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Updated: May 19, 2026
Evaluation of Left Ventricular Structure and Function using 3D Echocardiography
Published on: October 28, 2020
Four-dimensional blood flow-specific markers of LV dysfunction in dilated cardiomyopathy
Jonatan Eriksson1, Ann F Bolger, Tino Ebbers
1Division of Cardiovascular Medicine, Department of Medical and Health Sciences, Linköping University, Linköping, Sweden. jonatan.eriksson@liu.se
Insights
Patients with mild heart failure (HF) have altered blood flow patterns in the left ventricle (LV). These changes in diastolic flow routes and kinetic energy (KE) occur even with normal stroke volume (SV) and may indicate early LV dysfunction.
Area of Science:
- Cardiovascular Physiology
- Medical Imaging
- Biomedical Engineering
Background:
- Mild heart failure (HF) patients may present with normal left ventricular (LV) stroke volume (SV) despite underlying cardiac dysfunction.
- Altered intra-ventricular blood flow patterns have been observed in clinically compensated HF patients.
- Understanding these flow dynamics is crucial for early detection and management of LV dysfunction.
Purpose of the Study:
- To investigate intra-ventricular flow patterns in patients with mild heart failure (HF) and dilated cardiomyopathy (DCM).
- To compare the proportion of LV inflow directly to ejection and the preservation of inflow kinetic energy (KE) between DCM patients and healthy controls.
- To determine if altered flow patterns can serve as subclinical markers of LV dysfunction despite preserved stroke volume.
Main Methods:
- Four-dimensional MRI velocity and morphological data were acquired from 10 DCM patients and 10 healthy subjects.
- A validated method segmented LV end-diastolic volume (EDV) into four flow components.
- Kinetic energy (KE) was calculated for each component throughout the cardiac cycle.
Main Results:
- DCM patients had larger EDV and smaller ejection fraction but equivalent SV compared to healthy controls.
- The proportion of LV inflow directly to ejection was significantly smaller in DCM patients (P = 0.000).
- End-diastolic KE/mL of direct flow did not differ significantly between groups.
Conclusions:
- Mildly remodeled LVs in HF patients exhibit altered diastolic flow routes and impaired inflow KE preservation compared to healthy individuals.
- These flow-specific changes are detectable even in clinically compensated patients.
- Altered flow routes and energetics may serve as valuable subclinical markers for LV dysfunction.
Aims:
Patients with mild heart failure (HF) who are clinically compensated may have normal left ventricular (LV) stroke volume (SV). Despite this, altered intra-ventricular flow patterns have been recognized in these subjects. We hypothesized that, compared with normal LVs, flow in myopathic LVs would demonstrate a smaller proportion of inflow volume passing directly to ejection and diminished the end-diastolic preservation of the inflow kinetic energy (KE).
Methods And Results:
In 10 patients with dilated cardiomyopathy (DCM) (49 ± 14 years, six females) and 10 healthy subjects (44 ± 17 years, four females), four-dimensional MRI velocity and morphological data were acquired. A previously validated method was used to separate the LV end-diastolic volume (EDV) into four flow components based on the blood's locations at the beginning and end of the cardiac cycle. KE was calculated over the cardiac cycle for each component. The EDV was larger (P = 0.021) and the ejection fraction smaller (P < 0.001) in DCM compared with healthy subjects; the SV was equivalent (DCM: 77 ± 19, healthy: 79 ± 16 mL). The proportion of the total LV inflow that passed directly to ejection was smaller in DCM (P = 0.000), but the end-diastolic KE/mL of the direct flow was not different in the two groups (NS).
Conclusion:
Despite equivalent LVSVs, HF patients with mild LV remodelling demonstrate altered diastolic flow routes through the LV and impaired preservation of inflow KE at pre-systole compared with healthy subjects. These unique flow-specific changes in the flow route and energetics are detectable despite clinical compensation, and may prove useful as subclinical markers of LV dysfunction.
