Arterial buckling is associated with the abdominal aortic aneurysm (AAA). The disease can be caused by multiple contributing factors, including high blood pressure, aging, connective tissue disorders, atherosclerosis, genetic disease, and various pathologic changes in the arteries (Liu and Han 1192; Luetkemeyer et al. 70; Mrowiecki et al. 1258; Vandiver 1). However, despite the rise of the research on arterial buckling, its underlying mechanisms are still understudied (Lee et al. H873). The buckling instabilities in arteries are associated with high rates of mortality and disability, entailing healthcare, demographic, and socioeconomic problems. Given the detrimental consequences of this issue, this paper will focus on the exploration of arterial elastic instability and its relation to abdominal aortic aneurysm (AAA).
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Despite the existence of some controversy in research findings related to arterial buckling, elastic instability of the aorta is identified as the major factor contributing to abdominal aortic aneurysm (AAA). According to statistical data provided by Mrowiecki et al. (1258), an abdominal aortic aneurysm (AAA) occurs in approximately “8% of male patients over 60 years of age.” Aneurysm rupture is the most severe complication of abdominal aortic aneurysm, resulting in about 80% mortality. Elastic stability ensures healthy arterial functions and hemodynamic actions (Vandiver 2). The scales of the disease occurrence and its consequences predetermine the importance of research on elastic instability in arteries in general and the aorta in particular.
For the proper understanding of interconnections between arterial elastic instability and abdominal aortic aneurysm (AAA), the structure of the aortic walls should be considered. The aorta is the major artery in the human body that is divided by the diaphragm into the thoracic and abdominal aorta. Across the lifespan, the aorta transfers approximately 200 million liters of blood. Histologically, the walls of the aorta consist of three layers as follows: 1) a thin inner layer (tunica intima) lined with endothelium, 2) a thick layer (tunica media) characterized by the presence of elastin and collagen fibers, and 3) an outer layer (tunica adventitia) that contains mostly collagen, vasa vasorum, and lymph.
Because of its elasticity, the aorta functions as a “pump” during diastole, ensuring the coronary perfusion. The aorta possesses elastic stability and strength due to such extracellular components as collagen and elastin (Vandiver 1). Aortic elastin is primarily included in the extracellular matrix at the early stages of embryonic development. Elastic fibers are composed of cross-linked monomers and elastin-containing proteins, such as fibrillin-1, which are organized into a thin elastic membrane. Elastin is one of the most stable structural components of the aortic extracellular matrix, and the period of its biological half-life reaches decades, making the flexibility and elasticity the basic properties of the normal aortic wall. On the contrary, the destruction of elastin in the aortic tunica is the most frequent morphological abnormality specific to an abdominal aortic aneurysm.
Decreased amounts of elastic fibers in the aortic walls can be caused by various factors. Taking into account the etiology, factors contributing to abdominal aortic aneurysm are divided into congenital and acquired. Luetkemeyer et al. state that elastic instability is associated with genetic diseases that induce arterial tortuosities, such as cutislaxa, Loeys–Dietz syndrome, Williams syndrome, and hereditary arterial tortuosity syndrome (80). According to Lee et al., the degradation of arterial elastic stability is caused by increased blood flow, hypertension, and aging-related arterial tortuosity (H873). Liu and Han emphasize that high blood pressure, vascular diseases, atherosclerosis, and different pathologic changes in the aorta can diminish the mechanical stability and elasticity of the artery, causing its buckling and tortuosity (1192). Irrespective of its cause, abnormal elastic stability of the aortic wall results in the abdominal aortic aneurysm (AAA) characterized by the vessel tortuosity, the buckling in the aorta, and the increase in the diameter of the vessel in more than two times in comparison with its normal condition (“Part A—Theoretical Background” 2).
Macroscopically, aortic aneurysms are extended segments of the aorta of different sizes. The inner surface of an aneurysm contains atherosclerotic plaques, which are often calcified and ulcerated. Depending on the degree, location, and extension of abnormalities in the aortic wall, the shape of aneurysms can be saccular or fusiform. Saccular aneurysms occur when there is a localized change in one of the aortic walls, producing the cavity similar in its shape to a bag whose walls are buckling aortic fibers. Fusiform aneurysms are diffuse buckling of the entire perimeter of the abdominal aorta associated with a large circular lesion of the aortic segment. Saccular aneurysms are more inherent in inflammatory processes, while diffuse fusiform aneurysms are observed in individuals diagnosed with atherosclerosis.
The role of elastic instability in the formation of the abdominal aortic aneurysm can be proved from the engineering perspective. Referring to the concept developed by Holzapfel et al., Vandiver states that “At higher pressures, the collagen fibers are stretched, and the resulting mechanical response is anisotropic.” (3) The process of blood circulation in the abdominal aortic aneurysm is characterized by the sharp slowdown in the linear blood flow velocity and turbulence. This is clearly evident in the cineradiogram-based examination and confirmed by the flowmetry curve, which approximates the curve characteristic of complete occlusion.
The mechanisms of slow blood flow in the aneurysmal area can be represented as follows: the flow of blood rushes along the afflicted aortic walls, and the central stream slows down its speed due to the return of blood, caused by the turbulence, thrombotic masses, and the aortic bifurcation. After the formation of an abdominal aortic aneurysm that is twice as much as the diameter of the abdominal aorta, hemodynamics inside the cavity performs in accordance with the law of Laplace (Bucchi and Hearn 8). The pressure increases in direct proportion to the radius of the aorta at a constant magnitude. The pressure on the aortic wall rises disproportionately because the pressure itself enlarges the radius of the artery and decreases the wall thickness. If there are no elastic abnormalities in the aorta, the high pressure does not cause the rupture of the abdominal aortic aneurysm. However, a better insight into processes within the aorta can be provided by the “fluid-structure interaction model” (“Part B—Application and Comparison” 165).
Summing up, the elasticity of the aorta is an important auxiliary factor during the blood circulation due to a substantial reduction of the load on the heart and the amount of required energy. This is achieved by the fact that the heart does not overcome the inertia of the liquid column and frictional forces. The next portion of blood ejected by the left ventricle during systole is located in the initial section of the aorta due to its transverse extension. A significant portion of the contraction energy is converted into potential energy of elastic recoil of the aorta. A decrease in the aorta elasticity and an increase in peripheral resistance put a strain on the myocardium.
Elastic arterial instability is a significant determinant of the occurrence of abdominal aortic aneurysms (AAA). The disease progressive nature frequently leads to the rupture of an aneurysm, is associated with high risks of lethal outcome. Therefore, to study the elastic instability of the aorta is of paramount importance.
Bucchi, Andrea, and Grant E. Hearn. “Predictions of Aneurysm Formation in Distensible Tubes: Part A—Theoretical Background to Alternative Approaches.” International Journal of Mechanical Sciences, vol. 71, 2013, pp. 1-20.
“Predictions of Aneurysm Formation in Distensible Tubes: Part B—Application and Comparison of Alternative Approaches.” International Journal of Mechanical Sciences, vol. 70, 2013, pp. 155-170.
Lee, Avione Yvonne, et al. “Effects of Elastin Degradation and Surrounding Matrix Support on Artery Stability.” American Journal of Physiology. Heart and Circulatory Physiology, vol. 302, no. 4, pp. H873-H884.
Liu, Qin, and Hai-Chao Han. “Mechanical Buckling of Artery under Pulsatile Pressure.” Journal of Biomechanics, vol. 45, no. 7, 2012, pp. 1192-1198.
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Luetkemeyer, Callan M., et al. “Critical Buckling Pressure in Mouse Carotid Arteries with Altered Elastic Fibers.” Journal of the Mechanical Behavior of Biomedical Materials, vol. 46, 2015, pp. 69-82.
Mrowiecki, Wojciech, et al. “Inflammatory Aortic Abdominal Aneurysm–Immunophenotypic Characterization of Inflammatory Infiltrate.” Archives of Medical Science: AMS, vol. 10, no. 6, 2014, pp. 1258-1262.
Vandiver, Rebecca M. “Buckling Instability in Arteries.” Journal of Theoretical Biology, vol. 371, 2015, pp. 1-8.