How pulmonary valve regurgitation after tetralogy of fallot repair changes the flow dynamics in the right ventricle: An in vitro study

Moving beyond size: vorticity and energy loss are correlated with right ventricular dysfunction and exercise intolerance in repaired Tetralogy of Fallot

“…We have previously developed an in-vitro computational model of intracardiac flow in rTOF patients using conventional CMR imaging [ 18 – 20 ]. Through this computational model, we observed a pattern where the jet of PR disrupts the natural tricuspid inflow vortex at the RVOT, a finding also observed in an in-vitro pump study by Mikhail et al [ 16 ]. We conjecture that in rTOF patients this flow phenomenon can be quantified by 4D flow as patterns of vorticity and energy loss that are distinct from the normal RV and RV dilation patients.…”

“…Electromechanical dyssynchrony likely affected RV longitudinal wall motion [ 10 ], which in turn weakens the tricuspid inflow vortex. The competing nature between PI and tricuspid inflow is also observed in in-vitro studies [ 16 , 18 ], and may lead to abnormal hemodynamic forces in directed from the RVOT towards the RV base, as demonstrated by Sjoberg et al [ 45 ]. The vortex interaction and resultant hemodynamic forces likely contributes to altered mechanotransductive environment that leads to RV dysfunction [ 46 , 47 ].…”

“…In-vivo and in-vitro studies of aortic regurgitation in the left ventricle show that when the inflow vortex is interrupted by a colliding jet of insufficiency, there is increased vortical flow formation and energy loss [40][41][42]. rTOF patients in similar fashion have higher vorticity and energy loss from PR in the RVOT, as the local jet collision creates a distinct intracardiac topology which generates shear layers, small-scale turbulence or turbulent-like flow [16,[18][19][20]. This effect is determined by PR, inflow, RV geometry (e.g.…”

“…Beyond size, dilated RVs do not all share the same intracardiac flow characteristics. Both in-vivo and in-vitro studies have highlighted the unique pathophysiology of rTOF patients [16][17][18][19][20] that are fundamentally distinct from other forms of RV dilation. A recent echocardiographic case-control study by Moceri et al [17] demonstrated different RV strain patterns between rTOF and patients with atrial septal defects (ASD), despite similar RV size.…”

Ventricular flow analysis and its association with exertional capacity in repaired tetralogy of Fallot: 4D flow cardiovascular magnetic resonance study

“…RV direct flow, the effective propagation of the tricuspid inflow diastolic vortex into the RVOT, which can then be ejected in systole. This flow property has been studied in prior studies, both in-vivo and in-vitro (by computational fluid dynamics and particle velocimetry), in both normal healthy controls and rTOF patients [ 41 – 45 ]. Moreover, Michail and his colleague [ 45 ] showed that PR significantly altered the tricuspid inflow during diastolic phase with increasing viscous energy dissipation in the RV in an in-vitro study.…”