Author + information
- Michail I. Papafaklis, MD, PhD∗ ()
- ↵∗Michailideion Cardiac Center, Medical School, University of Ioannina, Stavrou Niarchou Avenue, Ioannina 45100, Greece
I read with great interest the article in iJACC by Choi et al. (1), who provided an innovative characterization of the hemodynamic force acting on individual plaques in a series of patients. By applying computational fluid dynamics in coronary computed tomography angiographic data, these investigators quantified the “axial plaque stress” (i.e., the hemodynamic stress acting on the longitudinal direction of stenotic lesions) and related that force to geometric lesion features.
A critical parameter in the elaborate characterization performed by the investigators is the assumption of hyperemic blood flow in all their computational fluid dynamics analyses. By applying boundary conditions of high blood flow, axial plaque stress values in this study actually represent the peaks in axial tensile stress that are induced by the hyperemia-triggered blood pressure drop over a lesion. According to fluid mechanics principles, the pressure drop across a stenosis results from the sum of the following: 1) viscous (frictional) losses along the entrance (entrance effects) and mostly at the throat of the stenosis; and 2) inertial (kinetic energy) losses downstream secondary to the sudden lumen expansion that creates zones of flow separation and recirculation. Both losses (primarily inertial) are rapidly augmented with increasing blood flow rates and are maximized under conditions of hyperemic blood flow. The nonlinear increase in inertial losses with increasing flow rates causes the pressure gradient on the upstream portion of an idealized symmetrical lesion (upstream vs. downstream morphology) to be significantly greater than that on the downstream portion of the lesion, and thus a net axial force that acts on the plaque from upstream to downstream governs under hyperemic conditions, as also shown in Figure 1 of the article (i.e., upstream axial plaque stress is higher than downstream stress) (1).
In contrast, under conditions of resting flow, the pressure gradient would be similar in the upstream and downstream portions of a symmetrical lesion, thus resulting in “neutralization” of the opposite-acting axial stresses in the upstream and downstream regions. Because the absolute rate of blood flow is critical for the value of axial plaque stress and the dominance of either net anterograde or retrograde axial plaque force, Choi et al. (1) could also investigate the relationship of the predicted axial plaque stress (including the pattern of the stress distribution) with the absolute rate of hyperemic flow, which, of note, is not known but is variably estimated for each patient according to a model used by these investigators.
The application of hyperemic blood flow for computing the peaks in axial plaque stress distribution also has important implications for the mechanism of the plaque rupture that one presumably intends to predict by using the proposed biomechanical approach. Hyperemic blood flow occurs during physical exertion, and thus axial plaque stress could be helpful in predicting exertion-triggered acute coronary syndromes but may not be relevant in predicting cardiac events at resting conditions (e.g., predicting myocardial infarctions or deaths at rest). Those events at resting conditions may be a result of sudden blood pressure surges translating into sudden peaks of local tensile stress acting perpendicularly to the endothelial surface (i.e., particularly related to the radial component of hemodynamic stress).
Finally, another issue I would like to raise is that hyperemic flow conditions have a great impact on the computed wall shear stress. Mean values of wall shear stress in the article were >10 Pa (= 100 dynes/cm2) in both upstream and downstream regions of the lesions studied (1). This value is much greater than the expected range of wall shear stress magnitude observed in arteries (2). Although the association of low shear stress (<1 to 1.5 Pa) with atherosclerosis development or progression and high-risk plaque features (vs. moderate or high shear stress) is well documented both in experimental models and in clinical studies (3), the pathophysiological implications of very high shear stress are not known. The transient peaks of the entire wall shear stress distribution that may occur under hyperemic blood flow conditions warrant further investigation.
Please note: The author has reported that he has no relationships relevant to the contents of this paper to disclose.
- American College of Cardiology Foundation
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