The patient with acute cardiovascular problems
Ian Peate, Helen Dutton in Acute Nursing Care, 2014
Atherosclerosis is a potentially serious condition where there is a progressive build-up of fatty deposits in the subintimal layer of medium and large arteries. It is a chronic condition and it can take several decades for these deposits to reach a level where there is significant disruption to the blood flow along the arteries. Atherosclerosis is a major risk factor for many different conditions involving a reduced blood flow. Collectively, these conditionsare known as cardiovascular disease (CVD).Examples of CVD include:Coronary artery disease and myocardial infarctionPeripheral artery diseaseStroke.
Atherosclerosis, Arteriolosclerosis and Vasculitis
Jeremy R. Jass in Understanding Pathology, 2020
Epidemiological studies have shown that the major risk factors of atherosclerosis are diet (i.e. one high in cholesterol), hyperlipidemia of genetic origin, hypertension, smoking and diabetes mellitus. Other risk factors include male gender, obesity, age and physical inactivity. In the past, two main theories were put forward to explain the growth of an atheromatous plaque. The first envisaged the insudation of cholesterol from the bloodstream into the intima, this in turn stimulating the proliferation of smooth muscle cells. The second theory focused on the progressive laying down and organisation of platelet thrombi. The contemporary view combines elements of both theories but views atherosclerosis as an inflammatory response to intimal injury (Ross & Fuster, 1996). The suggested steps are shown in Figure 25. Thrombosis is now viewed as a late complication of atheroma, rather than as a predisposing event. The sequence of events outlined in Figure 25 fits with the risk posed by hypercholesterolemia and the direct damaging influence of hypertension and cigarette smoke upon endothelial cells. Considerable research is under way to map the molecular steps involved in the above pathway, with the aim of developing therapeutic strategies to block the process of atherogenesis. However, a healthy diet, regular exercise and avoidance of tobacco would be a useful start to preventing this disease.
Stroke and Transient Ischemic Attacks of the Brain and Eye
Philip B. Gorelick, Fernando D. Testai, Graeme J. Hankey, Joanna M. Wardlaw in Hankey's Clinical Neurology, 2020
Fatty streaks: focal accumulations of subendothelial smooth muscle cells and macrophages containing lipid (cholesterol and cholesterol ester).Fibrous plaque: a central core of lipid and cell debris surrounded by smooth muscle cells, collagen, elastic fibers, and proteoglycans.A band of fibrous tissue (the fibrous cap) separates the lipid core (the atheroma) from the lumen of the vessel.Mature atheroma:Proliferated cells, predominantly smooth muscle cells.Lipids (cholesterol-esters) and lipid-laden macrophages (“foam cells”).Connective tissue elements such as elastins and glycosaminoglycans.Complicated lesions: mature fibrous plaque with various types of degenerative changes such as calcification (due to precipitation of calcium salts in the tissues), intraplaque hemorrhage or plaque rupture, intimal ulceration or erosion, and mural thrombosis and thromboembolism (Figure 12.61).Atherothrombosis occurs when the fibrous cap of an unstable atherosclerotic plaque ulcerates, erodes, or ruptures due to inflammation within the plaque, thus exposing circulating platelets and thrombin to subendothelial collagen, and initiating platelet activation and thrombosis. Thrombosis within a large artery may grow to occlude the artery (with or without causing symptoms), but more commonly causes ischemic stroke when it embolizes distally to occlude an intracranial branch artery. The main cause of atherosclerosis is prolonged exposure to causal risk factors, such as high BP, cigarette smoking, high blood glucose (diabetes), and high blood lipids (low-density lipoprotein-cholesterol [LDL-C] and apolipoprotein B lipoprotein [apoB]), in individuals genetically predisposed to form atheroma in response to these exposures. The traditional model of atherosclerosis presumes that the mass of cholesterol within very low-density lipoprotein particles, LDL particles, chylomicron, and lipoprotein (a) particles in plasma is the principal determinant of the mass of cholesterol that is deposited in the arterial wall and drives atherogenesis. However, each of these particles contains one molecule of apoB, and cholesterol can only enter the arterial wall within apoB particles. Hence, apoB particles are the basic unit of injury to the arterial wall. Trapping of apoB particles within the arterial wall is the fundamental step that initiates and drives atherosclerosis, from the first appearance of fatty streaks to the ultimate development of complex lesions that are vulnerable to endothelial erosion and plaque rupture. The more apoB particles within the lumen of the artery, the greater trapping of apoB particles within the arterial wall, and the greater the injury to the arterial wall. Hyperhomocysteinemia is an uncommon hereditary cause of atheroma, predisposing to it by injuring endothelial cells and increasing smooth muscle proliferation (Table 12.20).
A focus on inflammation as a major risk factor for atherosclerotic cardiovascular diseases
Published in Expert Review of Cardiovascular Therapy, 2016
Ida Gregersen, Sverre Holm, Tuva B Dahl, Bente Halvorsen, Pål Aukrust
Atherosclerosis is a dynamic, pathogenic process in the artery wall, with potential adverse outcome for the host. Acute events such as myocardial infarction and ischemic stroke often result from rupture of unstable atherosclerotic lesions. Understanding the underlying pathology of such lesions and why and when they rupture, is therefore of great interest for the development of new diagnostics and treatment. Inflammation is one of the key drivers of atherosclerotic plaque development and the interplay between inflammation and lipids constitutes the hallmark of atherosclerotic disease. This review summarizes the role of inflammation in atherosclerosis and presents some of the latest discoveries as well as unmet needs regarding the role of inflammation as major risk factor in atherosclerotic disease.
Foam cell origination from degenerated vascular smooth muscle cells in atherosclerosis: An ultrastructural study on hyperlipidemic rabbits
Published in Ultrastructural Pathology, 2020
Yong-Xin Ru, Hong-Cai Shang, Shu-Xu Dong, Shi-Xuan Zhao, Hao-Yue Liang, Chao-Jun Zhu
To clarify foam cell origination in atherosclerosis, a series of morphologic and ultrastructural alterations of vascular smooth muscle cells (VSMCs) and foam cells were studied by light and electron microscopy in atherosclerotic aortas from hyperlipidemic rabbits induced for 5 weeks. The study exhibited that VSMCs were severely degenerated and damaged, including irregular shapes, expanded mitochondria, aplenty lipid droplets, and disarranged myofilaments in cytoplasm in media adjacent to atheromatic bottoms. Most lipid laden cells shared interphase structures of VSMCs and foam cells, and some dissolved spindle cells contained lipid droplets, lipofuscin, and rod-like CCs in cytoplasm also. The result demonstrated that VSMCs were degenerated and transformed into foam cells in atherosclerosis, which was responsible for the accumulation of lipid and cholesterol crystals in atherosclerotic arteries.
Breastfeeding is associated with lower subclinical atherosclerosis in postmenopausal women
Published in Gynecological Endocrinology, 2020
Areti Augoulea, Eleni Armeni, Stavroula A. Paschou, Georgios Georgiopoulos, Kimon Stamatelopoulos, Irene Lambrinoudaki
Objective: To evaluate the association between a personal history of lactation and indices of subclinical atherosclerosis in postmenopausal women. Methods: We evaluated the association between a history of breastfeeding and indices of subclinical atherosclerosis (pulse wave velocity, PWV; intima-media thickness [IMT]; atherosclerotic plaque presence) in 197 parous postmenopausal women with history of breastfeeding. Results: Women who reported breastfeeding ≥6 months when compared with women who reported breastfeeding for 1–5 months exhibited significantly lower values of common carotid artery IMT (Model R2=15.7%, b-coefficient = −0.170, 95% CI: −0.208—0.001, p-value = .019) and lower odds of subclinical atherosclerosis (Model X2=28.127, OR = 0.491, 95% CI 0.318–0.999, p-value = .049), adjusting for traditional cardiovascular risk factors. Conclusions: Postmenopausal women with a history of breastfeeding for at least 6 months have a lower prevalence of subclinical atherosclerosis, independently of traditional cardiovascular risk factors. A longer duration of breastfeeding may have a beneficial effect on subclinical atherosclerosis later in life.
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