Interesting presentation of a broad complex tachycardia during the head up tilt table test

Abstract

Broad complex tachycardia (BCT) during head up tilt test (HUTT) is infrequent. Electrophysiology Study (EPS) plays an important part in further differentiation of BCT. We present a case of BCT during HUTT in a patient presenting with presyncope which later on EPS with 3D mapping was diagnosed as ventricular tachycardia. This case highlights the unusual occurrence of BCT during HUTT, the differential diagnosis of BCT and the utility of EPS to reliably identify the type and origin of BCT.

Background

Broad complex tachycardia (BCT) can be life-threatening and needs urgent evaluation and treatment. In patients with ischaemic heart disease (IHD), BCT is likely ventricular tachycardia (VT), that is, 80% of cases.¹ BCT could also be secondary to other causes like supraventricular tachycardia with aberrancy, pre-excited atrioventricular (AV) re-entry tachycardia secondary to Wolf-Parkinson-White syndrome, metabolic abnormalities and pacemaker mediated tachycardia. Reliably distinguishing VT from other causes of BCT has been the corner stone of its management. Occurrence of BCT during head up tilt test (HUTT) is uncommon, to our knowledge, there is only one study that has reported the incidence of BCT during HUTT to be around 0.04%.² The occurrence of VT and ventricular fibrillation in patients with IHD during HUTT with isoproterenol augmentation has also been reported.²

We describe a case of BCT induced during the HUTT without isoproterenol augmentation in a patient being evaluated for presyncope. This case lays emphasis on the differential diagnosis of BCT and workup of BCT to distinguish VT from other causes of BCT for appropriate patient’s management.

Case presentation

A 45-year-old man with background history of IHD and angioplasty to left anterior descending coronary artery 10 years ago presented to the cardiology clinic with symptoms suggestive of presyncope (dizziness and lightheadedness). The presyncope was primarily exertional; however, it also happened at rest occasionally. Patient did not describe situational symptoms that usually happen before reflex syncope. He needed preoperative clearance before anal fistula surgery. He denied any other significant cardiac symptoms that is, chest pain, shortness of breath and/or palpitations. His medications included aspirin, atorvastatin, and beta blocker.

As a part of workup for evaluation of presyncope before clearance for anal fistula surgery, his primary cardiologist advised him a transthoracic echocardiogram and a HUTT as cardiology team believed that symptoms could be vasovagal in nature. The echocardiogram showed left ventricular (LV) ejection fraction of 45%–50%, no diastolic dysfunction or significant valvular abnormality.

During HUTT, his resting ECG was normal (figure 1A) and also during the non-provocation phase of HUTT it was unremarkable but subsequently after administration of sublingual glyceryl trinitrate (GTN) 500 μg he developed a BCT at 139 beats/min (figure 1B). During the whole HUTT, he remained asymptomatic except during the BCT, when he had mild dizziness. The dizziness was spontaneous and occurred with the onset of BCT. We believe that the dizziness was likely because of decrease in cardiac output with VT. Furthermore, the patient’s systolic blood pressure did drop to about 20 mm Hg from 125/80 mm Hg to 105/70 mm Hg during HUTT, however, it did not drop significantly enough to cause haemodynamic compromise. There could be multiple mechanisms for dizziness without unstable blood pressure including loss of atrial kick during BCT due to AV dissociation, or retrograde activation of atrium during BCT (as in our case) or GTN induced vasodilation with mildly lower blood pressure as noted in our patient.

Figure 1.

(A) Resting normal ECG at initiation of HUTT, no delta waves are seen. (B) Broad complex tachycardia during provocation with sublingual glyceryl trinitrate. ECG shows QRS duration of 139 ms with a delta wave (yellow stars) that is usually characteristics of a WPW syndrome. However, the P waves (red arrows) are clearly visible in the ST segments. Therefore 1:1 VA conduction is seen on the ECG. Also the QRS transition is between V1 and V2 which suggests the tachycardia origin within the interventricular septum. HUTT, during head up tilt test. Leads I, II, III, aVR, aVL, aVF, V1-V5 are standard 12 ECG leads.

For further evaluation of BCT, he was referred to the cardiac electrophysiology team. His recent investigations and ECG traces during HUTT were reviewed in the clinic and an Electrophysiology Study (EPS) was scheduled to identify the type and origin of BCT. The main differentials were VT and antidromic atrioventricular reentry tachycardia (AVRT). The EPS was performed with fluoroscopy guidance. During the EPS, ventricular pacing was decremental with central coronary sinus activation while atrial pacing showed no pre-excitation or delta wave. Postdobutamine augmentation same BCT was induced with leftward axis and transition between V1 and V2 at a ventricular rate of 140beat/min. During BCT, the patient remained haemodynamically stable and his blood pressure was 95/65 mm Hg. BCT was confirmed as VT with AV dissociation with faster atrial pacing (figure 2).

Figure 2.

Broad complex tachycardia induced during EP study. Ventriculo-atrial (VA) dissociation and no change in morphology during atrial straight pacing.

The patient was counselled regarding VT and discussed regarding implantable cardioverter defibrillator (ICD), however, the patient refused ICD implantation. After discussion, we decided to go for a VT ablation with 3D mapping after anal fistula surgery. It was decided to treat him medically during this period on amiodarone therapy. The patient underwent anal fistula surgery uneventfully. Postsurgery patient had persistent symptoms of presyncope on stopping amiodarone. Successful VT ablation was then performed with 3D mapping. The 3D mapping identified the VT focus about 10 mm away from the his bundle.

Investigations

Echocardiogram

LV ejection fraction of 45%–50%. There was no diastolic dysfunction or significant valvular abnormality.

Heads up tilt table test

HUTT was done with sublingual glyceryl tri nitrate (GTN) provocation. During the procedure, the patient remained asymptomatic and his blood pressure remained stable. Provocative phase of HUTT was unremarkable and ECG showed no significant findings but subsequently during provocation with GTN 500 μg, BCT at rate of 139 beats/min with short RP interval was evident and there was no change of axis (figure 1).

Electrophysiology Study

EP study was performed initially with fluoroscopy guidance. During EP study, ventricular pacing was decremental with central coronary sinus activation while atrial pacing showed no pre-excitation. But no BCT was induced. So intravenous dobutamine infusion at 20 ug/min was used for tachycardia induction. BCT was then induced with leftward axis and transition between V1 and V2 at a ventricular rate of 140beat/min. During BCT, the patient remained haemodynamically stable. BCT was confirmed as VT with AV dissociation with faster atrial pacing (figure 2). Ventricular entrainment showed postpacing interval of 45 ms from mid ventricular septum and 110 ms from right ventricular apex which was suggestive of VT focus likely from mid-interventicular septum. Subsequently 3D electroanatomical mapping was used and it identified the VT focus about 10 mm away from the his bundle on the LV side.

Differential diagnosis

The main differentials for BCT seen on HUTT were following and EPS was done for delineation:

1. VT, that is, a fast rhythm originating from an abnormal ventricular focus.

2. AVRT with pre-excitation, that is, tachyarrhythmia that uses the accessory pathway for propagation of impulse from atria to ventricles.

Treatment

As the patient was diagnosed to have VT so he was counselled regarding device therapy with ICD and further demarcation of VT focus with 3D (Three-dimensional) mapping and ablation. It was initially agreed to proceed for anal fistula surgery on amiodarone. A Holter monitor was performed before and after starting patient on amiodarone. The Holter monitor postamiodarone showed no ventricular ectopics and no VT episodes thus the patient was proceeded for surgery. During the perioperative period, strict arrhythmia monitoring was done and electrolyte imbalance was avoided. Postsurgery patient underwent EP study and ablation with 3D mapping for the VT.

Outcome and follow-up

Patient is stable and free of symptoms on recent follow-up at 1-year postablation. His repeat Holter monitor did not show any BCT. He remained on aspirin, atorvastatin and B blocker therapy.

Discussion

HUTT with nitrate augmentation is a useful test for workup and management of patients presenting with pre syncope and syncope, addition of nitrate enhances the rate of positive tilt test while maintaining the specificity.³ To best of our knowledge although VF has been reported in patients undergoing HUTT with isoproterenol augmentation⁴ but no case of occurrence of VT has been reported. This the first case of BCT reported on HUTT with nitrate provocation. A BCT can either be VT in 80% of cases or a supraventricular tachycardia with aberrant conduction in remaining 20% of patients.¹

In our case appropriate workup was done with echocardiography and invasive EP study as per recent European Society of Cardiology (ESC) guidelines.⁵ But as focus of arrhythmia was found to be near his bundle so pros and cons of treatment with ablation were discussed with the patient as described above as ESC guidelines recommend ablation as class I treatment for VT in patients with IHD.⁵ Moreover, ablation has also been suggested as treatment modality of choice in a recent Survey by European Heart Rhythm Association among patients with cardiomyopathy and impaired EF (same as in our patient) as this study indicated that

VT ablation was preferred intervention in 62.0% of the responding centres in such cases, while medical therapy with amiodarone was instituted only in 19.7% of the responding centres.⁶ This approach for ablation as first line therapy before ICD implantation has also been advocated by well-known VTACH trial.⁷ Contemporary guidelines also recommend ICD therapy as class I indication in patients with syncope of undetermined origin with clinically relevant, haemodynamically significant VA induced at EP study.⁸

As our patient was scheduled for anal fistula surgery soon and he also had denied for ICD implant. So it was a tough scenario in terms of patient management while respecting patient’s autonomy. So we had to keep our patient on medical therapy with amiodarone along with beta blocker along with strict arrhythmia monitoring and avoidance of electrolyte imbalance in accordance with guidelines.⁵

Parahisian ventricular arrhythmias accounts for up to 10% of all idiopathic VTs⁹ and characterised by origin with in 10 mm of his cloud or those with earliest recorded activation in presence of a His potential after mapping of all nearby structures. Such VTs are difficult to ablate as there is high risk for AV block.¹⁰ Key idea when dealing with parahisian ventricular arrhythmias is to carry out thorough 3D mapping of all the nearby structures with a systematic approach before performing any ablation as AV block requiring permanent pacemaker occurs in about 10% of cases.¹¹ Recent literature in this respect has demonstrated that cryoablation yields successful results in up to 70% of the cases in patients with prior unsuccessful radiofrequency ablation.¹¹

Through this case we actually wanted to highlight the fact that the HUTT in patients with previous IHD could results in VT especially if syncopal symptoms are not typical of reflex vasovagal syncope. Thus HUTT with GTN provocation in patients with IHD should be avoided unless ischaemia has been completely ruled out as vasodilatation caused by GTN may alter the electrophysiological properties of myocardium leading to ventricular arrhythmias. The mechanisms known for causing arrhythmia include automaticity, re-entry and delayed after depolarisation. We believe that the mechanism of VT in our patient was likely due to automaticity. The other mechanism which could be possible in our patient is microre-entry. The mechanism by which vasodilation with GTN leads to either of those is because of localised ischaemia due to a phenomenon termed ‘coronary steal’. There is alteration of circulation patterns in coronary vessels which leads to a reduction in the blood flow.¹² When a coronary vasodilatory agent like GTN is used in a patient with coronary artery disease, there is diversion of blood away from those parts of the heart which are supplied by coronaries narrowed by atherosclerotic disease due to these narrowed vessels being already maximally dilated to compensate for the decreased blood supply.¹³ Due to dilatation of the resistance vessels in the coronary circulation by the GTN blood is shunted away from the myocardial areas these vessels supply and this may provoke or lead to arrhythmogenesis.

The VT during EPS with dobutamine occurred as dobutamine is known to increase automaticity of cardiac muscle. This increase in automaticity is further enhanced in ischaemic or fibrosed areas of the myocardium. Similar agents, that is, isoprenaline has been used frequently to induce arrhythmia during an electrophysiological study.

Patient’s perspective.

This section is written on basis of patient’s input in electrophysiology clinic on his follow-up visit after treatment for arrhythmia. It includes his perspective on his ailment and his experience throughout the course of management and effect of treatment.

• I was diagnosed to have this condition (Ventricular tachycardia) during my workup before surgery for anal fistula. I had history of cardiac event around 10 years back for which stent was placed. I have been very vigilant of my cardiac status and compliant to treatment and regular follow-up with my cardiologist since then. I had no significant complaints in this regard but started having dizziness occasionally around the time of my anal fistula ailment which required surgery. As I was worried in this regard so I discussed this with my cardiologist and was advised some extra tests before fitness for surgery by him. The results of these initial tests were bit concerning and added to my worries when I was already having surgery for anal fistula in coming days. So I was referred to heart rhythm disorder specialist. I was explained about this new heart rhythm issue and that it needed another procedure to clarify its cause and possible treatment before I could be declared fit for surgery.

• I was found to have a life threatening rhythm disorder named ‘ventricular tachycardia’ during procedure and was counselled by the electrophysiology team about the gravity of this new incidentally found illness. It was distressing for me as I had a surgery planned shortly back then. I was told that bad rhythm that was the cause of my new cardiac symptoms was a rare one and was not straight forward to treat during the same procedure, I was also guided for placement of cardiac device to treat this life rhythm disorder if needed in future. As I was very much distressed for upcoming surgery so i opted for medical treatment of this newly found rhythm disorder instead and was prescribed a new medication. I underwent anal fistula surgery safely. During my anal surgery heart rhythm disorder team worked in close cooperation with my surgeon and ensured that I had a safe procedure and hospital course.

• Few weeks after my recovery from anal surgery I started having same dizzy spells and I was advised to undergo same procedure as prior but with some new modality for treatment of my rhythm disorder. I was told that I had this rhythm originating from left lower chamber of my heart.

• I have been well after treatment of my rhythm disorder and luckily had no adverse effects of procedure. I am extremely thankful to all physicians who worked for my treatment and I would urge all cardiac patients to take their symptoms seriously and seek medical attention in time.

Learning points.

• Avoidance of head up tilt test in patients with history of ischaemic heart disease and suspicion of ischaemia.

• Importance of proper knowledge of differential diagnoses of broad complex tachycardia (BCT) as especially in a patient with predisposing risk factors for ventricular arrhythmias.

• Pathway for workup of BCT to reach the final diagnosis.

• Implications of ablations and risks with parahisian focus.

• Institution of proper treatment in long term.

• Perioperative management of patient with ventricular tachycardia.

• Modification of treatment plan in conjunction with patient’s autonomy.

Ethics statements

Patient consent for publication

Obtained.