Recently, Geiger et al reported that repaired tetralogy of Fallot patients (rTOF) revealed increased blood flow in the right pulmonary artery and significant vortical flow in pulmonary trunk during systolic period (1). However, the information regarding the energy transfer between input and output flow of right ventricle (RV) in rTOF patient is still unclear. We aim to investigate input- and output kinetic energy (KE) propagation, retrograde flow, and abnormal intraventricular flow patterns in rTOF.

This study recruited six rTOF patients (21.5±3.9 y/o; male/female: 3/3) and eight normal subjects (21.9±1.3 y/o; male/female: 4/4) without any known cardiovascular diseases. Images were acquired at a 3.0 Tesla MR scanner (Tim Trio or Skyra, Siemens, Erlangen, Germany). All subjects underwent flow-sensitive 4D phase-contrast MRI (TR/TE=10.8/2.9 ms, flip angle=7°, VENC=1.5 m/s, voxel size=1.17×1.17×3.5 mm³). The total scanning time was approximate 20 minutes.

A 3D angiogram was reconstructed by EnSight software (V10, CEI, Apex, NC) for visualizing intraventricular flow vectors and for quantifying flow-related indices. Two planes were determined manually at the tricuspid valve annulus and main pulmonary artery for computing input and output flow, respectively (Figure 1). The kinetic energy was calculated as: $$KE=\frac{1}{2}\times \rho_{blood} \times V_{voxel} \times v_{voxel}^2 $$ , where $$$\rho $$$ was blood density with a value of 1060 kg/m³, $$$ {V_{voxel}} $$$ denoted blood volume, and $$$ {v_{voxel}} $$$ represented the velocity of the voxel. An index of total KE was defined as the summation of forward flow KE during systole (output) or diastole (input). One-tailed Student t test was used to assess the statistical significance between normal and rTOF groups. A P value < 0.05 was considered statistically significant.

Table 1 summarizes basic characteristics of the study population. Compared with normal subjects, rTOF patients exhibited higher RV end systolic volume index (78.1±22.8 cm³/m² vs. 34.3±8.0 cm³/m², P<0.01) and increased RV end diastolic volume index (141.4±22.8 cm³/m² vs. 71.6±7.3 cm³/m², P<0.01), indicating that patients presented dilated RV. Further, rTOF patients exhibited significantly higher pulmonary regurgitation fraction than normal subjects (21.7±4.5% vs. 0.6±0.4%, P<0.001).

Figure 2 displayed time courses of forward and backward KE. The rTOF group displayed a larger peak RV output forward KE at 60 %ES than normal group (0.9±0.5 J vs. 0.3±0.1 J, P<0.05). Figure. 2b demonstrated that normal group displayed a backward KE close to zero within whole cardiac cycle. Moreover, rTOF group demonstrated a larger peak RV $$${output_{backward}}$$$ KE (0.3±0.2 J) at 160 %ES, reflecting the KE provided by regurgitant flow.

In Figure 3, rTOF group presented higher RV output total KE than normal group (P<0.01). Furthermore, most of the rTOF patients had higher output total KE than input total KE (4.3±2.2 J vs. 0.9±0.5 J, P<0.05).

Figure 4 displayed the velocity vector fields in 4-chamber view during diastole period of a 23-year-old normal male subject and a 22-year-old rTOF male patient. At peak diastolic phase (t=155%ES), normal subject displayed a high velocity filling jet into the ventricle along with LV lateral wall and RV septal wall. By contrast, the rTOF patient exhibited disturbing flow directed toward apex. At late diastolic phase (t=170 and 185%ES), normal subject demonstrated a clockwise vortex (white line) with reduced velocity in both LV and RV. In rTOF patient, however, the vortex was absent. Alternatively, the blood flow filled into ventricles with a high velocity, accompanying several local vortices.

We quantified ventricular input/output KE and characterized intraventricular flow for rTOF patients. The recruited rTOF patients show higher RV output KE and abnormal intraventricular flow patterns.

Namheon et al verified higher RV pressure at both end-diastole and end-systole in rTOF patients by using cardiac catheterization (2). In our work, KE of flowing blood from right atrium accumulated in RV chamber during diastole. In the meanwhile, regurgitant blood from pulmonary artery also flowed backward into RV, leading to increased RV volume and pressure. Consequently, higher RV output velocity and KE were displayed in the subsequent ejection to release the accumulated RV pressure.

A previous study associated altered vortex formation with LV pathology and inefficient heart pumping function (3). In the recruited rTOF patients, the disturbed ventricular filling patterns could be associated with the severe pulmonary regurgitation, which may alter the hemodynamic conditions of RV and limit the formation of the intraventricular vortex. As a result, low-efficient energy propagation of intraventricular flow may lead to RV overloading and deteriorated diastolic function.

In conclusion, the higher RV output total KE in rTOF patients suggested the RV overloading condition. The visualization of intraventricular vector field helped to comprehend the energy propagation and its influence on RV function.