Related Experiment Video
Updated: Aug 14, 2026

Implantation of a Carotid Cuff for Triggering Shear-stress Induced Atherosclerosis in Mice
Published on: January 13, 2012
Insights
Atherosclerosis complications may stem from engineering fatigue due to blood flow, not just lipid accumulation. Animal models support this fatigue hypothesis, suggesting hemodynamics play a key role in disease development.
Area of Science:
- Cardiovascular Science
- Biomedical Engineering
- Pathology
Background:
- Atherosclerosis involves vessel wall changes, but focus on lipid accumulation overshadows other aspects like complications.
- The prevailing lipid hypothesis inadequately explains atherosclerosis localization and complications.
Purpose of the Study:
- To propose and investigate the engineering fatigue thesis for atherosclerosis.
- To determine the role of hemodynamics in atherosclerosis development and complications.
Main Methods:
- Utilizing animal models with induced disturbances in blood flow.
- Observing morphological similarities to human atherosclerosis and its complications.
Main Results:
- Animal models with disturbed hemodynamics showed accelerated development of atherosclerosis-like disease and complications.
- Hemodynamics appear to influence dietary lipid accumulation, but combined factors do not fully replicate human atherosclerosis.
Conclusions:
- The engineering fatigue hypothesis, driven by hemodynamics, offers a plausible explanation for atherosclerosis and its complications.
- Hemodynamics are a critical factor in atherosclerosis, potentially more so than previously recognized by lipid-centric models.
Abstract:
Atherosclerosis is an ubiquitous disease effecting degenerative, proliferative and atrophic changes in the vessel wall. Preoccupation with intramural lipid accumulation has been at the expense of studies concerning other aspects of atherosclerosis including the complications. The current view of the lipid hypothesis fails to explain the localization or the complications. They can be accounted for by the thesis that atherosclerosis is due to hemodynamically-induced engineering fatigue. In animal models, in which gross disturbances of flow occur, the disease morphologically similar to atherosclerosis in man, together with the complications, can be reproduced at an accelerated rate, thus substantiating the fatigue hypothesis. Moreover, hemodynamics appears to govern dietary-induced lipid accumulation, but these two factors acting in concert will not reproduce atherosclerosis as it occurs in man.
Related Concept Videos
Arteries and Arterioles
Vascular Resistance
The primary determinants of vascular resistance are vessel diameter, blood viscosity, and vessel length. Among these, vessel diameter plays the most significant role due to the fourth power relationship described by...
Coronary Artery Disease II: Pathophysiology
Hypertension II: Pathophysiology
Atherosclerosis I: Introduction
Atherosclerosis II: Clinical Manifestations and Diagnostic Tests

