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PLoS One. 2015 Apr 16;10(4):e0124011. doi: 10.1371/journal.pone.0124011. eCollection 2015.

Assessment of wall elasticity variations on intraluminal haemodynamics in descending aortic dissections using a lumped-parameter model.

Author information

1
University Hospital and Research Institute Vall d'Hebron, Universitat Autònoma de Barcelona, Barcelona, Spain; Physense, DTIC, Universitat Pompeu Fabra, Barcelona, Spain.
2
Physense, DTIC, Universitat Pompeu Fabra, Barcelona, Spain; ICREA, Barcelona, Spain.
3
Biofluid, Tissue and Solid Mechanics for Medical Applications, Institute Biomedical Technology, Ghent University, Ghent, Belgium.
4
University Hospital and Research Institute Vall d'Hebron, Universitat Autònoma de Barcelona, Barcelona, Spain.

Abstract

Descending aortic dissection (DAD) is associated with high morbidity and mortality rates. Aortic wall stiffness is a variable often altered in DAD patients and potentially involved in long-term outcome. However, its relevance is still mostly unknown. To gain more detailed knowledge of how wall elasticity (compliance) might influence intraluminal haemodynamics in DAD, a lumped-parameter model was developed based on experimental data from a pulsatile hydraulic circuit and validated for 8 clinical scenarios. Next, the variations of intraluminal pressures and flows were assessed as a function of wall elasticity. In comparison with the most rigid-wall case, an increase in elasticity to physiological values was associated with a decrease in systolic and increase in diastolic pressures of up to 33% and 63% respectively, with a subsequent decrease in the pressure wave amplitude of up to 86%. Moreover, it was related to an increase in multidirectional intraluminal flows and transition of behaviour as 2 parallel vessels towards a vessel with a side-chamber. The model supports the extremely important role of wall elasticity as determinant of intraluminal pressures and flow patterns for DAD, and thus, the relevance of considering it during clinical assessment and computational modelling of the disease.

PMID:
25881158
PMCID:
PMC4399844
DOI:
10.1371/journal.pone.0124011
[Indexed for MEDLINE]
Free PMC Article

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