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Published on: May 8, 2012
Estimation of the axial wall strains induced by an arterial stenosis at peak flow
1University Hospital, Geneva, Switzerland. pierre_andre.doriot@hcuge.ch
Insights
Arterial stenoses significantly increase axial wall stress and strain at the stenosis entrance. This localized strain, particularly in coronary arteries, may exceed 10-20%, potentially triggering adverse biological processes.
Area of Science:
- Cardiovascular Mechanics
- Biomedical Engineering
- Arterial Physiology
Background:
- Atherosclerosis and restenosis studies have largely overlooked axial wall stress.
- Circumferential stress and biological factors have been prioritized over axial mechanics.
- Recent findings suggest arterial stenoses increase axial wall stress proximal to the stenosis.
Purpose of the Study:
- To investigate axial wall strains resulting from stenosis-induced axial stress.
- To model the impact of stenosis on axial wall mechanics using theoretical spring models.
- To assess the influence of surrounding tissues on strain distribution and magnitude.
Main Methods:
- Utilized a theoretical spring model to simulate arterial wall mechanics.
- Incorporated literature data on arterial mechanical properties.
- Analyzed relative wall elongations (axial strains) under varying stenosis severity and tissue absorption.
Main Results:
- High axial wall strains are concentrated at the stenosis entrance.
- Strain distribution depends on the absorption of axial forces by surrounding tissues.
- A 75% coronary artery stenosis can induce >10% axial strain at peak flow.
- Severe stenosis or high systolic pressure may lead to >20% axial strain.
Conclusions:
- Stenosis-induced axial strains are significant and localized at the stenosis entrance.
- The magnitude of axial strain is potentially influenced by surrounding tissue properties.
- These abnormal axial strains may induce deleterious biological processes in smooth muscle cells.
Abstract:
In the last 30 years, thousands of basic or clinical studies have been devoted to atherosclerosis or to the problem of restenosis after angioplasty. In these studies, axial stresses in the vessel wall have received practically no attention, contrary to circumferential stress and purely biological aspects. Based on a recent article describing how arterial stenoses can induce a considerable increase in axial wall stress during flow systole in the region immediately proximal to the stenosis entrance, we have used a simple (theoretical) spring model and data available in the literature on the mechanical properties of arteries to investigate the relative wall elongations (axial strains) resulting from the systolic increases in axial stress generated by the stenosis. The model shows that high axial wall strains are tightly limited to the stenosis entrance if the axial wall forces generating the supplementary stress are strongly absorbed by the tissues surrounding the vessel. Inversely, if this absorption is weak, the zone of high strains extends over a longer vessel segment upstream of the stenosis entrance. The maximum strain value, which is always situated at the stenosis entrance, appears to be relatively independent of the presence or absence of surrounding tissues. The simulation also shows that in a 3 mm coronary artery presenting a 75% diameter stenosis, the axial strain at the stenosis entrance can exceed 10% at peak flow, depending on the respective axial elasticities of vessel wall and surrounding tissues. In a more severe stenosis, or in case of a pathologically high systolic pressure, the maximum strain value might even exceed 20%. Since abnormal axial strains have been shown to induce abnormal biological processes in smooth muscle cells cultures, it is quite conceivable that such axial strains are deleterious, at least in arterial segments whose length normally does not vary.
