|
 |
| CASE REPORT |
|
| Year : 2017 | Volume
: 18
| Issue : 3 | Page : 83-87 |
|
|
Idiopathic fascicular left ventricular tachycardia
Yaser Alahmad, Nidal Ahmad Asaad, Salaheddin Omran Arafa, Shahul Hameed Ahmad Khan, Alsayed Mahmoud
Department of Cardiology, Heart Hospital, Hamad Medical Corporation, Doha, Qatar
| Date of Web Publication | 8-Nov-2017 |
Correspondence Address:
Nidal Ahmad Asaad
Department of Cardiology, Heart Hospital, Hamad Medical Corporation, P. O. Box 3050, Doha
Qatar
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/HEARTVIEWS.HEARTVIEWS_145_15
 Abstract | | |
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. Keywords: Left fascicular ventricular tachycardia, right bundle branch block narrow complex tachycardia
How to cite this article:
Alahmad Y, Asaad NA, Arafa SO, Ahmad Khan SH, Mahmoud A. Idiopathic fascicular left ventricular tachycardia. Heart Views 2017;18:83-7 |
| 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.[4],[5] It is also characterized by the absence of structural heart disease and classic electrocardiographic and electrophysiological features.[4],[6],[7]
Vagal maneuvers, adenosine, and lidocaine are ineffective in suppressing fascicular tachycardia.[4],[6],[8] In contrast, it is terminated or suppressed by calcium antagonists.[4],[5],[6],[7],[9]
| 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)
Click here to view |
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)
Click here to view |
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
Click here to view |
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%).[10],[11] 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.[13],[14]
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].
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.[17],[18] 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.[19],[20]
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
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.
| References | | |
| 1. | Zipes DP, Foster PR, Troup PJ, Pedersen DH. Atrial induction of ventricular tachycardia: Reentry versus triggered automaticity. Am J Cardiol 1979;44:1-8.  [ PUBMED] |
| 2. | Lerman BB, Stein KM, Markowitz SM. Mechanisms of idiopathic left ventricular tachycardia. J Cardiovasc Electrophysiol 1997;8:571-83. [ PUBMED] |
| 3. | Belhassen B, Rotmensch HH, Laniado S. Response of recurrent sustained ventricular tachycardia to verapamil. Br Heart J 1981;46:679-82. [ PUBMED] |
| 4. | Lin FC, Finley CD, Rahimtoola SH, Wu D. Idiopathic paroxysmal ventricular tachycardia with a QRS pattern of right bundle branch block and left axis deviation: A unique clinical entity with specific properties. Am J Cardiol 1983;52:95-100. [ PUBMED] |
| 5. | Ward DE, Nathan AW, Camm AJ. Fascicular tachycardia sensitive to calcium antagonists. Eur Heart J 1984;5:896-905. [ PUBMED] |
| 6. | Ohe T, Shimomura K, Aihara N, Kamakura S, Matsuhisa M, Sato I, et al. Idiopathic sustained left ventricular tachycardia: Clinical and electrophysiologic characteristics. Circulation 1988;77:560-8. [ PUBMED] |
| 7. | Andrade FR, Eslami M, Elias J, Kinoshita O, Nakazato Y, Marcus FI, et al. Diagnostic clues from the surface ECG to identify idiopathic (fascicular) ventricular tachycardia: Correlation with electrophysiologic findings. J Cardiovasc Electrophysiol 1996;7:2-8. [ PUBMED] |
| 8. | Griffith MJ, Garratt CJ, Rowland E, Ward DE, Camm AJ. Effects of intravenous adenosine on verapamil-sensitive “idiopathic” ventricular tachycardia. Am J Cardiol 1994;73:759-64. [ PUBMED] |
| 9. | Ohe T. Idiopathic verapamil-sensitive sustained left ventricular tachycardia. Clin Cardiol 1993;16:139-41. [ PUBMED] |
| 10. | Gaita F, Giustetto C, Leclercq JF, Haissaguerre M, Riccardi R, Libero L, et al. Idiopathic verapamil-responsive left ventricular tachycardia: Clinical characteristics and long-term follow-up of 33 patients. Eur Heart J 1994;15:1252-60. |
| 11. | Nakagawa M, Takahashi N, Nobe S, Ichinose M, Ooie T, Yufu F, et al. Gender differences in various types of idiopathic ventricular tachycardia. J Cardiovasc Electrophysiol 2002;13:633-8. |
| 12. | Ohe T, Aihara N, Kamakura S, Kurita T, Shimizu W, Shimomura K. Long-term outcome of verapamil-sensitive sustained left ventricular tachycardia in patients without structural heart disease. J Am Coll Cardiol 1995;25:54-8. |
| 13. | Nakagawa H, Beckman KJ, McClelland JH, Wang X, Arruda M, Santoro I, et al. Radiofrequency catheter ablation of idiopathic left ventricular tachycardia guided by a Purkinje potential. Circulation 1993;88:2607-17. |
| 14. | Tsuchiya T, Okumura K, Honda T, Iwasa A, Ashikaga K. Effects of verapamil and lidocaine on two components of the re-entry circuit of verapamil-senstitive idiopathic left ventricular tachycardia. J Am Coll Cardiol 2001;37:1415-21. |
| 15. | Nogami A, Naito S, Tada H, Oshima S, Taniguchi K, Aonuma K, et al. Verapamil-sensitive left anterior fascicular ventricular tachycardia: Results of radiofrequency ablation in six patients. J Cardiovasc Electrophysiol 1998;9:1269-78. |
| 16. | Lerman BB. Response of nonreentrant catecholamine-mediated ventricular tachycardia to endogenous adenosine and acetylcholine. Evidence for myocardial receptor-mediated effects. Circulation 1993;87:382-90. |
| 17. | Nakagawa H, Beckman KJ, McClelland JH, Wang X, Arruda M, Santoro I, et al. Radiofrequency catheter ablation of idiopathic left ventricular tachycardia guided by a Purkinje potential. Circulation 1993;88:2607-17. |
| 18. | Wen MS, Yeh SJ, Wang CC, Lin FC, Wu D. Successful radiofrequency ablation of idiopathic left ventricular tachycardia at a site away from the tachycardia exit. J Am Coll Cardiol 1997;30:1024-31. |
| 19. | Peichl P, Wichterle D, Pavlu L, Cihak R, Aldhoon B, Kautzner J. Complications of catheter ablation of ventricular tachycardia: A single-center experience. Circ Arrhythm Electrophysiol 2014;7:684-90. |
| 20. | Lamberti F, Di Clemente F, Remoli R, Bellini C, De Santis A, Mercurio M, et al. Catheter ablation of idiopathic ventricular tachycardia without the use of fluoroscopy. Int J Cardiol 2015;190:338-43. |
[Figure 1], [Figure 2], [Figure 3]
[Table 1]
|
