- Poster presentation
- Open Access
Left ventricular hemodynamic forces are altered in patients with dilated cardiomyopathy
© Eriksson et al; licensee BioMed Central Ltd. 2015
- Published: 3 February 2015
- Dilate Cardiomyopathy
- Hemodynamic Force
- Sphericity Index
- Adverse Cardiac Remodel
- Myocardium Initiate
Adverse cardiac remodeling is a key component of the failing heart. Increased diastolic wall stress plays a pivotal role in the development and progression of adverse cardiac remodeling. The forces generated by the left ventricular (LV) myocardium initiate blood flow, while the moving blood itself also exerts a force on the ventricular wall and heart valves. Abnormal hemodynamic forces may contribute to increased diastolic wall stress. We calculated LV hemodynamic forces from the moving blood, and hypothesized that these forces are mostly directed along the "mitral valve (MV) to apex axis" in the healthy LV, while the distribution is altered in myopathic LVs.
There was no significant difference in age (DCM: 49±14 years vs Healthy: 48±15, P=0.98) or heart rate (61±11bpm vs 67±10, P=0.22) between the groups, while LV ejection fraction (41±5% vs 61±3, P=0.00), LV end-diastolic volume (177±33ml vs 137±15, P=0.003) and LV sphericity index (0.75±0.12 vs 0.56±6, P<0.0003) was significantly different. The "SAx-max/LAx-max"ratio (figure 1) was significantly larger at both E- (0.53±0.18 vs 0.19±0.1, p<0.0001) and A-wave (0.52±0.24 vs 0.32±0.11, P<0.03) in the DCM group compared to normals. This implies that MV to apex directed flow-based forces in normal LVs are redirected towards the SAx direction in DCM LVs.
4D flow CMR data allow quantification of hemodynamic forces acting on the LV myocardium. The present data show that the distribution of hemodynamic forces is altered in LVs of DCM patients compared to LVs of healthy subjects.
This study was funded by the Swedish Heart-Lung foundation, the Swedish Research Council and the European Research Council.
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