Abstract
The aim of the study was to determine whether segmental interactions, as expressed by postsystolic shortening (PSS), affects RV mechanics and are connected with impaired systolic and diastolic function in rTOF children. Patients and Methods: 55 rTOF adolescent (study group), and 34 healthy volunteers (control group) were examined using classical Doppler flow (Doppler), Tissue Doppler Imaging (TDI) and Speckle Tracking Echocardiography (STE). PSS was found to occur when time to peak (TTP) was longer than pulmonary valve closure time (PVCT). TTP and strain were derived from RV lateral segments—basal (BL), medial (ML) and apical (AL) in STE. PVCT was measured from the beginning of QRS complex in the ECG to the termination of Doppler flow at the pulmonary valve. TDI was obtained at the lateral tricuspid annulus site and the systolic (S′), early (E′) and late diastolic (A’) peak velocities were measured along with isovolumic contraction (IVCT), and relaxation (IVRT) time. PW was used to measure early tricuspid inflow velocity (E) for calculating the E/E’ ratio. The TDI data in patients with PSS presence (TTP>PVCT) and those in whom it did not occur (TTP≤PVCT) were compared. Results: PSS in BL, ML and AL were observed respectively in: 27(51,9%), 9 (18%), and 8 (16,7%) patients. Mean values of TTP in BL, ML, and AL were respectively: 420.6±55.5ms, 389.8±50.0ms and 366.7±59.0ms. PVCT mean value was 396.6±33.5ms. In the study group, the mean E’ in TTP>PVCT was significantly lower (4.8±1.8 cm/s) compared to mean E’ in TTP≤PVCT (8.4±2.6 cm/s), p<0.01. The average E/E’ was significantly higher in TTP>PCVT than in TTP≤PVCT, respectively 21.6±7.3 vs 12.2±5.1, p<0.05. IVRT was significantly prolonged in TTP>PVCT compared to IVRT in TTP≤PVCT, respectively 95.9±38.7 vs 77.0±35.1, p<0.05. Furthermore, in TTP>PVCT, significantly higher strain in BL (-28.8±8.7%) was observed when compared to that parameter in TTP≤PVCT (-35.3±13.1%), p <0.05. Conclusions: Tissue Doppler Echocardiography and Speckle Tracking Echocardiography are useful techniques for detecting regional systolic and diastolic dysfunction in children after Tetralogy of Fallot surgical repair. Postsystolic shortening in the basal lateral segment is commonly seen in children after the Tetralogy of Fallot surgical repair, and is associated with altered right ventricular systolic and diastolic function.
Highlights
[1] Pulmonary regurgitation has been observed to be a major residual lesion associated with right ventricular (RV) volume overload, driving towards its dysfunction in rTOF patients. [2,3] the almost invariable presence of right bundle branch block (RBBB) in rTOF patients may play an important role in their long-term clinical outcomes, where it is likely that electrical and mechanical dysfunction are linked. [4,5] For the latter, RV abnormalities occur during both systole and diastole, with global and regional abnormalities in systole being well documented [6,7]
In our study we found a significant decrease in myocardial early diastolic velocity (E’) and isovolumic relaxation time prolongation (IVRT) within the right ventricle in patients in whom postsystolic shortening was detected when compared with the remaining subjects of the study group
Postsystolic shortening in the basal lateral segment is commonly seen in children after the Tetralogy of Fallot surgical repair, and is associated with altered right ventricular systolic and diastolic function
Summary
An increasing number of patients after Tetralogy of Fallot surgical repair (rTOF) has led to a growing adolescent population with postoperative cardiac sequels. [1] Pulmonary regurgitation has been observed to be a major residual lesion associated with right ventricular (RV) volume overload, driving towards its dysfunction in rTOF patients. [2,3] the almost invariable presence of right bundle branch block (RBBB) in rTOF patients may play an important role in their long-term clinical outcomes, where it is likely that electrical and mechanical dysfunction are linked. [4,5] For the latter, RV abnormalities occur during both systole and diastole, with global and regional abnormalities in systole being well documented [6,7]. One trial shows a PSS within the RV, where an elegant model of right ventricular lateral wall activation was presented [13] For this sequence early septal activation, as observed echocardiographically by a septal flash with concomitant lateral wall prestretch, follows contraction of the early stretched lateral wall. The subsequent late initiation of systolic RV lateral contraction (connected with RBBB) may be partially inefficient as it continues on after pulmonary valve closure. Another postulated mechanism responsible for the PSS phenomenon is passive post-systolic deformation after end-systolic stretch observed at the pulmonary/aortic valve closure [14,15]
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