Idiopathic Fascicular Left Ventricular Tachycardia.

Idiopathic left fascicular ventricular tachycardia (ILFVT) is characterized by right bundle branch block morphology and left axis deviation. We report a case of idiopathic left ventricular fascicular tachycardia in a young 31-year-old male patient presenting with a narrow complex tachycardia.

INTRODUCTION

Idiopathic left fascicular ventricular tachycardia (ILFVT) is a ventricular tachycardia (VT) characterized by right bundle branch block (RBBB) and left axis deviation (LAD) on electrocardiogram (ECG). It occurs predominantly in young males (15–40 years old) without structural heart disease.[1]

It represents 10%–15% of all idiopathic left VT seen in clinical practice today.[2] It was first described by Zipes et al. in 1979, when they reported three cases of right bundle branch block (RBBB) and left axis VT with a relatively narrow QRS (120–140 ms) in young patients.[1] In 1981, Belhassen et al. demonstrated that intravenous (IV) administration of verapamil significantly decreased the recurrence rate of idiopathic fascicular left VT (IFLVT) in afflicted patients.[3] It may be confused with either typical VT or supraventricular tachycardia.[45] It is also characterized by the absence of structural heart disease and classic electrocardiographic and electrophysiological features.[467]

Vagal maneuvers, adenosine, and lidocaine are ineffective in suppressing fascicular tachycardia.[468] In contrast, it is terminated or suppressed by calcium antagonists.[45679]

CASE PRESENTATION

A 31-year-old male patient presented to the emergency department with sudden onset of palpitations of 2 h duration. He has no history of chest pain, shortness of breath, or syncopal attack. He had experienced one similar episode 18 months previously that had responded to medical treatment in another hospital. No old medical report was available, and he could not recall what drugs he had been given. There was no significant past medical, family, or surgical history and he was not on any regular medication. He did not smoke and denied any use of alcohol or illicit drug.

Physical examination revealed blood pressure (BP) of 107/72 mm Hg and heart rate of 225 beats/min. On cardiac examination, S1 and S2 were normal, no murmurs, or additional sounds. The chest was clear on auscultation. ECG revealed a narrow complex tachycardia, RBBB, and LAD [Figure 1].

Figure 1

Electrocardiogram at admission showed narrow complex tachycardia, incomplete right bundle branch block (RBBB) with left axis deviation (LAD)

Intravenous adenosine, amiodarone and beta blocker wee tried but failed to terminate the arrhythmia. Cardiology consultation was sought and a diagnosis of fascicular tachycardia was suspected based on ECG findings of narrow complex tachycardia, RBBB and LAD. Additional doses of intravenous verapamil were given which slowed down the heart rate to 170 beats/min. The ECG revealed tachyarrhythmias with AV dissociation which suppots that the origin of tachyarrhythmia was from the left ventricle [Figure 2]. After 12 hours, patient developed shortness of breath and dizziness associated with hypotension with BP 81/50 mmHg. An electrical cardioversion was attempted but failed to terminate the arrhythmia.

Figure 2

Electrocardiogram demonstrated a narrow QRS complex tachycardia with atrioventricular dissociation after intravenous verapamil. The arrows point at the P waves in rhythm strip lead II (P and QRS complexes at different rate)

Subsequently, patient was admitted to the coronary care unit where serial ECGs were done. Laboratory tests revealed normal hemoglobin, liver function tests, renal function tests, serum electrolytes, and thyroid-stimulating hormone.

Initial transthoracic echocardiography during tachycardia revealed moderate global hypokinesia with left ventricular ejection fraction (LVEF) of 45%; other structures were normal. After obtaining informed consent, an electrophysiological study was performed. The electroanatomical bipolar voltage map did not show any area of the ventricular scar. The mechanism of the tachycardia was confirmed as reentry arising from the basal and mid septum. Multiple ablations were performed to the basal and mid septum, guided by Purkinje and P2 potential. The arrhythmia was terminated after ablation, and no arrhythmias could be induced after Isoprenaline administration. The final ECG showed sinus rhythm [Figure 3].

Figure 3

Electrocardiogram revealed normal sinus rhythm after successful catheter ablation therapy

After 24 hours, transthoracic echocardiography was repeated showing normal structures with normal LVEF of 60%. The patient was discharged from the cardiac department after 48 hours with cardiology follow up.

DISCUSSION

The evaluation and management of ventricular tachyarrhythmias are uniquely challenging. When evaluating patients with VT and ventricular fibrillation (VF), several initial distinctions should be made. These include:

Arrhythmia duration – sustained or non-sustained

Arrhythmia morphology – monomorphic VT, polymorphic VT, or VF

Associated symptoms – ranging from none to hemodynamic collapse and sudden cardiac arrest

Associated cardiac disease.

Malignant arrhythmias usually occur in the presence of significant structural heart disease (e.g., coronary heart disease with prior myocardial infarction, dilated cardiomyopathy, or hypertrophic cardiomyopathy). In this setting, ventricular arrhythmias carry a high risk of sudden cardiac death.

ILFVT generally presents in young adults (15–40 years) and mainly affects males (60%–80%).[1011] The most frequent clinical presentation is paroxysmal episodes of palpitations and dizziness. Syncope and sudden death are very rare. Tachycardiomyopathy has been described in the 6% of cases as a result of persistent tachycardia, and it is usually reversible after successful ablation.[12] Although most episodes occur at rest, exercise, emotional stress, and catecholamine infusion can act as triggers.

Although triggered activity was at first postulated as a potential mechanism,[1] later studies showed that IFLVT behaves electrophysiologically as a reentrant tachycardia.[1314]

On the surface ECG, the QRS duration in fascicular tachycardia can vary from 100 to 140 ms. The RS interval is uniformly <80 ms in contrast with VT associated with structural heart disease where the RS interval is generally >100 ms.[7] The electrocardiographical pattern varies depending on the site of origin of the tachycardia [Table 1].

Table 1

Illustration of types of fascicular ventricular tachycardia

The long-term prognosis of patients with fascicular VT without structural heart disease is very good. Arrhythmias in patients with sporadic and well-tolerated episodes of idiopathic left VT may not progress despite the absence of pharmacologic therapy.[12] Patients with moderate symptoms can be treated with oral verapamil (120–480 mg/day). The risk of hemodynamic collapse in cases of the wrong diagnosis makes it advisable to only administer verapamil in stable patients with an established diagnosis. However, unlike other idiopathic VT, IFLVT usually does not respond to vagal maneuvers, adenosine, or beta-blockers. This has been attributed to the fact that IFLVT depends on the slow entry of calcium in partially depolarized Purkinje fibers and not the Cyclic adenosine monophosphate mediated triggered activity occurring in the adenosine-sensitive VT.[16]

Radiofrequency catheter ablation is an appropriate management strategy for patients with severe symptoms or those intolerant or resistant to antiarrhythmic therapy. It could be performed successfully by targeting the earliest high-frequency Purkinje potential during VT.[1718] Ablation success rates as reported in various series vary between 85% and 95% and are generally higher in those patients with posterior IFLVT. Long-term success after catheter ablation is more than 92% with rare complications.[1920]

The most common complication is the development of left bundle branch or AV block. It is also possible to induce mitral regurgitation due to catheter entrapment in the chordae of the mitral valve leaflet in cases of transeptal puncture and aortic regurgitation due to damage to the aortic valve using a retrograde aortic approach.

CONCLUSION

Prompt recognition of this arrhythmia is necessary because it is curable with catheter ablation. In general, if standard methods including vagal maneuvers and adenosine administration fail to convert the arrhythmia and the 12 lead ECG shows a right bundle branch block picture with left axis deviation, a diagnosis of fascicular tachycardia should be considered. In the acute setting, first-line pharmacological treatment is Verapamil. Catheter ablation is an effective treatment method and is recommended when symptoms are severe or when pharmacological treatment is ineffective or poorly tolerated.

Declaration of patient consent

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Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.