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Mathematical Model of Aortic Coarctation to Elucidate Mechanisms of Vascular Remodeling
Author(s) -
Higareda Deidre J.,
Tran Nga V.,
Bustillos Jacob L.,
Nguyen Phuc H.,
Quick Christopher M.
Publication year - 2013
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.27.1_supplement.1217.24
Subject(s) - pulsatile flow , arterial stiffness , cardiology , pulse pressure , medicine , peripheral , mechanics , blood pressure , physics
Aortic coarctation is of interest to both clinicians and mechanobiologists, because it induces high upstream pulse pressures (PP) and vascular remodeling. Interpreting either clinical or experimental data to infer adaptive mechanisms is challenging: vascular remodeling induces changes in PP, and changes in PP induce vascular remodeling. Further complicating analysis, PP depends on the architecture of the systemic arterial network as well as the properties of each component artery—radius (r), wall thickness (h), and stiffness (E). The resulting complexity has made it difficult to test one of the most enduring hypotheses: high pulsatile wall stress (σ) causes arterial stiffening. Therefore, we used a classical human arterial system model with realistic architecture (Westerhof, 1968) to predict local PP from the r, h, and E of each of its 121 arterial segments. Assuming Laplace's Law, σ was calculated from local PP, r, and h. We then made vessels adaptive by assuming E increases linearly with σ. The result was a fundamental instability leading to positive feedback between changes in E and PP. Assuming instead that E decreases with σ not only led to realistic values of local vessel E and PP, it correctly predicted an increase in compliance upstream of a coarctation and a partial restoration of normal pulse pressure.