Controlling cardiac transport and plaque formation.

Area of Science:

• Cardiovascular science
• Biomedical engineering
• Hemodynamics

Background:

• Atherosclerosis involves LDL particle and macrophage infiltration into artery walls.
• Blood flow patterns, particularly low shear stress and high oscillations, influence LDL infiltration and plaque development.
• Plaque rupture often occurs near the minimum lumen area, prompting investigation into the role of adjacent plaques.

Purpose of the Study:

• To investigate the hemodynamic forces generated by a severe distal atherosclerotic plaque.
• To determine if these forces can destabilize a proximal, non-stenotic plaque and promote rupture.

Main Methods:

• Developed physical models of coronary artery stenoses (single and double).
• Utilized continuous Doppler particle image velocimetry (CDPIV) to analyze blood flow between stenoses.
• Measured hydrostatic pressure acting on the proximal plaque.

Main Results:

• A significant distal stenosis created disturbed blood flow with high shear rates and oscillatory patterns.
• These hemodynamic conditions, combined with high hydrostatic pressure, increased LDL and macrophage uptake in the proximal plaque.
• The disturbed flow enriched the lipid core, and high pressure induced stresses that can trigger plaque rupture.

Conclusions:

• Hemodynamic forces from a severe distal stenosis can destabilize a proximal plaque.
• This interaction promotes plaque vulnerability by enhancing lipid accumulation and internal stress.
• Understanding these mechanics is crucial for predicting and preventing atherosclerotic plaque rupture.