(Circulation. 2008;117:e300.)
© 2008 American Heart Association, Inc.
Correspondence |
Department of Pediatric Cardiology, Saarland University Hospital, Homburg/Saar, Germany
Department of Congenital Heart Disease, Paediatric Cardiology, Deutsches Herzzentrum Berlin, Berlin, Germany
Department of Pediatrics and Pediatric Cardiology Cairo University, Egypt
We read with great interest the article by Uebing et al,1 and we congratulate the authors on this important work. The authors have cited our work1,2 and compared their results on right ventricular delay to our published data on intraventricular left ventricular (LV) dyssynchrony. In our article, we concluded that LV asynchrony may exist in patients with right bundle-branch block after tetralogy of Fallot repair and that this electromechanical delay was associated with lower global and regional LV function as well as physical performance.2 We would like to comment on the authors critical remark about our article:
In contrast to the study by Uebing et al, we assessed electromechanical delay using tissue Doppler imaging–derived strain rather than tissue Doppler imaging–derived velocity as was used in the Uebing et al study.2 Tissue Doppler–derived velocity tracing is affected by global heart motion as well as by the tethering effect from adjacent structures, and accordingly it may not adequately reflect the mechanoelectrical interaction. This limitation is especially important to consider in the tetralogy of Fallot patient after surgical repair in whom noncontractile patches are present. In addition, in tissue Doppler imaging–derived velocity tracing, determining the onset of maximal rate of contraction is rather difficult because multiple velocity peaks are present, especially when a high frame rate is used. This difficulty explains the high interobserver variability found in the study by Uebing et al. The time interval between Q and onset of contraction was not measured in our study because this interval is difficult to assess with great accuracy. A plateau-like interval is usually present at the beginning of the strain curve tracing, making it very difficult to mark the beginning of myocardial deformation. In contrast, the maximal systolic deformation of the tissue Doppler imaging–derived strain curves is well defined by the aortic valve closure and can be obtained with great accuracy.2 In addition, the suggested methods by the authors for measurements of electromechanical delay are significantly influenced by noncontractile material and scars in the reconstructed right ventricular outflow tract.
We do not agree, as Uebing et al assert, that the measured delay in our study is related to the heart rate because no statistical difference was found relative to this factor in our patients with or without LV dyssynchrony.2 The LV intraventricular delay in our study did not correlate with the QRS duration; accordingly we did not assume that it is related to LV asynchrony. QRS duration may not necessarily be related to electromechanical dyssynchrony in the LV, an important issue when cardiac resynchronization is considered for the systemic LV in these patients. In the study by Uebing et al on right ventricular dyssynchrony, no data were provided on pulmonary regurgitation. In this clinical setting, it is extremely important to illustrate the effect of pulmonary regurgitation on right ventricular dilatation and dyssynchrony.3 Nevertheless, the study by Uebing et al may present additional information on the electromechanical disturbance in these patients.
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2. Abd El Rahman MY, Hui W, Yigitbasi M, Dsebissowa F, Schubert S, Hetzer R, Lange PE, Abdul-Khaliq H. Detection of left ventricular asynchrony in patients with right bundle branch block after repair of tetralogy of Fallot using tissue-Doppler imaging-derived strain. J Am Coll Cardiol. 2005; 45: 915–921.
3. Abd El Rahman MY, Abdul-Khaliq H, Vogel M, Alexi-Meskishvili V, Gutberlet M, Lange PE. Relation between right ventricular enlargement, QRS duration, and right ventricular function in patients with tetralogy of Fallot and pulmonary regurgitation after surgical repair. Heart. 2000; 84: 416–420.
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