Europace Advance Access published online on July 14, 2007
Europace, doi:10.1093/europace/eum138
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CASE REPORT
Reversible left ventricular dyssynchrony and dysfunction resulting from right ventricular pre-excitation
Department of Cardiology, First Affiliated Hospital of Nanjing Medical University, 300 Guangzhou Road, Nanjing 210029, P.R.China
Manuscript submitted 7 April 2007. Accepted after revision 19 June 2007.
* Corresponding author. Tel: +86 2583672050; fax: +86 2583717168. E-mail address: kjcao{at}njmu.edu.cn
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Abstract |
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We report observations in a 7-year-old girl with right ventricular pre-excitation due to an accessory atrioventricular pathway (AP), and depressed cardiac function. Echocardiographic findings consisted of left ventricular (LV) dilatation with asynchronous ventricular wall motion and diminished LV ejection fraction. Electrophysiological study revealed a para-Hisian AP. She underwent successful AP ablation, after which asynchronous ventricular wall motion disappeared. Cardiac size and function were normal after 3 months follow-up. These findings suggest that ventricular pre-excitation leading to asynchronous ventricular motion was a possible cause of LV dilation and dysfunction and that catheter ablation reversed undesirable cardiac remodelling in this patient.
Key Words: Pre-excitation, Accessory pathway, Catheter ablation, Cardiomyopathy
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Introduction |
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Supraventricular tachycardia (SVT) is very common in patients with accessory atrioventricular pathways (APs), and in occasional patients, the tachycardia can be incessant and induce a cardiomyopathy. On the other hand, although occasional episodes of SVT are not usually associated with the development of ventricular dysfunction, the possibility exists that abnormal ventricular activation resulting from antegrade conduction over an AP (ventricular pre-excitation) could cause sustained atrial-ventricular, interventricular, and intraventricular dyssynchrony. In this report, we present observations in a patient with right ventricular pre-excitation and depressed cardiac function whose left ventricular (LV) function substantially improved after successful AP catheter ablation.
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Case report |
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A 7-year-old girl was referred to our hospital after two fainting episodes during vigorous exercise within the previous 6 months. She felt palpitation before each fainting episode. There was no family history of cardiomyopathy and no history of her having had a viral illness in the recent past. The troponin I was in normal range. An electroencephalogram was obtained as part of the evaluation for possible seizure disorder, and the result was negative. Her electrocardiogram (ECG) revealed a short PR interval (80 ms) and long QRS duration (180 ms) (Figure 1, left panel). A delta wave was apparent, and the overall QRS appearance suggested a left bundle branch block (LBBB) appearance, compatible with right ventricular pre-excitation. Echocardiogram (Echo) revealed LV dilatation (LVDd = 52 mm), reduced LV ejection fraction (LVEF = 46%), and moderate mitral valve regurgitation. Tissue Doppler imaging (TDI) revealed asynchronous LV wall motion.
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The patient underwent electrophysiology study and an AP ablation procedure on the fifth hospital day. Electrophysiology study showed a para-Hisian AP (Figure 2) with both antegrade and retrograde conduction properties. The AP did not exhibit decremental conduction, and effective refractory periods were identical (300 ms) in both antegrade and retrograde directions. An orthodromic SVT with LBBB (aberrant conduction) was induced by right ventricular apex programmed stimulation (Figure 3). During the SVT episode, her symptoms were similar to those experienced during spontaneous tachycardia.
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A sharp QS deflection preceding the surface ECG delta wave onset by 20 ms was present on the unipolar electrogram at the successful ablation site. The delta wave disappeared during radiofrequency energy delivery (temperature setting was 55°C, and the energy titrated from 10 to 30 W), and a low-amplitude His deflection was recorded on the bipolar electrogram (Figure 4). After ablation, SVT could not be induced in the drug-free state or during isoproterenol infusion. Normal atrial-ventricular conduction was documented at the end of the procedure. Prior to discharge, an Echo showed that the LVEF had slightly improved (53%), and TDI indicated that asynchronous ventricular wall motion had disappeared. She was discharged without any medication.
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At the 6 month follow-up visit, she remained free of symptoms. A delta wave was no longer observed on the ECG recording (Figure 1, right panel), and echocardiographic findings revealed that both her cardiac size and LVEF had returned to normal (LVDd = 44 mm, LVEF = 63%).
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Discussion |
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The principal finding in this report was the resolution of cardiac chamber enlargement and normalization of LV function within a few months of successful elimination of right ventricular pre-excitation by radiofrequency ablation in a young patient who presented with a cardiomyopathic picture. In this case, a paroxysmal supraventricular tachyarrhythmia function was the most possible reason for fainting episode, especially, given the diminished LV function. However, the mechanism of her LV dilation and ventricular dysfunction was not so readily explained given the absence of evidence for familial disease, a recent illness (e.g. causing myocarditis), or a drug-induced cardiomyopathy. In addition, incessant tachycardia causing a tachycardia-induced cardiomyopathy seemed unlikely given no history of long-standing palpitation and the findings at EP study that excluded susceptibility to asymptomatic incessant tachycardia such as that associated with the permanent form of junctional reciprocating tachycardia. On the other hand, since her ECG showed constant LBBB-like pattern with short PR interval due to manifest right ventricular pre-excitation, it seemed reasonable to attribute the reversible LV dysfunction to that cause.
Left bundle branch block causes asynchronous ventricular wall motion, which has the potential to progress to ventricular dysfunction and mitral regurgitation1
–3. In this regard, Blanc et al.4 recently demonstrated reversibility by LV-based pacing of an apparent cardiomyopathic picture triggered by long-standing LBBB in patients with no other evident cause for LV dysfunction. Presumably, effective ‘elimination’ of the LBBB pattern, and its associated intraventricular dyssynchrony (as we hypothesize in our patient), was the basis for LV functional improvement. In addition, it has become widely accepted on the basis of relatively recent clinical trials5–7 that long-term right ventricle apical pacing promotes heart failure progression due to the deterioration of LV function. Again, it seems likely that pacing results in a scenario essentially equivalent to LBBB-induced ventricular dyssynchrony and adverse effect on LV structure and function. Finally, there have been several reports8,9 describing patients with frequent (>20%) premature ventricular complexes from right ventricle outflow tract (RVOT-PVCs), LV dilation, and LVEF reduction. Successful catheter ablation of PVCs reversed their LV dilatation and dysfunction. It is presumed that the ROVT-PVCs, which manifested LBBB-like morphology, gave rise to LV dyssynchrony and dysfunction.
On the basis of these previous observations, it seems plausible that right ventricular pre-excitation in our patient led to interventricular and intraventricular dyssynchrony. The short PR interval (80 ms) also could give rise to atrial-ventricular dyssynchrony. After successful ablation, her PR interval and duration of QRS complex became normal; Echo verified that dyssynchrony wall motion had disappeared.
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Conclusions |
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Given the previous reports regarding the potential impact of LBBB or LBBB-like activation pattern on ventricular function, as well as our observation in this patient, it seems possible that APs producing right ventricular pre-excitation leading to comparable ventricular dyssynchrony could be a possible cause of reversible LV dilatation and ventricular dysfunction. Consequently, in patients with a manifest right-sided AP and depressed cardiac function, catheter ablation to eliminate pre-excitation may have beneficial effects on cardiac function beyond eliminating their susceptibility to recurrent tachyarrhythmias.
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Acknowledgements |
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We would like to thank Professor David G. Benditt for his revision of the manuscript.
Conflict of interest: none declared.
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References |
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[1] Littmann L, Symanski JD. Hemodynamic implications of left bundle branch block. J Electrocardiol (2000) 33:115–21.[CrossRef][Web of Science][Medline]
[2] Xiao HB, Lee CH, Gibson DG. Effect of left bundle branch block on diastolic function in dilated cardiomyopathy. Br Heart J (1991) 66:443–7.
[3] Bradley DJ, Bradley EA, Baughman KL, Berger RD, Calkins H, Goodman SN, et al. Cardiac resynchronization and death from progressive heart failure: a meta-analysis of randomized controlled trials. JAMA (2003) 289:730–40.
[4] Blanc JJ, Fatemi M, Bertault V, Baraket F, Etienne Y. Evaluation of left bundle branch block as a reversible cause of non-ischaemic dilated cardiomyopathy with severe heart failure. A new concept of left ventricular dyssynchrony-induced cardiomyopathy. Europace (2005) 7:604–10.
[5] Tops LF, Schalij MJ, Holman ER, Erven L, van der Wall EE, Bax JJ. Right ventricular pacing can induce ventricular dyssynchrony in patients with atrial fibrillation after atrioventricular node ablation. J Am Coll Cardiol (2006) 48:1642–8.
[6] Lieberman R, Padeletti L, Schreuder J, Jackson K, Michelucci A, Colella A, et al. Ventricular pacing lead location alters systemic hemodynamics and left ventricular function in patients with and without reduced ejection fraction. J Am Coll Cardiol (2006) 48:1634–41.
[7] Tse HF, Lau CP. Selection of permanent ventricular pacing site: how far should we go? J Am Coll Cardiol (2006) 48:1649–51.
[8] Takemoto M, Yoshimura H, Ohba Y, Matsumoto Y, Yamamoto U, Mohri M, et al. Radiofrequency catheter ablation of premature ventricular complexes from right ventricular outflow tract improves left ventricular dilation and clinical status in patients without structural heart disease. J Am Coll Cardiol (2005) 45:1266–8.
[9] Yarlagadda RK, Iwai S, Stein KM, Markowitz SM, Shah BK, Cheung JW, et al. Reversal of cardiomyopathy in patients with repetitive monomorphic ventricular ectopy originating from the right ventricular outflow tract. Circulation (2005) 112:1092–7.
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