What is this? VT versus SVT

Abstract

We present a patient who had a wide QRS tachycardia; it was initially difficult to determine whether it was superventricular tachycardia (SVT) or ventricular tachycardia (VT). By some criteria (sinus capture beats, pseudo-δ waves and wide QRS) the patient's ECG was suggestive of VT of epicardial origin. On the coronary angiogram it was found that this patient had significant coronary artery disease. He was stented with three stents and later had a full electrophysiological study .We present here the ECGs and the differential diagnosis and a brief review of the diagnostic features of epicardial VT.

Background

It is always difficult to make a decision whether a given broad QRS tachycardia is superventricular tachycardia (SVT) or ventricular tachycardia (VT). Wellens, Brugada and Miller have all described various criteria to differentiate VT from SVT.¹ This distinction is of specific importance to the physician who mans the casuality service. They would have to make fast decisions on this and treat the emergencies appropriately. Hence we describe a rather difficult case, and its solution.

Case presentation

A 60-year-old patient presented with chest pain of more than 15 min duration and a fast cardiac rhythm. The admitting physician thought that he had coronary artery disease (CAD) non-st elevation myocardial infarction, on 17 January 2013 (admission ECG; figures 1 and 2). ECG 1 showed a wide QRS tachycardia of rate 120–140/min with varying RR intervals. In lead 2 there was a possible sinus capture beat. V6 also showed a very wide beat. ECG 2 on 17 January 2013 showed a varying rate, wide QRS tachycardia 0.12 s, with a rate of 150–160/min, the ECG showed frank sinus capture beats. V4–V6 showed slurring of the initial part of the QRS. His rhythm was believed to be one of the following:

1. Atrial fibrillation, possible due to an accessory pathway/a pre-excited tachycardia;

2. Ventricular tachycardia, due to the acute coronary syndrome;

3. Atrial fibrillation alone.

Figure 1.

The ECG of the patient showing a wide QRS tachycardia. A sinus capture beat in lead 2.

Figure 2.

A wide QRS tachycardia showing intermittent sinus capture beats (in V1, V5 and V6.) δ waves/pseudo-δ waves are seen in V5 and V6.

He was admitted to the intensive coronary care unit. He was managed with intravenous amiodarone bolus, 2 (150 mg) and then 900 mg in 500 mL as an infusion, the infusion was given at the rate of 1 mg/min for 4 h and 0.5 mg/min after this. After 2 days he reverted to sinus rhythm.

His ECG 3 showed (figure 3): sinus rhythm with rate 78/min, with PR interval 0.08 s and the initial part of the QRS in V4–V6 showed a slurring and possible δ wave. Leads 2,3 and avf also had changes suggestive of positive δ waves.

Figure 3.

ECG in sinus rhythm showing δ waves that are positive in V1–V6, note that 2, 3 avf are positive, suggestive of a left lateral or a left anterolateral accessary pathway.

With this ECG the possibility of a left anteroseptal pathway or a left lateral accessory pathway were thought off. The differential diagnosis of epicardial VT² in which pseudo-δ waves are seen was also kept in mind. It might have been possible that the patient had CAD and developed VT earlier or later.

He was planned for coronary angiogram (CAG) and electrophysiology (EP) study and radiofrequency (RF) ablation if possible.

Investigations

His echocardiogram showed left ventricle internal diameter diastole/S 4.13/2.29 ejection fraction 76%. Interventricular septum (IVS) d 1.7 cm and posterior wall diameter in diastole 1.19 cms. He had regional wall motion abnormality in the left anterior descending (LAD) territory and stage 1 diastolic dysfunction. His risk factors were age, male, systemic hypertension, type 2 diabetes mellitus and he was an ex-smoker. His total cholesterol was −230 mg, low-density lipoprotein 176 mg/dL, high-density lipoprotein 44 mg/dl, triglyceride 145 mg/dL and very low-density lipoprotein negative.

On 25 February 2013 he had his CAG that showed a normal left main coronary artery with LAD a type 3 vessel. The LAD had a discrete eccentric 80% lesion. His left circumflex artery was normal. His right coronary artery (RCA) showed two discrete lesions of 70% eccentric mid-RCA and distal RCA showed an 80% lesion.

Since he needed time to arrange his finances the RF ablation was deferred.

On 18 March 2013 he underwent percutaneous coronary intervention to the LAD and RCA and three stents were placed mid-LAD-2.75X23 Xience V (DES) and in the RCA 2.25X12 Xience V was placed in the mid-RCA and 3×23 Xience V (DES) in the proximal RCA. All vessels had thrombolysis in myocardial infarction score 3 flow and the patient was stabilised and sent home.

Since his finances were exhausted he had to go to the nearby centre to do his EP study and further tests. At this time we thought that the tachycardia could be VT as he definitely had coronary lesions. We also thought that he might have had a myocardial or epicardial type of VT.

In the neighbouring centre an EP study showed that the earliest atrial activation was in CS (coronary sinus) 1,2; distal CS) on ventricular pacing consistent with a left anterolateral pathway (figures 4–9). So radiofrequency ablation was carried out. His δ wave disappeared. The protocol briefly was: incremental ventricular pacing showed eccentric non-decremental conduction with ventriculo-atrial time (VA) fusion at the distal CS. The earliest A was observed at the distal CS suggestive of left lateral pathway. Atrial pacing showed increasing degrees of pre-excitation with the morphology suggestive of a left lateral pathway. The effective refractory periods of the accessary pathway (AP) were 280 and 270 ms for antegrade and retrograde effective refractory periods. The tachycardia was easily inducible with atrial and ventricular protocols. The tachycardia cycle length was 420 ms. Entrainment suggested atrioventricular reciprocating tachycardia. The mitral annulus was mapped and (after septal puncture) and at the 2 o’clock position the A and V were fused and the signals were the earliest. So RF ablation was performed in sinus rhythm and A and V separation occurred in 2 s and the tachycardia was non-inducible after this and the δ wave disappeared. Post-RF ablation the retrograde protocols showed VA dissociation. His basal intervals are shown in figure 9. His cycle length was 764 ms and his basal AH interval was 66 ms and his basal HV interval was 30 ms.

Figure 4.

The intracardiac recording showing a one one relationship of A and V, denoting it is a superventricular tachycardia. No A V dissociation seen.

Figure 5.

Intracardiac atrial pacing at 600 ms. Note atrial pacing does not entrain the tachycardia showing it is not a VT.

Figure 6.

The intracardiac ECG showing atrial pacing at 370 ms.

Figure 7.

The fused A and V before ablation and their separation after ablation (in the later half of the image) showing successful ablation of the pathway.

Figure 8.

Postradiofrequency ablation showing VA dissociation.

Figure 9.

The patient's basal intervals are given here. His cycle length was 764 ms and his basal AH interval was 66 ms and his HV interval was 30 ms.

Further briefly the patient also had evidence of dual AV nodal pathways/physiology but no echo or atrioventricular nodal re-entry tachycardia could be induced.

Differential diagnosis

• Atrial fibrillation with a wide QRS

• Pre-excited tachycardia(SVT)

• VT, even may epicardial VT.

Outcome and follow-up

The patient is fine and comes for follow-up. He has no tachycardia.

Discussion

A few words about how to distinguish SVT from VT. Issa¹ has summarised it simply.

First look at the AV relationship: dissociated P waves and A/V ratio less than 1 favours VT. The presence of fusion beats and capture beats favours VT.

Next look at the QRS duration: more than 160 ms in left bundle branch block (LBBB) morphology or more than 140 ms in right BBB (RBBB) morphology tachycardia favours VT.¹ Further if the QRS is narrower during the VT or tachycardia than in sinus rhythm, it means it is VT. Then utilising the previous criteria described by Marriot, for Marriots central lead 1 lead, if the onset QRS to peak of the QRS is more than 50 ms it is VT.

Next look at the QRS axis: an axis shift of >40° between normal sinus rhythm (NSR) and wide complex tachycardias (WCT), a north west axis or a left axis deviation in a patient with RBBB or a right axis deviation in an LBBB morphology again favours VT.

Precordial QRS concordance:

Positive concordance or negative concordance favour VT.

QRS morphology: in RBBB tachycardias: here monophasic R, biphasic qR complexes or broad R (more than 40 ms) in lead V1, or the rabbit ear sign, with the left rabbit ear higher, rS in V6 or contralateral BBB in WCT and NSR all favour VT.

The QRS morphology in LBBB pattern WCT of a broad initial R wave greater than 40 ms in V1 or V2, R wave in lead V1, during the wide complex tachycardia taller than the R wave during NSR, notching of the S wave in V1 or RS interval more than 70 ms in V1 or V2 all of these favour VT. A Q or QS in lead V6 favours VT. Negative QRS deflection in V6 favours VT.

So our patient has some features that superficially resemble VT, that too VT of epicardial origin. (Such as pseudo-δ wave, wide complexes, capture beats and negative QRS in V5 and V6.) But the EP study showed this was only an ordinary anterolateral pathway.

What are the ECG features of an epicardial VT? To review

The epicardial origin of a VT is suspected when the following features are present.^{2 3} A pseudo-δ wave of >34 ms, intrinsicoid deflection in V2 >than 85 ms and shortest RS duration more than 120 ms and maximum deflection index more than 0.55 (2.3). These VTs have an RBBB morphology usually.

Vallas et al⁴ have defined the ECG criteria for epicardial VT in non-ischaemic dilated cardiomyopathy. They are the following—they identified a step-wise algorithm to identify epicardial VT. They studied the QRS from 16 epicardially ablatable VTs and eight endocardial mapped VTs. They found that a q wave in lead 1 was found in 90% of the epicardial VTs and only in 4% of endocardial VTs (p<0.001) and it correctly identified 14/16 epicardial VTs (sensitivity of 88% and specificity of 88%). No other single criterion was helpful in identifying the site of origin of the VT in non-ischaemic dilated cardiomyopathy (DCM). But four of the following criteria could identify epicardial VTs. These were—Q in lead 1, a pseudo-δ wave of ≥ 75 ms. A maximum deflection index of ≥0.59.

Identifying that a possible VT is from the epicardium is not easy. Pacing from the epicardium⁵ has been used to identify the epicardial origin of a VT. Inada et al⁵ describe a patient who had cardiomyopathy, prior cardiac surgery and recurrent VT that failed endocardial ablation. They realised that the patient had an epicardial lead (of the biventricular internal cardioverter defibrillator) that was placed over the myocardial scar. So they paced from this epicardial lead during a VT. They found entrainment with concealed fusion with a long stimulus to QRS interval meaning it was an epicardial VT. So they performed surgical cryoablation of the VT at this site and the VT was terminated.

Berruezo et al⁶ analysed 14 cases of VT that could not be ablated through the endocardial route and compared the ECG findings of this group to those who were successfully ablated from the endocardial route. They found that the epicardial VTs had a pseudo-δ wave. This had a duration of less than or equal to 34 ms; they had an intrinsicoid deflection time of greater than or equal to 85 ms and on measuring the narrowest RS complex this was more than 121 ms and these had a sensitivity of more than 75% and specificity of more than 80% identifying epicardial VT. They thought that on pacing patients with suspected epicardial VT, while pacing from the epicardium, activation of the myocardium occurred through the myocardial cells and so it was wide and had a pseudo-δ wave. But pacing from the endocardium utilised the specific His Purkinjee fibres so the QRS was narrow. So they also showed that on endocardial pacing, VTs of endocardial origin are narrow and on epicardial pacing, VTs of epicardial origin are wider. And the two groups were statistically significantly different.

No ECG feature consistently predicted an epicardial LV-VT origin in infarct-related tachycardias.⁷ The epicardial VTs had longer QRS durations (189±32 ms in epicardial vs 179±37 ms in endocardial, p=0.28) but similar pseudo-δ durations was 38±27 vs 47±27 ms (p=0.2), similar intrinsicoid deflection times 93±35 vs 86±32 ms (p=0.4) and the shortest RS times were not different in epicardial versus endocardial VTs in postmyocardial infarction patients (97±38 vs 99±32 ms (p=0.77) and median deflection index 0.82±0.25 versus 0.87±0.22 (p=0.43). So in postmyocardial infarction VTs these criteria may not help.

In another article Berruezo et al⁸ described a young man with almost a normal heart developing a ventricular tachycardia. He was a 23-year-old man who caused a traffic accident due to syncope. His ECG had small q waves in 2,3, avf. and slight elevation of the of ST segment in these leads and premature ventricular complexes with RBBB morphology and superior axis. His echocardiogram was normal. He developed a monomorphic VT at the rate of 220/min. His CAG was normal. He underwent a left ventricular (LV) angiogram that showed a normal EF and a small aneurysm of the inferolateral wall. This patient had an incessant arrhythmia. This VT appeared to have the criteria for epicardial VT. So an epicardial mapping was performed and in the area of the aneurysm there was a diastolic fragmented potential in sinus rhythm and an electrogram in this region was 18 ms earlier than the pseudo-δ wave, so RF ablation was performed here (temperature 60° and voltage 55 W). The VT stopped and was no longer inducible. This fitted in with the Ouyang syndrome–the exercise induced subepicardial VT of re-entrant origin seen in patients with inferolateral aneurysms in patients with normal coronaries. Until today only four cases have been described (until 2006).

Just a word on how epicardial origin VTs became important—they were first described in Chagas’ disease. In this condition 70% of the VTs are epicardial.⁹ Hsia et al⁹ described the technique of epicardial space entry by percutaneous means for VT ablation in the 1990s.

Learning points.

• All patients with fusion beats and capture beats may not have ventricular tachychardia (VT).

• If a δ wave is seen during a wide QRS tachycardia pre-excited tachycardia or epicardial VTs both should both be considered.

• The first step in any electrophysiological study is a coronary angiogram, as the arrhythmia may be secondary to a recent the acute coronary syndromes or myocardial infarction.

• As is already well known an acute myocardial infarction can have an arrhythmia due to a bypass tract.