lead aVR and Vereckei criteria favoring VT. With the fact that 80% WCTs are VTs, it is absolutely reasonable to presume that this VT. He received Amiodarone and was converted to sinus.
Image 2. ECG after conversion shows pre-excitation
ECG after conversion in sinus rhythm shows delta wave (positive in inferior leads and V1, and negative in lead aVL). This is suggestive for left sided accessory pathway.
Image 3. Locations of accessory pathways (from Das and Zipes Electrocardiography of Arrhythmias)
If we now compare ECG in sinus rhythm with pre-hospital WCT, we could say it was antidromic AV reentry tachycardia (AVRT).
Image 4. Example how PAC induce antidromic AVRT.
They transferred him in hospital, where the ECG #2 was recorded.
Image 5. The first WCT recorded in hospital
This is WCT with a rate of about 160 bpm/min and very similar morphology to the pre-hospital WCT (Image 1). The only difference is slightly irregular rhythm. The cardiologist read this as AF+WPW, but I have doubts about that. If the atrial rhythm was really AF, it would produce much faster ventricular response, not only 160/min. In theory, this may be atrial flutter with variable conduction associated with WPW, but I’m still leaning toward antidromic AVRT. The reason for irregularity could be cycle length changes. In AVRT this could happen because of one of these:
a) The tachycardia CL usually changes as a result of changes in AV nodal conduction properties mostly owing to changes in autonomic tone.
b) Tachycardia CL can also change if the patient has dual AV nodal pathways and the conduction via the AV node alternates between slow and fast AV nodal pathways. Alternatively, AVRT can change to AVNRT.
c) Tachycardia CL changes can occur if the patient has more than one AP. (Das and Zipes)
He was hospitalized in Coronary unit, received Amiodarone and converted again.
The same episode of palpitations happened next day.
Image 6. WCT recorded second day in hospital
This is WCT with the same QRS complexes morphology in the limb leads as the first two, but with different findings in precordial leads. There is a positive concordance, strongly suggestsive of VT, according to classic Brugada criteria.
However, there is another Brugada’s paper, not so famous - Steurer G, et al. The Differential Diagnosis on the Electrocardiogram BetweenVentricular Tachycardia and Preexcited Tachycardia. Clin. Cardiol. 1994;17:306-308.
Algorithm for the differential diagnosis between VT and preexcited tachycardia on the 12-lead surface ECG (SE 75%, SP 100%):
1) Predominantly negative QRS complexes in the precordial leads V4 to V6? YES=VT
2) Presence of a QR complex in one or more of the precordial leads V2 to V6? YES=VT
3) AV relation different from 1:1? (More QRS complexes than P waves?) YES=VT
NO= Pre-excitated tachycardia
According to this paper, this is pre-excited tachycardia.
One to remember: our hearts don’t read algorithms. This is example that WCT can have positive concordance and still not be VT.
During all these later episodes he was hemodynamically stable with normal vitals. They decided to transfer him into EP unit and he agreed with ablation this time.
Waiting for ablation, during two days, he had several WCT episodes with same ECG…
Image 7. WCT with different morphology than previous
What happened here? This WCT is completely different than all recorded previously. This is AFL with 2:1 conduction and rate-related LBBB. Accessory pathway is not included in this tachycardia. Again Amiodarone was given and he was converted.
Image 8. Sinus rhythm recorded just after conversion
Beside the same pre-excitation pattern as previous sinus ECG, there are diffuse STDs (probably caused by tachycardia) and one PAC at the end of strip.
Third day narrow complex tachycardia was recorded two times (with identical morphology).
Image 9. Narrow complexes tachycardia in same patient
“Wow! Is there the end here?”-you are probably asking.
This is SVT with P wave after QRS complex (best seen in lead I, II and V1). So, here are two options:
1) AFL with 2:1 conduction (the Bix rule: “If “P” wave is between QRS complexes, the most likely there is another “P” hidden into QRS complexes, favoring AT or AFL). But I’m not sure this is AFL: the rate is nearly the same when rate-related LBBB appeared (in several ECGs).
2) The other option is orthodromic AVRT, as short RP SVT.
He finally got in the Cath lab and they performed left lateral accessory pathway ablation. In short, this is the Cath lab report: …”Intracardiac recording revealed the earliest local activity in the ablation catheter placed in lateral mitral annulus (V-delta 35ms; A:V 2:1). Using conventional RF energy (50W, 60 C, 120sec) after 7 second the loss of pre-excitation was registered…After that, the absence of accessory pathway was proven with differential pacing from RV and LV. During whole procedure the only recorded arrhythmia was antidromic AVRT, which was successfully converted in sinus with over-drive pacing. No VT was induced. (They didn’t mention the other accessory pathway from 1992. at all!) After ablation there were no signs of pre-excitation in ECG.
Image 10. Post-ablation ECG
I’m not sure why there was difference between two EP studies and why another pathway wasn’t seen now.
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