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Arteropathies, Microcirculation and Vasculitis
Published in Mary N. Sheppard, Practical Cardiovascular Pathology, 2022
Arteriosclerosis affects both arteries and arterioles. There is gradual replacement of vascular smooth muscle cells by collagen (Fig. 11.1) and deposition of plasma proteins in the smooth muscle to produce hyaline change. This process is accelerated by age, hypertension and diabetes mellitus. Arteriosclerosis lowers the compliance of the arterial tree, and contributes to the age-related increase in systolic blood pressure. Arteriosclerosis differs from atherosclerosis in that there is no intimal lipid deposition with resultant inflammation.
Dyslipidemia
Published in Jahangir Moini, Matthew Adams, Anthony LoGalbo, Complications of Diabetes Mellitus, 2022
Jahangir Moini, Matthew Adams, Anthony LoGalbo
Atherosclerosis is defined as the development of atheromas, which are intimal plaques collecting in the lumens of medium- and large-sized arteries such as the coronary, carotid, and cerebral arteries. The aorta and its branches as well as the major arteries in the extremities can be affected. The patchy plaques are made up of lipids, inflammatory and smooth muscle cells, and connective tissue. Atherosclerosis is related to dyslipidemia, diabetes mellitus, cigarette smoking, family history, hypertension, obesity, and a sedentary lifestyle. Once the plaques grow or rupture, blood flow can be reduced or obstructed. Atherosclerosis is the most common form of arteriosclerosis, which describes disorders that thicken arterial walls and cause them to lose elasticity. Atherosclerosis is very serious, since it results in coronary artery disease (CAD) and cerebrovascular disease (CVD). There are also nonatheromatous forms, which are called arteriolosclerosis and Mönckeberg arteriosclerosis.
Food Interactions, Sirtuins, Genes, Homeostasis, and General Discussion
Published in Chuong Pham-Huy, Bruno Pham Huy, Food and Lifestyle in Health and Disease, 2022
Chuong Pham-Huy, Bruno Pham Huy
Mechanisms for the prevention of arteriosclerosis by antioxidants have been proposed. The mechanism of oxidized LDL cholesterol has been suggested as the atherogenic factor that contributes to heart disease (2). Dietary antioxidants neutralize oxidized LDL cholesterol (bad cholesterol), thereby preventing atherosclerosis, a disease of the arteries characterized by the deposition of fatty material on their inner walls. In addition, phytochemicals have been shown to have roles in the reduction of platelet aggregation, modulation of cholesterol synthesis and absorption, and reduction of blood pressure. Recently, C-reactive protein, a marker of systemic inflammation, has been reported to be a stronger predictor of cardiovascular disease than LDL cholesterol, suggesting that inflammation is a critical factor in cardiovascular disease (2, 7). Inflammation not only promotes initiation and progression of atherosclerosis but also causes acute thrombotic complications of atherosclerosis. Therefore, the anti-inflammatory activity of phytochemicals obtained from the combination of different plant foods may play an important role in the prevention of CVDs (2).
Relationship between ambulatory arterial stiffness index and the severity of angiographic atherosclerosis in patients with H-type hypertension and coronary artery disease
Published in Clinical and Experimental Hypertension, 2023
Li Dong, Jing Liu, Yan Qin, Wen-Juan Yang, Liang Nie, Hua-Ning Liu, Qing-Hua Hu, Yu Sun, Wen-Yan Cao
According to epidemiological data statistics from China, patients with H-type hypertension account for about 80.3% of the total number of patients with hypertension (15); accordingly, the prevention and treatment of hypertension in China should be focused on. Patients with H-type hypertension have a higher risk of target organ damage, including to the heart, brain and kidney, than patients without H-type hypertension (16). In particular, the disease is closely related to the occurrence of CAD and is considered to be an independent risk factor for cardiovascular disease. Arteriosclerosis is a very important predictor of cardiovascular and cerebrovascular events, such as myocardial infarction, stroke and heart failure, and is an abnormal embodiment of arterial structure and function and an important marker of arterial stiffness (17).
Bidirectional role of reactive oxygen species during inflammasome activation in acrolein-induced human EAhy926 cells pyroptosis
Published in Toxicology Mechanisms and Methods, 2021
Liping Jiang, Songsong Luo, Tianming Qiu, Qiannan Li, Chunteng Jiang, Xiance Sun, Guang Yang, Cong Zhang, Xiaofang Liu, Lijie Jiang
Atherosclerosis, which is a chronic inflammatory disease, is the leading cause of mortality worldwide (Soehnlein and Libby 2021; Xu et al. 2021). Early stages of atherogenesis characteristics are endothelial cell dysfunction, persistent inflammatory response, and changed vascular homeostasis (Mehta and Malik 2006; Badimón et al. 2009). Arterial inflammation is triggered by endothelium, ultimately results in endothelial cell activation and recruited inflammatory cells to the blood vessels (Mudau et al. 2012). Genetic, lifestyle, and environmental factors would all contribute to the occurrence of arteriosclerotic vascular disease. Epidemiological studies have shown evidence of the link between cigarette smoke and atherosclerosis (Barnoya and Glantz 2005; Raghuveer et al. 2016; Arnett et al. 2019). However, the mechanism of tobacco smoke-induced atherosclerosis remains unclear.
Ventricular-arterial coupling: definition, pathophysiology and therapeutic targets in cardiovascular disease
Published in Expert Review of Cardiovascular Therapy, 2021
Sahrai Saeed, Hannes Holm, Peter M Nilsson
Arterial stiffening is a common feature of aging, also called arteriosclerosis, which is inevitable [6,25]. It is important to differentiate atherosclerosis from arteriosclerosis. The former is referred to as narrowing of the arteries due to intimal calcification and plaque formation, while the latter is referred to as age-related dilation of the arterial (aortic) lumen and thickening of the medial layer; i.e. increased arterial stiffness [25]. Age-related changes in arterial stiffness typically involve fragmentation and degeneration of elastin, relative increase in collagen content, intima-media thickness and cross-linking of collagen fibers, which can be promoted by enzymatic or mechanical mechanisms [26]. When the aorta becomes rigid/stiff either due to advanced aging or by the influence of cardio-metabolic risk factors, it loses its buffer function and the forward pressure waves propagate rapidly, with a progressive increase in downstream velocity, and backward pressure waves returning to the heart early in systole [22]. The repetitive high energy pressure waves generated by the heart are directly transmitted to the brain and kidneys without buffering (less impedance mismatch), damaging the microvasculature of these end-organs [27].