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  • M. FllerC. ReithmannA. BeckerT. RempA. KmentG. Steinbeck

    Bundle branch reentrant tachycardiain a patient with a calcified bicuspidaortic valve and normal ventricular function

    Clin Res Cardiol 95:168173 (2006)DOI 10.1007/s00392-006-0343-5

    Received: 23 May 2005Accepted: 2 November 2005Published online: 12 January 2006

    Dr. med. Markus FllerPriv.-Doz. Dr. med.Christopher Reithmann (


    )Dr. med. Alexander BeckerDr. med. Thomas RempProf. Dr. med. Gerhard SteinbeckMedizinische Klinik IKlinikum GrohadernUniversitt MnchenMarchioninistr. 1581377 Mnchen, GermanyTel.: +49 /897095-3060Fax. +49 /897095-8830E-Mail: christopher.reithmann@med.uni-muenchen.de

    Dr. med. Axel KmentAbteilung fr Innere MedizinKrankenhaus WeilheimJohann-Baur-Str. 482362 Weilheim, Germany

    n Summary We report the caseof a bundle branch reentranttachycardia (BBRT) in a 40-year-old patient with a calcified bicus-pid aortic valve and normal leftventricular function. The ventri-cular tachycardia was eliminatedby successful radiofrequency ab-lation of the right bundle branch.As the aortic valve annulus is inclose proximity to the specializedconduction system, premature de-generation of a bicuspid aorticvalve may involve the bundle ofHis and the proximal bundlebranches by invading calcifica-tions. We speculate that calcifica-tions invading the proximal bun-dle branches from the bicuspidaortic valve may have created thesubstrate for the BBRT in this pa-tient.

    n Key words Bundle branchreentrant tachycardia bicuspid aortic valve radiofrequency catheter ablation


    Case reportA 40-year-old man presented with poorly toleratedsustained monomorphic broad complex tachycardiawith a left bundle branch block (LBBB) morphologyand a ventricular rate of 230/min, requiring electri-cal cardioversion (Fig. 1). There was no history ofpalpitations or syncope. The patient was a lifelongnonsmoker with no history of alcohol or substanceabuse. There was no history of hypertension, dia-betes mellitus, vascular disease, congestive heart fail-ure, congenital heart disease or chronic lung disease.He had no family history of sudden cardiac death.There was no significant increase of biochemical

    markers of myocardial ischemia, and electrolyteswere within the normal range. A subsequent ECG re-vealed sinus rhythm with a PR interval of 0.16 s, aQRS duration of 0.09 s and a superior QRS axis.Transthoracic echocardiogram showed a bicuspidaortic valve with calcification of the aortic valve andthe aortic ring with aortic stenosis of moderate se-verity and mild aortic regurgitation. The size andfunction of the right ventricle and left ventricle werenormal. The patient was treated with amiodaronebut over the course of the following days he experi-enced several non-sustained episodes of broad com-plex tachycardias with the same ECG morphologydocumented by Holter monitoring.

  • The patient was referred to our institution forfurther evaluation and therapy. The transesophagealechocardiography identified eccentric closure of theaortic valve (M-mode recording), restricted motionof the bicuspid valve during systole (Fig. 2A) andmarked calcifications of the aortic valve and aorticring (Fig. 2B). Cardiac catheterization confirmed anormal sized left ventricle with normal left ventricu-lar ejection fraction (LV-EF 81%) and a normal sizeand function of the right ventricle. Aortic pressurewas 102/69 mmHg and left ventricular pressure was142/011 mmHg. The pressure gradient across theaortic valve was 40 mmHg. According to the Gorlinformula, the aortic valve orifice area was calculatedto be 1.3 cm2. Angiography documented a mild aor-tic regurgitation. Coronary artery disease was ex-cluded by coronary angiography.

    At electrophysiologic study, atrio-His (AH) interval(90 ms) and His-ventricular (HV) interval (40 ms)were normal. Atrial premature stimulation and burstpacing were performed and showed no evidence ofpre-excitation. With stimulation from the right ventri-cular apex, a sustained LBBB morphology tachycardiacould reproducibly be induced and was identical tothe clinical tachycardia. During the tachycardia, VA

    block and 1 :1 VA conduction were alternately regi-strated (Fig. 3A and B). His bundle activity occurredbefore each QRS complex and was followed by a rightbundle branch (RB) deflection with a short RB-V in-terval (20 ms) preceding every QRS complex. Sponta-neous variations in ventricle-to-ventricle intervalswere preceded by identical changes in RB-RB inter-vals. The ventricular tachycardia could easily be ter-minated by overdrive pacing.

    The electrophysiological findings indicated a bun-dle-branch reentrant tachycardia (BBRT). The pa-tient underwent successful ablation of the right bun-dle branch (Fig. 4). After ablation, no further tachy-cardia was inducible using a standard programmedstimulation protocol with up to 3 extra-stimuli at2 sites and 4 cycle lengths (600 ms, 500 ms, 400 ms,330 ms) without or with orciprenaline infusion. ThePR intervals before and after ablation of the rightbundle branch were identical (PR 0.16 s).

    A pre-discharge exercise test (maximum 200 W,3 min) did not provoke any ventricular arrhythmias.Several Holter ECG recordings in-hospital and afterdischarge from the hospital showed no ventriculartachycardias. Inappropriate sinus tachycardia with aheart rate response of up to 140/min to moderate ex-

    169M. Fller et al.Bundle branch reentrant tachycardia and bicuspid aortic valve

    Fig. 1 12-lead ECG obtained at hospital admissionshowing a regular broad-complex tachycardia with aleft bundle branch block (LBBB) morphology, ventri-cular rate 230/min

  • ercise was noted but resolved within one month.Oral therapy with metoprolol was initiated and en-docarditis prophylaxis was recommended. Duringthe follow-up of 4 months, the patient experiencedno further episodes of either morphology of ventri-cular tachycardias.


    The case highlights the occurrence of BBRT in a pa-tient with a bicuspid aortic valve and normal ventri-cular systolic function. Marked calcifications of thebicuspid aortic valve and the aortic ring with anaortic stenosis of moderate severity were found. Dueto the proximity of the bundle of His and the proxi-

    170 Clinical Research in Cardiology, Volume 95, Number 3 (2006) Steinkopff Verlag 2006

    Fig. 2 Transesophageal echocardiography with multiplane imaging. A Leftventricular outflow tract: Eccentric closure of the aortic valve in M-moderecording (left) and restricted motion and sclerosis of the bicuspid aortic

    valve (right) in 2D-recording. B Bicuspid aortic valve: Marked calcifications ofthe aortic valve annulus



  • mal bundle branches to the aortic valve, calcifica-tions invading the proximal bundle branches may bethe substrate of conduction abnormalities of theHis-Purkinje system associated with the BBRT. How-ever, a mere coincidence of BBRT and a bicuspidaortic valve is also possible. The patient was curedof the ventricular tachycardia by ablation of theright bundle branch. Little data is available in theliterature concerning ICD implantation in a patientwith BBRT, bicuspid aortic valve and normal leftventricular systolic function.

    n Diagnosis of bundle branch reentrant tachycardia

    The diagnostic features leading to the diagnosis of aBBRT were (1) a typical LBBB tachycardia morphol-ogy, (2) an intermittent ventriculo-atrial block, (3)reproducible induction and termination of the BBRTby programmed ventricular stimulation, (4) a Hisbundle potential and RB potential preceding eachQRS complex, (5) variations in the V-V intervalsbeing preceded by similar changes in the RB-RB in-

    tervals and (6) non-inducibility of the VT after abla-tion of the right bundle branch.

    A common finding in patients with BBRT is prolon-gation of the baseline HV interval and/or the QRScomplex duration. Our patient had a normal HV inter-val and a normal QRS duration with a rSr morphol-ogy during sinus rhythm. In a recent review of 13 pa-tients with BBRT [9], 6 patients had an apparentlynormal His Purkinje conduction (HV 55 ms), butsignificant prolongation of the HV interval developedduring tachycardia suggesting functional, rather thanfixed conduction block in the His Purkinje system.

    n Bundle branch reentrant tachycardiain valvular heart disease

    BBRT is typically associated with dilative cardiomyo-pathy and poor left ventricular function [26]. Otherdiseases associated with conduction delay and BBRTinclude myotonic dystrophy [11, 14], hypertrophiccardiomyopathy [12], Ebstein anomaly [1] and val-vular surgery [13]. There have also been reports of

    171M. Fller et al.Bundle branch reentrant tachycardia and bicuspid aortic valve

    Fig. 3 Surface ECG and intracardiac tracings during theventricular tachycardia from high right atrium (HRA),His-Bundle (HB), proximal and distal right bundle branch(RBprox and RBdist) and right ventricular apex (RVA):Evidence of VA-block (A) and 1 : 1 VA-conduction (B)during ventricular tachycardia

  • cases of BBRT in patients without ventricular dys-function or valvular disease, whose only underlyingsubstrate for this arrhythmia is an abnormality ofthe His-Purkinje system [3, 10, 15]. To our knowl-edge, only one case of a BBRT in a patient with a bi-cuspid aortic valve, mild aortic stenosis and normalventricular function has been reported [7].

    In a series of 31 patients with sustained mono-morphic VT who had undergone valvular surgery, 9(29%) had BBRT [13]. Because the valvular annuliare in close proximity to the specialized conductionsystem, conduction abnormalities may develop orworsen by the excision of the native valve and its re-placement. Hemorrhagic lesions involving the Hisbundle and the bundle branches in patients aftervalve replacement have been reported [8]. We specu-late that calcifications


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