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The Coronary Arteries: Atherosclerosis and Ischaemic Heart Disease
Published in Mary N. Sheppard, Practical Cardiovascular Pathology, 2022
Examination of the intimal surface of the human aorta opened longitudinally at autopsy shows plaques with considerable variation in their macroscopic appearances (Figs. 2.1–2.5). Studies of cohorts of individuals of different ages who die from noncardiac disease allow inferences to be made about the temporal sequence of the development of the different forms of plaque. The earliest lesion which is visible to naked eye examination is the fatty streak. This is a flat yellow dot or streak on the intima. Fatty streaks are the only lesions found in children up to 10 years of age. Although it seems likely that not all fatty streaks progress, they are considered the starting point in sequential plaque development (Fig. 2.6). Histologically, the fatty streak consists of a focal collection of lipid-filled macrophages over which there is an intact endothelial surface (Fig. 2.7). This lesion has been called Stage II by the American Heart Association (AHA) committee on plaque nomenclature.1 Stage I is the adhesion of monocytes to the intact endothelial surface through which they subsequently move to enter the intima and become the foam cells of the fatty streak.
Dyslipidemia
Published in Jahangir Moini, Matthew Adams, Anthony LoGalbo, Complications of Diabetes Mellitus, 2022
Jahangir Moini, Matthew Adams, Anthony LoGalbo
The prognosis for atherosclerosis is based on the level of the disease progression. With only the presence of fatty streaks, prognosis is good with proper treatment. Once fibrous plaques develop, prognosis is fair since the likelihood of serious outcomes is much more likely. However, with adequate treatment and lifestyle changes, many patients still are treated effectively. Once fibrous plaques have ruptured, prognosis is poor due to constriction of blood flow. Timely disease management may still save the life of the patient, but many patients do not survive this stage of the disease.
The patient with acute cardiovascular problems
Published in Peate Ian, Dutton Helen, Acute Nursing Care, 2020
Fatty streaks are non-pathological lesions in the coronary arteries; they are present in most people around the age of 20 and are thought to be the precursors of atheromatous plaques. The progression into pathological lesions is influenced by both genetic and lifestyle factors (Mageed 2018). During the early stages of this disease, lipids are deposited into the sub-intimal space where they combine with monocytes to form large bulky cells called foam cells. As the cells proliferate, the amount of space needed for them is reduced, and they slowly start to force the endothelial layer of the arterial wall out into the lumen of the artery. As a result, the diameter of the lumen becomes slowly more narrow (stenosis) (see Figure 6.17). The patient might be asymptomatic throughout the early phases of atherosclerosis build-up. By the time that symptoms of chest pain (angina) and breathlessness occur during activity, the disease will already be quite advanced in the coronary arteries.
Role of protein deimination in cardiovascular diseases: potential new avenues for diagnostic and prognostic biomarkers
Published in Expert Review of Proteomics, 2021
Liqun Mao, Rowann Mostafa, Esra Ibili, Justyna Fert-Bober
Stage II, Formation of lipid layer or fatty streak. The characteristics of stage II are the recruitment of leukocytes and formation of foam cells. The recruited monocytes, neutrophils, and macrophages secrete proinflammatory cytokines (e.g., IL-1β and TNF-α), enzymes (e.g. myeloperoxidase), reactive oxygen species (ROS) that promote further retention and modification of LDLs, as well as many other mediators [120,121]. oxLDLs can activate lesional T cells to secrete proinflammatory cytokines TNF-α, TNF-β, IFN-γ, and IL-2 that can activate macrophages and vascular cells to promote inflammation [113,122]. oxLDLs and cytokines like TNF-α and IL-1β can activate nuclear factor-κB (NF-κB) through canonical NF-κB activation pathways, and the upregulation of NF-κB aggravates chronic inflammation throughout the atherogenesis [120,121]. Notably, PAD4 was shown to citrullinate NF-κB p65 subunit in neutrophils and enhance its interaction with importin-α3 to enter the nucleus and led the expression of proinflammatory mediators, including TNF-α and IL-1β, as confirmed invitro by the inhibition of PAD [123].
Bioinformatics analysis reveals the landscape of immune cell infiltration and immune-related pathways participating in the progression of carotid atherosclerotic plaques
Published in Artificial Cells, Nanomedicine, and Biotechnology, 2021
Liao Tan, Qian Xu, Ruizheng Shi, Guogang Zhang
Since the advent of microarrays, they have provided thousands of gene expression datasets. Microarrays have been widely used to predict the underlying targets for the prevention and therapy of carotid atherosclerotic plaques. In this study, infiltrating immune cells and their immunological gene functions and pathways in plaque carotid artery tissues were analysed using the gene matrices GSE28829, GSE41571, and GSE43292 obtained from the GEO dataset. Only inflammation-related atherosclerotic carotid plaque datasets were included. According to the pathological morphological staging method of the American College of Cardiology, the early-stage lesions were characterised by scattered macrophage foam cells, fatty streaks, intimal thickness, and resident stability. However, advanced plaques are characterised by deep ulceration, disruptions of the lesion surface, haematoma or haemorrhage, and thrombotic deposits [23]. The results from CIBERSORT showed that the infiltrated immune cell subsets were similar in early and advanced plaques. M2 macrophages, M0 macrophages, naive B cells, CD8 T cells, and CD4 memory resting T cells represented the top five infiltrating fractions in carotid artery atherosclerosis. Inversely, there were fewer CD4 naive cells and eosinophils. The results of the composition of carotid atherosclerotic plaques from CIBERSORT is consistent with previous studies that used flow cytometry and single cell sequencing [24–27]. Single cell sequencing of human carotid atherosclerotic plaques in a mouse atherosclerosis model showed that T cells and macrophages dominate the immune landscape of atherosclerotic plaques.
Effects of Egg Consumption and Choline Supplementation on Plasma Choline and Trimethylamine-N-Oxide in a Young Population
Published in Journal of the American College of Nutrition, 2018
Bruno S. Lemos, Isabel Medina-Vera, Olga V. Malysheva, Marie A. Caudill, Maria Luz Fernandez
Cardiovascular disease (CVD) is the leading cause of death worldwide (1). Research targeting the pathogenesis, development, and causes of CVD in various populations is of great interest. Currently, accumulation of fat in the arterial wall can prompt a cascade of events that may result in heart attack, stroke, or death (2). This occurs when low-density lipoprotein (LDL) particles are modified (3) and consequently enter the intima where macrophages engulf them, resulting in foam cell formation (4). The uptake of modified LDL, either oxidized or acetylated, is mainly mediated by scavenger receptors (5) expressed on the surface of macrophages. Eventually, foam cells within the arterial intima will accumulate and form a fatty streak. This will then result in a fibrous cap, at some point rupturing to cause a thrombus (6), which is the main trigger of ischemic events.