CORRESPONDENCE: LETTER TO THE EDITOR
Local Blood Pressure Rather Than Shear Stress Should Be Blamed for Plaque Rupture
Arnold P.G. Hoeks, PhD*,
Koen D. Reesink, PhD,
Evelien Hermeling, MSc and
Robert S. Reneman, MD, PhD
* Department of Biophysics, Cardiovascular Research Institute Maastricht, University Maastricht, P.O. Box 616, 6200 MD Maastricht, the Netherlands (Email: A.Hoeks{at}bf.unimaas.nl).
A recent article (1) published in the Journal corroborates the hypothesis that shear stress triggers fibrous cap rupture. In 20 patients with considerable lumen narrowing (maximum area reduction of 80 ± 7%), ulcerative plaque rupture preferentially occurred in areas with locally high wall shear stresses (WSS), estimated by means of computational modeling. However, the authors of this study do not answer the basic question of whether local WSS distribution is indeed related to plaque rupture.
Hemodynamics is an interplay between pressure, flow, and morphology. The study by Fukumoto et al. (1) mainly considers the interaction between flow and morphology under steady-state conditions. Compared with an unaffected site, the increase in WSS around a plaque can be estimated to be a factor of 10 assuming simple circular geometries. For a normal WSS of 0.6 Pa (2), the mean WSS within the stenosis will remain <10 Pa, which might be too low to initiate plaque rupture directly, as acknowledged by the authors.
The article does not fully appreciate the influence of local blood pressure within a stenosis, although this pressure was calculated as well. Let us consider the hemodynamics in the vicinity of a stenosis (3), where in a steady-state situation the sum of potential energy (local blood pressure) and kinetic energy (local blood velocity) is constant (Bernoulli equation): an increase in velocity induced by geometry decreases local pressure (3). An area reduction of 80% converts to an increase in velocity by a factor of 5, and the associated pressure decrease will be 1.1 kPa (8.4 mm Hg), which is 100 times greater than the WSS. In the longitudinal direction, the pressure gradient across the wall also goes down by 8.4 mm Hg and is partially restored distal to the stenosis.
Now let us assume that the vasa vasorum function properly (4). Then, within the arterioles supplying the plaque, blood pressure highly depends on the blood pressure proximal to the stenosis, despite frictional losses along the arterioles. Because of high stenotic blood flow velocities, not only a high WSS but also a substantial pressure gradient develops across the wall towards the lumen. This situation is opposite to normal conditions where the transmural pressure gradient is directed outward.
Pulsatile conditions aggravate the situation. High-grade stenoses cause strong pulse wave reflections, increasing the proximal pulse pressure by almost a factor of 2. The pulsatile transmural pressure and the longitudinal pressure gradient into the stenosis contribute to (position-dependent) wall and plaque deformation. Because of the fragility of plaque structures (5), this deformation will very likely contribute to cap rupture. The pressure gradient across a plaque may contribute to the release of thrombogenic material into the lumen.
Wall shear stress plays an important role in atherogenesis but is merely coincidental with plaque rupture. The combination of high velocities due to lumen narrowing, the vasa vasorum, plaque composition, and structure and pressure wave reflection induce longitudinal and transmural pressure gradients and plaque deformation, contributing to plaque rupture. A small residual lumen generates high inward pressure gradients and inward "bleeding."
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1. Fukumoto Y, Hiro T, Fujii T, et al. Localized elevation of shear stress is related to coronary plaque rupture: a 3-dimensional intravascular ultrasound study with in-vivo color mapping of shear stress distribution J Am Coll Cardiol 2008;51:645-650.[Abstract/Free Full Text]2. Reneman RS, Arts T, Hoeks AP. Wall shear stress—an important determinant of endothelial cell function and structure—in the arterial system in vivo. Discrepancies with theory. J Vasc Res 2006;43:251-269.[CrossRef][Web of Science][Medline] 3. Holen J, Waag RC, Gramiak R. Doppler ultrasound in aortic stenosis: in vitro studies of pressure gradient determination Ultrasound Med Biol 1987;13:321-328.[CrossRef][Web of Science][Medline] 4. Ritman EL, Lerman A. The dynamic vasa vasorum Cardiovasc Res 2007;75:649-658.[Abstract/Free Full Text] 5. Virmani R, Kolodgie FD, Burke AP, et al. Atherosclerotic plaque progression and vulnerability to rupture: angiogenesis as a source of intraplaque hemorrhage Arterioscler Thromb Vasc Biol 2005;25:2054-2061.[Abstract/Free Full Text]
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