Shi-Ying Ke1, Meng-Chu Chang1, Ming-Ting Wu2, Ken-Pen Weng3,4, and Hsu-Hsia Peng1
1Department of Biomedical Engineering and Environmental Sciences, National TsingHua University, Hsinchu, Taiwan, 2Department of Radiology, Kaohsiung Veterans General Hospital, Kaohsiung, Taiwan, 3Department of Pediatrics, Kaohsiung Veterans General Hospital, Kaohsiung, Taiwan, 4Department of Pediatrics, National Yang-Ming University, Taipei, Taiwan
Synopsis
We aimed to investigate the interaction between
myocardial kinetic energy (KEmyo) and intraventricular KE (KEven) in left- and right-ventricle (LV, RV) for repaired tetralogy of Fallot (rTOF)
patients. The rTOF group displayed
higher systolic RV KEven, earlier LV myocardial
diastolic time-to-peak (TTPmyo), earlier RV TTPmyo in both
systole and diastole, earlier LV TTPven in both systole and
diastole, and earlier RV TTPven in systole. In conclusion, from an insight of energy conversion, rTOF
patients demonstrated undermined interaction between LV KEmyo and KEven in an
early stage. The
dilated RV potentially have impacts on the RV KEven in rTOF
patients.
Introduction
Patients with repaired tetralogy of Fallot (rTOF)
is the most common form of cyanotic congenital heart.1 The kinetic
energy (KE) is a measure of the amount of work involved directly in moving blood.2 The disturbed intraventricular
KE in left and right ventricles (LV, RV) in rTOF patients was studied using 4D
flow MRI.3,4 Previous
study verified that altered RV hemodynamics interacted with severe pulmonary
regurgitation (PR).5 Moreover, the association of RV myocardium adapted to pressure
overload of rTOF patients was reported.6 Although these studies
mentioned the myocardial and intraventricular KE, the potential impact of the
myocardial KE on intraventricular flow KE has not been discussed thoroughly. In
this study, we aimed to investigate the interaction between myocardial and
intraventricular KE in both LV and RV for rTOF patients in an early stage with
preserved cardiac function. Method
The study population comprised 48 rTOF patients
(22.2±4.0 y/o; male/female: 29/19) and 46 age-matched normal volunteers (21.7±1.2
y/o; male/female: 28/18).
Images were acquired at a 3-T clinical MR
scanner (Tim Trio or Skyra, Siemens, Erlangen, Germany) with prospective ECG
triggering and navigator-echo to synchronize with cardiac and respiratory
motion, respectively. All subjects were imaged using 2D dark-blood fast
low-angle shot sequence for tissue phase mapping (TPM) acquisitions. The
protocol parameters were as follows: TR/TE = 6.5/4.2 ms, pixel size = 1.17 x
1.17 mm2, slice thickness = 6 mm, flip angle = 7°, acceleration
factor = 5,Venc=15 and 25 cm/s for in-plane and through-plane motions,
respectively, and temporal resolution=26 ms. The 4D flow dataset was acquired
by TR/TE=10.8/2.9 ms, voxel size=3.2x1.4x3.5 mm3, flip angle=7°,
Venc=150 cm/s, and temporal resolution=41.6 ms.
A
self-developed program was employed to calculate the longitudinal (vz),
radial (vr), and circumferential (vØ) velocities in LV
and RV and the corresponding myocardial KE (KEmyo).
The voxel-wise KEmyo was calculated
as: $$KE_{myo}=\frac{1}{2}×ρ_{myo}×V_{myo}×v_{myo}^2 (1)$$where ρmyo was myocardial density with
a value of 1050 kg/m3, Vmyo denoted voxel volume, and vmyo represented the voxel velocity.
In the current work, we added upthree-directional components of KE as
total KE.
As shown in Figure 1, the ROIs of LV and RV were
manually determined in a 4-chamber view for calculation of intraventricular KE
as follows:$$KE_{ven}=\frac{1}{2}×ρ_{ven}×V_{ven}×v_{ven}^2 (2)$$
where ρven was blood density with a
value of 1060 kg/m3, Vven denoted voxel volume, vven and represented the voxel
velocity. The time frame was normalized to the individual period of end
systolic time and was presented as the percentage of the end-systole
(%ES). Two-tailed Student t test and Pearson correlation were performed
when appropriate. P < 0.05 was
considered as statistical significance.Results
Table 1
illustrated that rTOF
patients showed
significant higher RVESVI (33.9
± 7.6 cm3/m2 vs. 57.2 ± 31.2 cm3/m2, P<0.001) and RVEDVI (76.7
± 13.3 cm3/m2 VS. 116.6 ± 44.5 cm3/m2, P<0.001) than normal volunteers. Nevertheless, rTOF group
demonstrated preserved RV and LV ejection fraction (RVEF and LVEF, both P>0.05). Figure 2 displayed the time courses of KEmyo
and KEven .The
systolic and diastolic peak KEmyo in rTOF group were similar to normal group in both LV and
RV. The KEven of LV showed no substantial difference between
normal and rTOF groups. In contrast, rTOF group displayed significant
higher RV KEven in diastole (0.04 ± 0.02 mJ vs. 0.07 ± 0.04 mJ, P<0.001). As illustrated
in Figure 3, rTOF patients presented earlier LV myocardial diastolic time-to-peak
(TTPmyo) and earlier RV TTPmyo in both systole and
diastole than normal volunteers (P<0.05~0.001).
For intraventricular flow,
rTOF group showed earlier LV TTPven in both systole and diastole and
earlier RV TTPven in systole (P<0.05~0.001, Figure 3c,d).In
Figure 4a, normal volunteers presented moderate correlation between KEmyo and KEven in
LV (R=0.388, P<0.05).
In rTOF group, the RV KEven was correlated with RV
end-diastolic volume (R=0.424, P<0.05). Discussion and Conclusions
In this
study, we explored the interaction of KEmyo and KEven in both
LV and RV of rTOF patients. The rTOF presented earlier TTPmyo and
TTPven of KE and moderate correlation between RV KEven and
RVEDV.
In our study, the rTOF patient’s time to peak is earlier than
normal. This finding suggested that the early TTP in myocardial and
intraventricular KE may be beneficial to the rTOF. In the current work, the positive
correlation between LV KEmyo and KEven in the normal group
indicated the normal interaction between myocardium and intraventricular flow. The
absence of this interaction in rTOF patients reflected the disordered
incoherence of myocardium and intraventricular flow in a relatively early
stage, i.e. with preserved global LVEF.
Previous study reported that higher intracardiac
vorticity of rTOF patients could be relevant with regard to the development of RV dilation.7 In this study, the positive correlation
between RV KEven and RVEDV in the rTOF group indicated that the dilated RV have impacts on the RV
KEven which reflected the increased and disturbed intraventricular
flow. In
conclusion, from an insight of energy conversion, rTOF patients
demonstrated undermined interaction between LV myocardium and intraventricular flow
in an early stage. The dilated RV potentially have impacts on the RV KEven
in rTOF patients. Acknowledgements
No acknowledgement found.References
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