Biomedical subjects

Pierre-André Doriot

Publications and source records attributed to Pierre-André Doriot.

3 recordsLinked to original sources

PubMed2004

Residual stenosis poststenting and subsequent decrease in the proximal reference diameter are correlated: excessive axial wall stress is a plausible explanation.

PURPOSE: To test the hypothesis that edge restenosis in stented lesions might be due to an increase in axial wall stress in the adjacent proximal vessel segment by examining whether the proximal reference diameters of conventionally stented lesions are reduced at follow-up and whether this reduction depends on the degree of residual stenosis poststenting. METHODS: The literature published in the past 5 years dealing with restenosis following implantation of standard stents was screened for the availability of (1) reference vessel diameters poststenting, (2) mean residual stenosis poststenting, and (3) mean reference vessel diameters at follow-up in the same patients or groups of patients. Data collected from 11 publications were pooled and used to compute the change in reference segment diameter over time. These differences were compared to the residual stenosis poststenting by nonlinear regression. RESULTS: The reduction in the mean reference diameters over time and the mean residual stenosis poststenting appear to be strongly correlated (r2 = 0.838), which supports the idea that the evolution of a stenosis adjacent to a stent margin depends on the severity of the residual stenosis. CONCLUSIONS: This finding indicates that edge restenosis might be due to excessive axial wall stress. It may also explain, at least partly, why edge restenosis is observed with catheter-based brachytherapy and radioactive or drug-eluting stents.

Arterial Occlusive Diseases↗

PubMed2003

Some unusual considerations about vessel walls and wall stresses.

The "zero-stress state" of blood vessels is usually defined with respect to the atmospheric pressure p(a) ( approximately 750 mmHg). As a consequence, circumferential and axial wall stresses due to a positive transmural pressure can only be positive and thus, by definition, only tensile. If the zero-stress state were defined with respect to vacuum pressure (0 mmHg), the compressive stress -p(a) generated by p(a) everywhere in the wall would, however, be included so that negative (=compressive) wall stresses would formally become possible. In order to examine the consequences this alternative definition would have for arteries, we have compared radial, circumferential, and axial stresses calculated "conventionally" to the values they take when the zero-stress state is defined "correctly" by reference to the vacuum pressure. It turns out that, under normal physiologic conditions, axial stress and perhaps also circumferential stress might well be compressive in many elastic and conductance arteries, contrary to the intuitive conviction of many people. Since the type of stresses a vessel wall is submitted to may be highly relevant for its structure and mechanical properties, this unconventional way of considering wall stresses may reveal unsuspected relationships between wall stresses on one side, and wall structure, vessel growth, adaptation and repair processes, atherosclerosis, angioplasty or stenting on the other side. Similar considerations might also prove useful with regard to cardiac hypertrophy.

Blood Pressure↗

PubMed2003

Estimation of the supplementary axial wall stress generated at peak flow by an arterial stenosis.

Mechanical stresses in arterial walls are known to be implicated in the development of atherosclerosis. While shear stress and circumferential stress have received a lot of attention, axial stress has not. Yet, stenoses can be intuitively expected to produce a supplementary axial stress during flow systole in the region immediately proximal to the constriction cone. In this paper, a model for the estimation of this effect is presented, and ten numerical examples are computed. These examples show that the cyclic increase in axial stress can be quite considerable in severe stenoses (typically 120% or more of the normal stress value). This result is in best agreement with the known mechanical or morphological risk factors of stenosis progression and restenosis (hypertension, elevated pulse pressure, degree of stenosis, stenosis geometry, residual stenosis, etc). The supplementary axial stress generated by a stenosis might create the damages in the endothelium and in the elastic membranes which potentiate the action of the other risk factors (hyperlipidaemia, diabetes, etc). It could thus be an important cause of stenosis progression and of restenosis.

Arterial Occlusive Diseases↗