BackgroundMeasurement of intracardiac kinetic energy (KE) provides new insights into cardiac hemodynamics and may improve assessment and understanding of heart failure. We therefore aimed to investigate left ventricular (LV) KE time curves in patients with heart failure and in controls.MethodsPatients with heart failure (n = 29, NYHA class I-IV) and controls (n = 12) underwent cardiovascular magnetic resonance (CMR) including 4D flow. The vortex-ring boundary was computed using Lagrangian coherent structures. The LV endocardium and vortex-ring were manually delineated and KE was calculated as ½mv2 of the blood within the whole LV and the vortex ring, respectively.ResultsThe systolic average KE was higher in patients compared to controls (2.2 ± 1.4 mJ vs 1.6 ± 0.6 mJ, p = 0.048), but lower when indexing to EDV (6.3 ± 2.2 μJ/ml vs 8.0 ± 2.1 μJ/ml, p = 0.025). No difference was seen in diastolic average KE (3.2 ± 2.3 mJ vs 2.0 ± 0.8 mJ, p = 0.13) even when indexing to EDV (9.0 ± 4.4 μJ/ml vs 10.2 ± 3.3 μJ/ml, p = 0.41). In patients, a smaller fraction of diastolic average KE was observed inside the vortex ring compared to controls (72 ± 6 % vs 54 ± 9 %, p < 0.0001). Three distinctive KE time curves were seen in patients which were markedly different from findings in controls, and with a moderate agreement between KE time curve patterns and degree of diastolic dysfunction (Cohen’s kappa = 0.49), but unrelated to NYHA classification (p = 0.12), or 6-minute walk test (p = 0.72).ConclusionPatients with heart failure exhibit higher systolic average KE compared to controls, suggesting altered intracardiac blood flow. The different KE time curves seen in patients may represent a conceptually new approach for heart failure classification.

Background: Pressure-volume (PV) loops provide a wealth of information on cardiac function but are not readily available in clinical routine or in clinical trials. This study aimed to develop and validate a noninvasive method to compute individualized left ventricular PV loops. Methods: The proposed method is based on time-varying elastance, with experimentally optimized model parameters from a training set (n=5 pigs), yielding individualized PV loops. Model inputs are left ventricular volume curves from cardiovascular magnetic resonance imaging and brachial pressure. The method was experimentally validated in a separate set (n=9 pig experiments) using invasive pressure measurements and cardiovascular magnetic resonance images and subsequently applied to human healthy controls (n=13) and patients with heart failure (n=28). Results: There was a moderate-to-excellent agreement between in vivo-measured and model-calculated stroke work (intraclass correlation coefficient, 0.93; bias, −0.02±0.03 J), mechanical potential energy (intraclass correlation coefficient, 0.57; bias, −0.04±0.03 J), and ventricular efficiency (intraclass correlation coefficient, 0.84; bias, 3.5±2.1%). The model yielded lower ventricular efficiency ( P <0.0001) and contractility ( P <0.0001) in patients with heart failure compared with controls, as well as a higher potential energy ( P <0.0001) and energy per ejected volume ( P <0.0001). Furthermore, the model produced realistic values of stroke work and physiologically representative PV loops. Conclusions: We have developed the first experimentally validated, noninvasive method to compute left ventricular PV loops and associated quantitative measures. The proposed method shows significant agreement with in vivo-derived measurements and could support clinical decision-making and provide surrogate end points in clinical heart failure trials.

Intracardiac blood flow is driven by hemodynamic forces that are exchanged between the blood and myocardium. Previous studies have been limited to 2D measurements or investigated only left ventricular (LV) forces. Right ventricular (RV) forces and their mechanistic contribution to asymmetric redirection of flow in the RV have not been measured. We therefore aimed to quantify 3D hemodynamic forces in both ventricles in a cohort of healthy subjects, using magnetic resonance imaging 4D flow measurements. Twenty five controls, 14 elite endurance athletes, and 2 patients with LV dyssynchrony were included. 4D flow data were used as input for the Navier-Stokes equations to compute hemodynamic forces over the entire cardiac cycle. Hemodynamic forces were found in a qualitatively consistent pattern in all healthy subjects, with variations in amplitude. LV forces were mainly aligned along the apical-basal longitudinal axis, with an additional component aimed toward the aortic valve during systole. Conversely, RV forces were found in both longitudinal and short-axis planes, with a systolic force component driving a slingshot-like acceleration that explains the mechanism behind the redirection of blood flow toward the pulmonary valve. No differences were found between controls and athletes when indexing forces to ventricular volumes, indicating that cardiac force expenditures are tuned to accelerate blood similarly in small and large hearts. Patients' forces differed from controls in both timing and amplitude. Normal cardiac pumping is associated with specific force patterns for both ventricles, and deviation from these forces may be a sensitive marker of ventricular dysfunction. Reference values are provided for future studies. Biventricular hemodynamic forces were quantified for the first time in healthy controls and elite athletes (n = 39). Hemodynamic forces constitute a slingshot-like mechanism in the right ventricle, redirecting blood flow toward the pulmonary circulation. Force patterns were similar between healthy subjects and athletes, indicating potential utility as a cardiac function biomarker.

Kinetic energy (KE) of atrial blood has been postulated as a possible contributor to ventricular filling. Therefore, we aimed to quantify the left (LA) and right (RA) atrial blood KE using cardiac magnetic resonance (CMR). Fifteen healthy volunteers underwent CMR at 3 T, including a four-dimensional phase-contrast flow sequence. Mean LA KE was lower than RA KE (1.1 ± 0.1 vs. 1.7 ± 0.1 mJ, P < 0.01). Three KE peaks were seen in both atria: one in ventricular systole, one during early ventricular diastole, and one during atrial contraction. The systolic LA peak was significantly smaller than the RA peak (P < 0.001), and the early diastolic LA peak was larger than the RA peak (P < 0.05). Rotational flow contained 46 ± 7% of total KE and conserved energy better than nonrotational flow did. The KE increase in early diastole was higher in the LA (P < 0.001). Systolic KE correlated with the combination of atrial volume and systolic velocity of the atrioventricular plane displacement (r(2) = 0.57 for LA and r(2) = 0.64 for RA). Early diastolic KE of the LA correlated with left ventricle (LV) mass (r(2) = 0.28), however, no such correlation was found in the right heart. This suggests that LA KE increases during early ventricular diastole due to LV elastic recoil, indicating that LV filling is dependent on diastolic suction. Right ventricle (RV) relaxation does not seem to contribute to atrial KE. Instead, RA KE generated during ventricular systole may be conserved in a hydraulic "flywheel" and transferred to the RV through helical flow, which may contribute to RV filling.