ObjectivesIndications for pulmonary valve replacement (PVR) in patients with pulmonary regurgitation (PR) after repaired tetralogy of Fallot (rToF) are debated. We aimed to compare right (RV) and left ventricular (LV) kinetic energy (KE) measured by 4D-flow magnetic resonance imaging (MRI) in patients to controls, to further understand the pathophysiological effects of PR.MethodsFifteen patients with rToF with PR > 20% and 14 controls underwent MRI. Ventricular volumes and KE were quantified from cine MRI and 4D-flow, respectively. Lagrangian coherent structures were used to discriminate KE in the PR. Restrictive RV physiology was defined as end-diastolic forward flow.ResultsLV systolic peak KE was lower in rToF, 2.8 ± 1.1 mJ, compared to healthy volunteers, 4.8 ± 1.1 mJ, p < 0.0001. RV diastolic peak KE was higher in rToF (7.7 ± 4.3 mJ vs 3.1 ± 1.3 mJ, p = 0.0001) and the difference most pronounced in patients with non-restrictive RV physiology. KE was primarily located in the PR volume at the time of diastolic peak KE, 64 ± 17%.ConclusionThis is the first study showing disturbed KE in patients with rToF and PR, in both the RV and LV. The role of KE as a potential early marker of ventricular dysfunction to guide intervention needs to be addressed in future studies.Key Points • Kinetic energy (KE) reflects ventricular performance • KE is a potential marker of ventricular dysfunction in Fallot patients • KE is disturbed in both ventricles in patients with tetralogy of Fallot • KE contributes to the understanding of the pathophysiology of pulmonary regurgitation • Lagrangian coherent structures enable differentiation of ventricular inflows Electronic supplementary materialThe online version of this article (10.1007/s00330-018-5385-3) contains supplementary material, which is available to authorized users.

Four-dimensional (4D) flow magnetic resonance imaging (MRI) enables quantification of kinetic energy (KE) in intraventricular blood flow. This provides a novel way to understand the cardiovascular physiology of the Fontan circulation. In this study, we aimed to quantify the KE in functional single ventricles. 4D flow MRI was acquired in eleven patients with Fontan circulation (median age 12 years, range 3–29) and eight healthy volunteers (median age 26 years, range 23–36). Follow-up MRI after surgical or percutaneous intervention was performed in 3 patients. Intraventricular KE was calculated throughout the cardiac cycle and indexed to stroke volume (SV). The systolic/diastolic ratio of KE in Fontan patients was similar to the ratio of the controls’ left ventricle (LV) or right ventricle (RV) depending on the patients’ ventricular morphology (Cohen´s κ = 1.0). Peak systolic KE/SV did not differ in patients compared to the LV in controls (0.016 ± 0.006 mJ/ml vs 0.020 ± 0.004 mJ/ml, p = 0.09). Peak diastolic KE/SV in Fontan patients was lower than in the LV of the control group (0.028 ± 0.010 mJ/ml vs 0.057 ± 0.011 mJ/ml, p < 0.0001). The KE during diastole showed a plateau in patients with aortopulmonary collaterals. This is to our knowledge the first study that quantifies the intraventricular KE of Fontan patients. KE is dependent on the morphology of the ventricle, and diastolic KE indexed to SV in patients is decreased compared to controls. The lower KE in Fontan patients may be a result of impaired ventricular filling.Electronic supplementary materialThe online version of this article (doi:10.1007/s00246-016-1565-6) contains supplementary material, which is available to authorized users.

We recently presented and validated a clinically available, noninvasive method for generation of pressure-volume (PV) loops from time-resolved ventricular volumes and brachial pressure (Seemann et al., 2019). The method is based on estimation of left ventricular pressure as the product of elastance from a mathematical model and volume from cardiac magnetic resonance imaging.While the previous method produced valid data at resting heart rates, its performance was impaired at high heart rates, such as in children or during exercise. To address this limitation, we present an improved method. This new method takes into account the heart rate-dependent relative duration of systolic and diastolic phases of the cardiac cycle (Chung et al., 2004). The aim of the present study was to develop the model into allowing for higher heart rates when the diastolic fraction of the cardiac cycle shortens and to