Response to Letter Regarding Article, “Right Ventricular Mechanics and QRS Duration in Patients With Repaired Tetralogy of Fallot: Implications of Infundibular Disease”
We thank Dr Abdul-Khaliq and his colleagues for their interest in our study1 and for their comments to Circulation. We submit that apparent differences between our 2 studies1,2 are largely methodological in origin. In order to isolate the potential effects of activation, we measured the time interval from Q to onset of motion using M-mode with its high repetition rate. Abdul-Khaliq et al used strain imaging to measure the time interval to maximum strain, which they took to coincide with aortic valve closure (A2).2 This latter interval also includes ventricular ejection and is thus potentially influenced by loading conditions. As we pointed out in our article, we had very similar results when we took the time interval to peak shortening velocity, which is inscribed at mid ejection and thus subjected to similar influences.1
We take issue with Abdul-Khaliq et al, however, on the subject of rate dependence. We note that heart rate was not found to be a significant determinant in the particular circumstances of their study. However, the time from Q to A2 has been extensively investigated in the setting of the systolic time intervals, and its rate dependence has been clearly documented.3 Such dependence must always be recognized among other potential confounding factors when any time interval that includes ventricular ejection is studied.
A wide scatter was present in the severity of pulmonary regurgitation in our group of patients with repaired tetralogy. The extent of outflow tract asynchrony, however, did not correlate with pulmonary regurgitation but rather with markers of right ventricular outflow tract disease such as akinetic area size or with whether an outflow tract patch was used at the time of repair. It is thus apparent that the degree of pulmonary regurgitation does not necessarily reflect the extent of right ventricular outflow tract damage at the time of tetralogy repair.4
We fully agree with Abdul-Khaliq et al as to the limitations of tissue Doppler in assessing the timing of ventricular motion, limitations that we referred to in our report and which were also underscored by the recent Predictors of Response to Cardiac Resynchronization Therapy (PROSPECT) study.5
Uebing A, Gibson DG, Babu-Narayan SV, Diller GP, Dimopoulos K, Goktekin O, Spence MS, Andersen K, Henein MY, Gatzoulis MA, Li W. Right ventricular mechanics and QRS duration in patients with repaired tetralogy of Fallot: implications of infundibular disease. Circulation. 2007; 116: 1532–1539.
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.
Lewis RP, Rittogers SE, Froester WF, Boudoulas H. A critical review of the systolic time intervals. Circulation. 1977; 56: 146–158.
Davlouros PA, Kilner PJ, Hornung TS, Li W, Francis JM, Moon JC, Smith GC, Tat T, Pennell DJ, Gatzoulis MA. Right ventricular function in adults with repaired tetralogy of Fallot assessed with cardiovascular magnetic resonance imaging: detrimental role of right ventricular outflow aneurysms or akinesia and adverse right-to-left ventricular interaction. J Am Coll Cardiol. 2002; 40: 2044–2052.