Key result
Patient-specific computational modeling demonstrated that high-LDL concentration sites in the healthy state correspond to plaque locations, and hypertension increases regions of high-LDL concentration.
Population
Three-dimensional, patient-specific computational model of a human left coronary artery derived from…
Comparison
Computational fluid dynamics simulation of LDL… vs Simulation under normal operating pressure and…
Design
Preclinical
Authors
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Supports mechanistic hypotheses on hypertension and plaque progression; leaves open translation to human therapy.
Patient-specific computational modeling demonstrates that hypertension increases regions of high LDL concentration and that existing plaques alter local hemodynamics to promote downstream LDL accumulation, supporting clinical observations of plaque growth.
Olgaç et al. (2009) studied Coronary artery disease (n=1). Hypertensive operating pressure (120 mmHg) and diseased arterial state vs. Normal operating pressure (70 mmHg) and healthy arterial state was evaluated on Spatial shear stress distribution and LDL concentration. Patient-specific computational modeling demonstrated that high-LDL concentration sites in the healthy state correspond to plaque locations, and hypertension increases regions of high-LDL concentration.
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