A patient-specific numerical modeling of the spontaneous coronary artery dissection in relation to atherosclerosis
Introduction
Spontaneous coronary artery dissection (SCAD) is a commonly observed clinical complication of angioplasty [1], which can trigger myocardial infarction (MI). SCAD initiates from a tiny tear in the intima layer of the arterial wall [2] and propagates to the interface of the intima-media [3]. The dissected layer of the arterial wall due to SCAD can partially or totally occlude the lumen, invoking downstream ischemia [4], [5].
Dissection of the arterial wall is clinically difficult to diagnose [2], therefore, a tiny crack in the intima layer can easily propagate to the media by the passage of time under the blood flow shear and normal stresses. Numerical methods, such as finite element (FE), not only can evaluate the critical stresses and strains at the dissection site but also analyze the propagation pattern of a crack in the intima layer under various diastolic and systolic pressures. So far, numerical studies in regard of the fracture of the arterial wall mostly have been focused on the aortic tissues. Gültekin et al., developed a phase-field approach to investigate the fracture of an aortic tissue [6]. Rajagopal et al., developed a mathematical model to predict a tear initiation and propagation in an aortic tissue [7]. A simplified FE model of the aorta was used to calculate the stresses at the crack site of the intima and media layers of the aorta [8]. Some other researchers instead of using the FE modeling approach, tried to address the fracture of the arterial tissues using continuum mechanics on a basis of the collagen and elastin fibers overstretching [9], [10], [11], [12], [13]. Three factors in their studies have been introduced as the pathogenesis of the aortic dissection, including the hemodynamics alterations which affect the load distribution on the arterial wall, the mechanical environment changes owing to the presence of a small initial lesion [7], and remodeling of the arterial tissue because of the blood pressure alteration [14].
Although non-atherosclerotic SCAD is typically a culmination of disease pathways that predispose arterial beds to injury [15] in both the intima and media layers [16], atherosclerosis has not been confidently accepted as the main reason of arterial dissection [17], [18]. The reason is related to the medial layer atrophy and scarring from atherosclerosis which limit the propagation of the dissection [19]. An anisotropic extension of the irreversible isotropic cohesive element model was used to simulate the fracture of a plaque [20] and fracture of a healthy aortic tissue [21]. The dissection mechanisms as a result of balloon angioplasty in an atherosclerotic coronary artery was investigated using a simplified FE model and cohesive interface modeling [22]. Although the mechanisms of crack initiation and propagation of the plaque in an atherosclerotic coronary artery were documented, still there is a lack of knowledge on the differences between these mechanisms among the healthy and atherosclerotic human coronary arterial walls. Therefore, this study was aimed at numerically simulating the initiation and propagation of a crack in the intraluminal and radial locations of the healthy and atherosclerotic human coronary arterial wall using virtual crack extension (VCE) method [23] of extended FEM (XFEM). To augment the accuracy of the numerical results, the elasto-plastic mechanical properties of the healthy and atherosclerotic human coronary arteries were experimentally measured using uniaxial tensile test and incorporated into our FE model. The parameters of fracture mechanics, such as the crack tip opening displacement (CTOD), crack tip opening angle (CTOA), and strain energy release rate (J-integral) at the dissection site for both the healthy and atherosclerotic human coronary arterial patient-specific models were calculated and compared. The results will have practical implications in extending our understanding of the role of the atherosclerosis in the SCAD initiation and propagation during a cardiac cycle.
Section snippets
Experimental measurements
Coronary arteries of 12 cadavers, including 6 healthy and 6 atherosclerotic male individuals aged 51 ± 12 (Mean ± SD) and 56 ± 13 years, respectively, were excised during autopsy within 5 h post-mortem. The atherosclerosis cadavers were selected according to their medical history approved by doctors of hospitals and legal medicine organization (data not reported here). All procedures were carried out following agreement of the institutional review board of Basir hospital, Tehran, Iran based on
Experimental results
The elasto-plastic mechanical properties of the healthy and atherosclerotic human coronary arteries were calculated and summarized in Table 1. The elastic modulus and yield stress of the healthy coronary tissues were significantly (n = 6, p ≤ 0.05, post hoc Scheffe method) higher than that of the atherosclerotic one. However, no statistical differences were observed in regard of the yield strain values (Table 1).
Numerical results
The numerical simulations were conducted in a cardiac cycle, with the minimum
Discussions
A tear in the coronary arterial wall occurs when the stress due to blood flow exceeds the ultimate strength of any of the layers, i.e., intima, media, and adventitia. The critical pressure required for the onset of propagation and subsequent SCAD depends on the tensile strength and geometry of the arterial wall. Due to the importance of these two parameters in SCAD simulation, the fresh human healthy and atherosclerotic coronary arterial walls were removed from cadavers for the experimental
Conclusions
The relation between SCAD and atherosclerosis is a controversial clinical issue. The question that how the initial crack because of SCAD can mechanically propagate into the interface of the intima-media and trigger a false lumen has still not been answered. This study, for the first time in the fields of SCAD and fracture biomechanics of the arterial tissues, was aimed at calculating the fracture parameters of the healthy and atherosclerotic human coronary arterial walls using VCM of XFEM.
Funding
This research received no specific grant from any funding agency in the public, commercial, or not-for-profit sectors.
Ethical issues
The use of experimental on the human body was approved by the committee of the Basir hospital with the letter ID of 65998/510-987-97. This study was also entirely adhered to the declaration of the Helsinki in 2008.
Declaration of Competing Interest
None declared.
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