Uncommon cause of wide complex tachycardia - Anterior fascicular ventricular tachycardia

Ramadan Fouad Arafa; Hussein Heshmat; Rajesh Rajan; Peter A Brady

doi:10.4103/ACCJ.ACCJ_7_18

CASE REPORT

Year : 2019 | Volume : 1 | Issue : 1 | Page : 37-38

Uncommon cause of wide complex tachycardia - Anterior fascicular ventricular tachycardia

Ramadan Fouad Arafa¹, Hussein Heshmat², Rajesh Rajan³, Peter A Brady⁴
¹ Department of Cardiology, Fujairah Hospital, Fujairah, UAE
² Department of Cardiology, Fujairah Hospital, Fujairah, UAE; Department of Cardiology, Cairo University, Giza, Egypt
³ Department of Cardiology, Sabah Al-Ahmed Cardiac Center, Kuwait City, Kuwait
⁴ Department of Electrophysiology, Mercy Heart Health System, Lowa City, USA

Date of Submission	28-Nov-2018
Date of Decision	18-Oct-2019
Date of Acceptance	22-Oct-2019
Date of Web Publication	13-Dec-2019

Correspondence Address:
Dr. Ramadan Fouad Arafa
P O Box 7498, Fujairah
UAE

Source of Support: None, Conflict of Interest: None

DOI: 10.4103/ACCJ.ACCJ_7_18

Abstract

A 24-year-old female presented to the emergency room with sudden-onset palpitations and shortness of breath for 4 h. We report a rare cause of anterior fascicular ventricular tachycardia.

Keywords: Anterior fascicular ventricular tachycardia, palpitations, wide QRS complex tachycardia

How to cite this article:
Arafa RF, Heshmat H, Rajan R, Brady PA. Uncommon cause of wide complex tachycardia - Anterior fascicular ventricular tachycardia. Ann Clin Cardiol 2019;1:37-8

How to cite this URL:
Arafa RF, Heshmat H, Rajan R, Brady PA. Uncommon cause of wide complex tachycardia - Anterior fascicular ventricular tachycardia. Ann Clin Cardiol [serial online] 2019 [cited 2023 Mar 26];1:37-8. Available from: http://www.onlineacc.org/text.asp?2019/1/1/37/273004

Introduction

In majority of the cases, fascicular tachycardia associated with underlying structural heart disease. It originates from the region of the posterior fascicle (or occasionally the anterior fascicle) of the left bundle branch and is partly propagated by the His-Purkinje network, which gives rise to narrow QRS complexes (0.11–0.14 s). Consequently, this arrhythmia is commonly misdiagnosed as supraventricular tachycardia (SVT).^[1]

Case Report

A 24-year-old female presented to the emergency room with sudden-onset palpitations and shortness of breath for 4 h. She denied associated chest pain, presyncope, or syncope. She admitted two similar episodes of shorter duration in the last 6 months, for which she did not seek medical attention. On examination at the time of admission, her heart rate was 203/min and regular; blood pressure was 112/80 mmHg. The remaining examination was unremarkable. A 12-lead electrocardiogram (ECG) obtained during symptoms is shown in [Figure 1]. Subsequent evaluation revealed no evidence of structural heart disease.

Figure 1: 12-lead ECG showing anterior fasicular ventricular tachycardia

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ECG showed wide QRS complex tachycardia with right bundle branch block (RBBB) morphology and right-axis deviation. The QRS duration is 110 ms. AV dissociation is present.

Carotid massage, valsalva maneuver, and adenosine injection failed to revert to sinus rhythm. Verapamil 2.5 mg injection intravenous (iv) was given, and it was reverted to sinus rhythm [Figure 2].

Figure 2: ECG after the administration of IV Verapamil 2.5mg

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She was continued on verapamil. Hospital stay was eventless and discharged on verapamil tablets.

Discussion

In the vast majority of cases, a wide complex tachycardia is due to ventricular tachycardia (VT), especially in the presence of structural heart disease such as prior myocardial infarction. VT can be seen in the absence of structural heart disease, the so-called “normal heart” VT. Most commonly, normal heart VT arises from the right or, less commonly, the left ventricular outflow tract. This origin results in an ECG pattern of left bundle branch block type with QRS transition beyond lead V3 or V4. Another type of normal heart VT is “verapamil-sensitive” VT which arises from the fascicular fibers of the left ventricle. Because the circuit arises within left ventricular myocardium, the ECG pattern is RBBB in V1 with a rightward or leftward axis depending on whether the exit point is the anterior or posterior fascicle. Usually, in the emergency room, the exact diagnosis of fascicular tachycardia seems difficult. It is commonly seen in young patients with no structural heart diseases. The arrhythmia may mimic either SVT or VT. Capture beats and fusion beats may be present on suggesting the diagnosis of VT rather than SVT.^[2] Our patient was initially diagnosed as SVT with RBBB, but the lack of response to vagal stimulation and adenosine made this diagnosis is less likely. The correct diagnosis was suggested by the presence of a broad complex tachycardia with a RBBB morphology and right-axis deviation. The QRS duration in fascicular tachycardia can vary from 100 to 140 ms.^[3] The RS interval is uniformly <80 ms in contrast with VT associated with structural heart disease where the RS interval is generally >100 ms.^[3] After reversion to sinus rhythm, nonspecific ST segment and T wave changes may be seen, most commonly in the inferior or lateral chest leads.^[4]

Fascicular tachycardia has been classified into three subtypes: (a) left posterior fascicular VT with a RBBB pattern and left-axis deviation (common form); (b) left anterior fascicular VT with RBBB pattern and right-axis deviation (uncommon form, like our patient); and (c) upper septal fascicular VT with a narrow QRS and normal-axis configuration (rare form).^[5]

The pharmacological treatment of choice for fascicular tachycardia is iv verapamil.^[3],[4] However, propranolol may be used to terminate and cure the attack of fascicular tachycardia.^[6] Misdiagnosis of SVT is common and is mainly due to its dramatic response to calcium channel block. Sotalol and amiodarone have also been reported to be effective.^[7] Vagal maneuvers, adenosine, and lignocaine have no effective.^[8] Recurrences may be prevented by long-term, oral verapamil.^[7] Radiofrequency ablation has been reported to be successful in >80% of patients and complications are infrequent.^[9]

Conclusion

In most cases, a broad complex tachycardia should be presumed to be VT, especially in the presence of structural heart disease. Less commonly, VT may arise in the normal heart and may respond to adenosine or verapamil. However, before administering these agents, careful analysis of the 12-lead ECG should be undertaken to confirm the diagnosis. In all confirmed cases, iv verapamil is the drug of choice.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.

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