the main trunk of the left bundle branch is not part of the re-entry circuit of verapamil-sensitive...
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Journal of Arrhythmia 28 (2012) 232–234
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Journal of Arrhythmia
1880-42
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Case Report
The main trunk of the left bundle branch is not part of the re-entry circuit ofverapamil-sensitive idiopathic left ventricular tachycardia
Eiichiro Nakagawa, MD, PhDa,n, Masahiko Takagi, MD, PhDb, Yukio Abe, MDa, Rhyshi Komatsu, MD,PhDa, Kazuo Haze, MD, PhDa, Takahiko Naruko, MD, PhDa, Akira Itoh, MD, PhDa
a Department of Cardiology, Osaka City General Hospital, 2-13-22 Miyakojima-hondori, Miyakojima-ku, Osaka 534-0021, Japanb Department of Internal Medicine and Cardiology, Osaka City University Medical School, 1-4-3 Asahi-machi, Abeno-ku, Osaka 545-8585, Japan
a r t i c l e i n f o
Article history:
Received 8 November 2011
Received in revised form
29 November 2011
Accepted 6 December 2011Available online 24 April 2012
Keywords:
Verapamil-sensitive idiopathic left
ventricular tachycardia
Left main bundle branch
Left bundle branch block
Ventricular tachycardia circuit
Left ventricular mapping
76/$ - see front matter & 2012 Japanese Hea
x.doi.org/10.1016/j.joa.2011.12.001
esponding author. Tel.: þ81 6 6929 1221; fax
ail address: [email protected] (E. N
a b s t r a c t
We report the case of a 19-year-old man with verapamil-sensitive idiopathic left ventricular tachy-
cardia (ILVT), who had paroxysmal palpitations for 3 years. Programmed right atrial and ventri-
cular stimulation easily induced ventricular tachycardia (VT) with QRS duration of 125 ms, right bundle
branch block pattern, and right inferior axis, which are characteristics of ILVT. Left ventricular
endocardial mapping accidentally produced a complete left bundle branch block and provoked
prolongation of the QRS duration of VT, which was 143 ms. However, no changes occurred in the
cycle length, inducibility, or maintenance of VT. The VT was eliminated successfully by catheter
ablation at the pre-Purkinje potential (PP) recording site. These findings suggest that the main trunk of
the left bundle branch is not a critical component of the re-entry circuit of ILVT.
& 2012 Japanese Heart Rhythm Society. Published by Elsevier B.V. All rights reserved.
1. Introduction
Idiopathic left ventricular tachycardia (ILVT) with a rightbundle-branch block (RBBB) configuration and superior or leftaxis is a distinct entity that arises in the left ventricle, mostlybecause of a reentry mechanism and is usually verapamil sensi-tive [1–6]. Although this type of tachycardia has been suggestedto originate from the Purkinje network [1,5], its precise re-entrycircuit and slow conduction zone remain unclear. However,radiofrequency (RF) catheter ablation has been reported tosuccessfully eliminate this arrhythmia from the left-hand side ofthe interventricular septum, where the earliest Purkinje potential(PP) and late diastolic potential are recorded during ventriculartachycardia (VT). In addition, catheter ablation targeting of theleft posterior fascicle was shown to be another therapeuticstrategy for curing ILVT [7]. These observations raise the possibi-lity that anterior or posterior fascicles compose a critical part ofthe re-entry circuit of ILVT. However, there have been no reportsdescribing the role of the main trunk of the left bundle branch inthe mechanism of ILVT. In this report, we present results indicat-ing the role of main trunk of the left bundle branch in the re-entrycircuit of ILVT in a patient.
rt Rhythm Society. Published by E
: þ81 6 6929 1091.
akagawa).
2. Case report
A 19-year-old man was referred to our hospital in June 2006with a 3-year history of paroxysmal palpitations. An ambulatoryelectrogram monitor showed a regular wide QRS tachycardia. Thepatient was admitted to our hospital for an electrophysiologicalstudy and RF catheter ablation. An initial physical examinationrevealed normal findings and the laboratory parameters were withinnormal limits. A standard 12-lead electrocardiogram obtained duringsinus rhythm showed no abnormalities; other examinations,including a chest roentgenogram and echocardiogram, showedno evidence of structural heart disease or other abnormalities.After obtaining written informed consent, we performed an electro-physiological study and catheter ablation for the regular wideQRS tachycardia. Under fluoroscopic guidance, a 4-Fr quadripolarelectrode catheter, two 5-Fr decapolar electrode catheters, a 5-Frquadripolar electrode catheter (Irvine Biomedical Inc., Irvine, CA,USA), and a 2.5-Fr micro-sized mapping catheter with 8 electrodes(Cardima Inc., Fremont, CA, USA) were introduced into the highright atrium, His-bundle region, left ventricular septum, rightventricular apex, and coronary sinus, respectively, through thefemoral veins and artery. The intracardiac electrocardiogramshowed an atrial-His interval of 85 ms and a His-ventricularinterval of 47 ms at baseline. Right atrial burst pacing and rightand left ventricular burst pacing easily induced tachycardia with aQRS duration of 125 ms, an RBBB pattern, inferior axis, and a cycle
lsevier B.V. All rights reserved.
E. Nakagawa et al. / Journal of Arrhythmia 28 (2012) 232–234 233
length of 320 ms (Fig. 1). Ventriculoatrial dissociation wasobserved during tachycardia and the diagnosis of VT was subsequently established. Ventricular stimulations from the rightventricular apex with constant cycle lengths 10, 20, and 30 msshorter than that of the VT cycle length were performed duringVT and manifest entrainment was confirmed. In addition, a PPpreceding ventricular activation and dull mid-diastolic potential
Fig. 1. A 12-lead electrocardiogram recording of ventricular tachycardia (VT)
induced by atrial burst pacing. Atrial and right and left ventricular burst pacing
easily induced tachycardia with a QRS duration of 125 ms, a right bundle-branch
block pattern, an inferior axis, and a cycle length of 320 ms.
Fig. 2. Intracardiac electrogram of the left and right ventricles during ventricular tach
143 ms. There were no differences in the local ventricular activation sequences of the lef
rhythms with narrow and wide QRS duration. The cycle lengths of the VT rhythms we
preceding PP (pre-PP) were recorded simultaneously during theVT at the mid-septum of the left ventricle, which is characteristicof verapamil-sensitive ILVT. During left ventricular outflow map-ping, we observed a slight spontaneous conversion of the QRSmorphology during VT with prolongation of the QRS durationfrom 125 ms to 143 ms and an identical inferior axis andtachycardia cycle length. A reverse morphological change of theQRS was observed as well. Intracardiac electrograms showed thatthere were no differences in the left ventricular activationsequences between VT with narrow QRS duration and that withwide duration (Fig. 2). RF catheter ablation and left ventricularmapping were performed using a 7-Fr quadripolar ablationcatheter with a 4-mm distal electrode, an embedded thermistor,and a deflectable tip (Marins, Medtronic Inc., Minneapolis, MN,USA). Left ventricular endocardial mapping at the left ventricularoutflow tract accidentally produced a complete left bundle-branch block (CLBBB), and thereafter, only VT with a wide QRSduration of 143 ms was induced (Fig. 3). In addition, no conver-sions of the QRS morphology and no changes of the VT cyclelength were observed. The earliest ventricular activation duringVT was found at the apical septum of the left ventricle, andRF catheter ablation at the basal third of the mid-septum, wherepre-PP and PP were recorded during tachycardia, successfullyeliminated the VT. After ablation, a new diastolic potentialappeared during sinus rhythm at the lower and more basal sitecompared with the successful ablation site; this has beenobserved in some patients with verapamil-sensitive ILVT aftersuccessful ablation [8].
Our study patient underwent follow-up without any anti-arrhythmic medication and has not experienced VT recurrencesduring the 60-month follow-up period.
3. Discussion
The major finding in this case is that the incidental occurrenceof CLBBB in a patient with verapamil-sensitive ILVT had no effecton the inducibility, maintenance, or cycle length of the VT. On the
ycardia (VT) with a narrow QRS duration of 125 ms and a wide QRS duration of
t ventricular base (CS) and the right basal ventricular septum (HIS) between the VT
re the same: 320 ms.
Fig. 3. A 12-lead electrocardiogram recording of accidentally induced complete
left bundle branch block (CLBBB) morphology and the ventricular tachycardia (VT)
with a wide QRS duration induced by premature ventricular beats. Left ventricular
endocardial mapping at the left ventricular outflow tract produced a CLBBB, and
thereafter, only VT with a wide QRS duration of 143 ms was induced.
E. Nakagawa et al. / Journal of Arrhythmia 28 (2012) 232–234234
other hand, it changed the QRS morphology of the VT with awider QRS duration. These findings indicate that the main trunkof the left bundle branch is not a critical component of the re-entry circuit of verapamil-sensitive ILVT.
The mechanism of verapamil-sensitive ILVT has been sug-gested as re-entry with an excitable gap and a slow conduction,because the VT can be induced, entrained, and terminated byprogrammed ventricular or atrial stimulation [1–6]. In addition,previous studies have suggested that the re-entry circuit isconfined to the posterior Purkinje system and that the ventricularmyocardium is involved in the circuit [5–7]. Previous studies haveshown successful catheter ablation achieved at the site of theearliest recorded PP or pre-PP, particularly at the inferoposteriorleft ventricular septum during sustained VT [5,9], and at the siteof abnormal potential in the mid-inferior septum within theposterior fascicular network during sinus rhythm [6]. In ourcase, catheter ablation could eliminate VT and was performed atthe basal third of the mid-septum, where pre-PP and PP wererecorded during tachycardia. However, the entire re-entrantcircuit and slow conduction zone remain unclear, and there have
been no reports describing patients with verapamil-sensitive ILVTin the presence of CLBBB. To the best of our knowledge, this is thefirst report of verapamil-sensitive ILVT, which was not influencedby the incidental occurrence of CLBBB.
The slight morphological change of the VT with QRS wideningoccurred transiently during LV outflow mapping and was perpe-tuated by the occurrence of CLBBB. However, the LBBB did notaffect other VT characteristics, such as left ventricular activationpattern, cycle length, VT induction, or maintenance. This suggeststhat the conduction block of the main trunk of the left bundlebranch did not have any effects on VT circuit, and it changed theventricular activation pattern by prolonging the conduction timefrom the VT circuit to the right ventricle. This might also raise thepossibility that the re-entrant circuit of verapamil-sensitive ILVTwas localized within the left ventricle.
In the present case report, we showed that the left main trunkof the His-Purkinje system is not a critical component of the re-entry circuit of verapamil-sensitive ILVT.
Conflict of interest
No conflict of interest declared.
References
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