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Mechanical Effects of Cardiovascular Drugs and Devices
Published in Michel R. Labrosse, Cardiovascular Mechanics, 2018
One of the most prevalent diseases of the cardiovascular system is atherosclerosis, which has been reviewed in Chapter 7. Atherosclerosis is the buildup of cholesterol plaque in the walls of the arteries. The initial lesion usually occurs decades before clinically significant effects are observed; thus, treatment of lesions has evolved as the primary remedy for vessel narrowing due to atherosclerosis. The lesion is marked by intracellular lipid accumulation, forming a fatty streak in the vessel wall. Further lipid accumulation expands to an extracellular lipid pool, which provides a site for calcification. This is followed by increased proliferation of smooth muscle and collagen deposition. When the lesion is severe, it erupts through the vessel wall, attracting platelets and forming a thrombus at the site. Atherosclerosis occurs all over the body but is most problematic in the peripheral, coronary, and cerebral arteries, which feed important capillary beds.
Intravascular Ultrasound for Molecular Imaging
Published in Robert J. Gropler, David K. Glover, Albert J. Sinusas, Heinrich Taegtmeyer, Cardiovascular Molecular Imaging, 2007
The most dangerous form of cardiovascular disease is atherosclerotic coronary artery disease, which leads to narrowing and stiffening of arteries supplying blood to the heart. Atherosclerosis arises from repeated injury, subsequent inflammation, and repair of the vascular wall. Endothelial injury leads to an inflammatory response and lipid accumulation mostly from low-density lipoprotein cholesterol in the blood. Endothelial cells, along with macrophages, promote rapid lipid accumulation leading to fatty streaks or foam cells. At this stage, atherosclerosis is mostly reversible with appropriate changes to risk factors (smoking, exercise, healthy diet, etc.). If atherosclerosis continues, a plaque (atheroma) forms around a lipid core. A stable plaque (fibroatheroma) is characterized by a thick fibrous cap composed of smooth muscles cells and a small lipid core. In contrast, rupture-prone plaque is often characterized by a large lipid core and a thin fibrous cap. They are sometimes referred to as vulnerable plaques. Note that the lipid core is highly thrombolytic. Upon rupture, lipids interact with the blood to induce thrombosis, artery blockage, and ultimately myocardial infarction. If the atheroma stabilizes, smooth muscle cell proliferation can prevent rupture but still lead to calcification and severe fibrosis. Continued plaque growth can lead to severe stenosis and myocardial ischemia. Recent studies have shown that plaque rupture, not vessel occlusion, is the leading cause of these acute events (6–7).
Elements of Continuum Mechanics
Published in Clement Kleinstreuer, Biofluid Dynamics, 2016
Based on cell culture and in vivo studies over the past decade, a working model of atherogenesis has been developed. Initiation of atherosclerosis involves monocyte migration through a dysfunctional endothelium (Ross, 1999). Advanced intimal proliferation lesions of atherosclerosis may occur by at least two pathways as described by Ross (1986): Monocytes attach to the endothelium which may continue to secrete growth factors. Sub-endothelial migration of monocytes may lead to fatty-streak formation and release of growth factors. Fatty streaks may become directly converted to fibrous plaques through the release of growth factors from macrophages or endothelial cells or both. Macrophages may also stimulate or injure the overlying endothelium. In some cases, macrophages may lose their endothelial cover and platelet attachment may occur, providing three possible sources of growth factors, i.e., platelets, macrophages, and endothelial cells. Some of the smooth muscle cells in the proliferative lesion itself may form and secrete growth factors as well. As the atherosclerotic lesion progresses, there are gaps in the endothelial surface within which lipid-filled monocytes are impacted, and the presence of foam cells in peripheral blood suggests that some are emigrating from the intima. Platelets then adhere to the exposed connective-tissue matrix underlying the endothelial defects, and this is the stage in which a true thrombogenic dimension is involved in atherosclerosis. The attached platelets play a major role in plaque growth by stimulating smooth muscle cell migration and proliferation even though they may not significantly influence initiation.
Basic pathogenic mechanisms of atherosclerosis
Published in Egyptian Journal of Basic and Applied Sciences, 2020
Hamad Abdulsalam Hamad Alfarisi, Zenab B. Hamad Mohamed, Muhammad Bin Ibrahim
The earliest histopathological lesion of atherosclerosis is the development of fatty streaks in the vascular wall at predilection points such as arterial branching sites where the laminar blood flow is disturbed [23,24]. A complex multiple processes of inflammation and oxidation are implicated in the development of fatty streaks in which LDL-c metabolism specifically appeared as a key factor [25]. The biomechanical forces at arterial branching areas found to be the triggering factor of endothelial dysfunction creating barrier impairment (endothelial misalignment), proinflammatory process and prothrombotic function [18,24]. Once endothelial dysfunction induced, fatty streaks develop due to exposure of matrix proteoglycans and loss of confluent elastic layer of blood vessel lumen which commonly found at arterial bifurcation sites [26]. Recent updates indicate the role of hypercholesterolemia as a direct cause of endothelial dysfunction by changing the endothelial permeability hence allowing the migration of LDL-c into the vascular wall [21]. Figure 3 illustrates the overall pathogenesis of atherosclerosis as an integrated process between oxidative stress and inflammatory process.
The vascular protective effects of trihoney in hypercholesterolemic atherosclerotic rabbits, a comparative study with atorvastatin
Published in Egyptian Journal of Basic and Applied Sciences, 2022
Hamad Abdulsalam Hamad Alfarisi, Muhammad Bin Ibrahim, Zainab Bubakr Hamad Zubi
Atherosclerosis is defined as a chronic inflammatory disease of the inner wall of large- and medium-sized arteries [1]. This condition may lead to several vascular complications such as heart attack, acute coronary syndrome (ACS), stroke, peripheral arterial disease, or even death [2,3]. The earliest histopathological lesion of atherosclerosis is the fatty streaks which further progresses to atherosclerotic plaque in the vascular wall at predilection points such as arterial branching sites where the laminar blood flow is disturbed [4,5].
Carotid hemodynamic response to external pressure and comparison with induced-stenosis progression: a fluid-structure interaction study
Published in Computer Methods in Biomechanics and Biomedical Engineering, 2022
Kshitij Shakya, Dalchand Ahirwar, P. M. Nabeel, Shubhajit Roy Chowdhury
Atherosclerosis is an inflammatory disease of the medium and large arteries such as carotid, aorta, coronary and peripheral arteries (Mantella et al. 2021). It is a prominent cause of death worldwide due to its role in the development of cardiovascular disease and its chronic nature (Khamehgir-Silz et al. 2021; Libby 2021). The injury to the arterial wall induces an inflammatory response which can lead to intimal thickening and the initiation of atherosclerosis (Shabbir et al. 2021). Additionally, high cholesterol, hypertension, and high shear stress in blood vessels increase the formation of lesions (Mohmmad-Rezaei et al. 2021; Zhang 2021). The endothelial cells forming the uppermost layer of the lumen act as a selective barrier between blood and the vessel wall and make it easy for the low-density lipoprotein to diffuse through the endothelium, which, however, is suggested to be the primary source of plaque lipids (do Brito Valente et al. 2021; Kato et al. 2021). The atherosclerotic plaque is classified as early plaques where lipid droplets are found in the intima, and fatty streaks are visible with layers of foam cells. In the intermediate plaques, lipid core is formed with new fibrous tissue overlying it and sometimes causes calcification and miscellaneous features accompanied by surface disruption, intraplaque haemorrhage, and thrombosis (Sakakura et al. 2013; Babaniamansour et al. 2020). Carotid artery stenosis, a consequence of atherosclerosis, is an important cause of stroke. Atherosclerotic plaque in the carotid artery can occur from the aortic arch to cerebral arteries along the carotid artery axis (Heck and Jost 2021). However majority of the stroke events happen due to plaque at the carotid artery bifurcation region. In a study, it was found that, among the total patients who suffered ischemic strokes, 20–30% of them were closely related to carotid atherosclerosis (Dalai and Datla 2021). Carotid artery stenosis can be either symptomatic like a transient ischemic attack (TIA) or asymptomatic.