Abstract
We hypothesized that the direction of global left ventricular (LV) hemodynamic forces during diastolic filling are concordant with the main flow axes in normal LVs, but that this pattern would be altered in dilated and dysfunctional LVs. Therefore, we aimed to assess the LV hemodynamic filling forces in a group of healthy subjects and compare them to the results from a group of patients with dilated cardiomyopathy (DCM). Ten healthy subjects and 10 DCM patients were enrolled. Morphological short- (SAx) and long-axis (LAx) images and 4D flow MRI data were acquired at 1.5T. The LV pressure gradients were computed from the 4D flow data using the Navier-Stokes equations. By integrating the pressure gradients over the LV volume at each time frame, the magnitude and direction of the global hemodynamic force was calculated over the cardiac cycle. The hemodynamic forces acting in the SAx- and LAx-directions were used to calculate the "SAx-max/LAx-max"-ratio for the early (E-wave) and late (A-wave) diastolic filling. In the LAx-plane, the temporal progression of the hemodynamic force followed a consistent pattern in the healthy subjects. The "SAx-max/LAx-max"-ratio was significantly larger at both E-wave (0.53±0.15 vs. 0.23±0.12, P<0.0001) and A-wave (0.44±0.21 vs. 0.26±0.09, P<0.03) in the DCM patients compared to the healthy subjects. 4D flow MRI data allow quantification of LV hemodynamic forces acting on the LV myocardial wall. The LV hemodynamic filling forces showed a similar temporal progression among healthy subjects, whereas DCM patients had forces that were more heterogeneous in their direction and magnitude during diastole.
Highlights
Heart failure represents the final stage of the continuum of cardiovascular diseases
This study aims to extend the previously proposed hypothesis that the direction of global left ventricular (LV) hemodynamic forces are concordant with the main flow axes in normal LVs, but that this pattern would be altered in dilated and dysfunctional LVs
The directional pattern was consistent during early filling, but there was a wider range in the magnitude of the hemodynamic force (Fig. 5A)
Summary
Heart failure represents the final stage of the continuum of cardiovascular diseases. Cardiac remodeling is a key component of heart failure that progresses from adaptive to maladaptive as the disorder worsens (Hill and Olson 2008). Increased myocardial wall stress during diastole contributes to the development and progression of adverse cardiac remodeling (Mann 2004). During LV diastolic filling, blood in the left atrium (LA) is accelerated due to the pressure difference between the LA and the LV. After entering the LV, the speed is reduced.
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