Atheroma refers to small fatty lumps that develop inside blood vessels (arteries). These form as patchy areas of plaque and contribute to the hardening of arteries, a condition known as atherosclerosis
Arteriosclerosis Atherosclerosis
A condition where the arteries become narrowed and hardened.
Atheroma
An atheroma, or atheromatous plaque, is an abnormal accumulation of material in the inner layer of the wall of an artery; it is present in the arteries of most adults. The material consists of mostly macrophage cells, or debris, containing lipids, calcium and a variable amount of fibrous connective tissue. The accumulated material forms a swelling in the artery wall, which may intrude into the channel of the artery, na…
Where does an atheroma develop?
Atheromas can occur in any artery, but they are most dangerous in the medium-to-large arteries of the heart, arms, legs, brain, pelvis, and kidneys. They don't just suddenly arise after an unhealthy meal. They accumulate over many years, often starting in childhood.
Where is the major site of atherosclerosis disease?
The most important sites for clinically significant atherosclerotic disease in humans are the coronary arteries, with progression to atherothrombotic events and subsequent myocardial infarction.
What are the 4 steps of atheroma formation?
Atherogenesis can be divided into five key steps, which are 1) endothelial dysfunction, 2) formation of lipid layer or fatty streak within the intima, 3) migration of leukocytes and smooth muscle cells into the vessel wall, 4) foam cell formation and 5) degradation of extracellular matrix.
Where do Atheromas tend to form in the vasculature?
Diseases of the Aorta Aortic atheromas, also known as “atheromata,” result from an accumulation of lipids, macrophages, connective tissue, and calcium within the intimal layer of the aortic wall.
Which arteries are most commonly affected by atherosclerosis?
The arteries in the heart (coronary arteries), neck (carotid arteries) and the legs are affected most often.
Which artery is most susceptible to atherosclerosis?
Overall, the coronary arteries are considered as the most susceptible vessels to atherosclerosis in the entire human vasculature [42].
What is the first step in the formation of an atheroma?
The first step in atherogenesis is trapping the lipoprotein in the lesion site. Although, LDL-C cannot pass through the firm endothelial junctions, it can rapidly enter the endothelial cells through endocytosis.
What are the three types of atherosclerosis?
There are three recognized types of arteriosclerosis: atherosclerosis, arteriolosclerosis, and Monckeberg medial calcific sclerosis.
What is the difference between atheroma and atherosclerosis?
Atherosclerosis is a potentially serious condition where arteries become clogged with fatty substances called plaques, or atheroma.
Where are atheromatous plaques most commonly found quizlet?
Location of Atherosclerotic aneurysms are usually found in: 1) abdominal aorta....Endothelial dysfunction.Fatty streak formation.Plaque growth and maturation.Unstable fibrous plaque.
Where in the vessel the atheromatous plaques are deposited?
They form patchy deposits (atheromas, also called plaques) covered with a fibrous cap in the lining of the artery wall. With time, calcium accumulates in the plaques. Plaques may be scattered throughout medium-sized and large arteries, but they usually start where the arteries branch.
What is the definition of atheroma?
1 : an abnormal fatty deposit in an artery. 2 dated : fatty degeneration of the inner coat of the arteries.
Which artery is the most common to have blockage?
When this happens, patients may go into cardiac arrest. Statistically, Niess said widow-makers are more likely to lead to brain injury and irregular heartbeat. Although blockages can occur in other arteries leading to the heart, the LAD artery is where most blockages occur.
Is the aorta the main artery?
The aorta is the main artery that carries blood away from your heart to the rest of your body. The blood leaves the heart through the aortic valve. Then it travels through the aorta, making a cane-shaped curve that allows other major arteries to deliver oxygen-rich blood to the brain, muscles and other cells.
What is atherosclerosis of aorta?
What is atherosclerosis of the aorta? Having atherosclerosis (say "ath-uh-roh-skluh-ROH-sis") of the aorta means that a material called plaque (fat and calcium) has built up in the inside wall of a large blood vessel called the aorta. This plaque buildup is sometimes called "hardening of the arteries."
What is arteriosclerosis disease?
Arteriosclerosis occurs when the blood vessels that carry oxygen and nutrients from the heart to the rest of the body (arteries) become thick and stiff — sometimes restricting blood flow to the organs and tissues.
Where do atheromas accumulate?
Arteries are composed of multiple layers of tissue, and atheromas can accumulate in the tunica intima layer that is between the endothelium lining and the smooth-muscle middle layer of the artery wall.
Where can atheromatous plaque be found?
However, the exact origins of atheromatous plaque are not well understood. These fatty streaks can be found in the artery walls of infants but are usually absorbed. But in certain cases, incomplete absorption may contribute to atheromatous plaque later in life.
What is atheroma?
Atheroma refers to small fatty lumps that develop inside blood vessels (arteries). These form as patchy areas of plaque and contribute to the hardening of arteries, a condition known as atherosclerosis.
What are the effects of atheromatous plaque?
Effects of atheromas include: Narrowing of an artery: This results in an incomplete supply of blood to the affected tissue found beyond the site of the blockage.
What are the complications of an atheroma?
Complications of atheroma. Atheromas and the narrowing or complete blockage of arteries can lead to several complications. When the fibrous cap covering plaque breaks down, platelets involved in blood clot formation become activated. When enough platelets reach the site of the plaque, a blood clot forms, causing ischemia and infarction.
What happens when an atheroma ruptures?
When this occurs, it can trigger the circulatory system to produce a blood clot (thrombosis) at the site of the atheroma. This can lead to a complete blockage of blood flow at the affected site, potentially causing a heart attack.
What are the causes of atheroma?
What are the causes and symptoms of atheroma? Atheromas are composed of mostly macrophage cells (a type of white blood cell) or debris, containing lipids (fats), calcium, and a variable amount of connective tissue. When these materials accumulate, they lead to the narrowing of the artery they are attached to.
Where does atheroma occur?
Atheroma occurs in large elastic and muscular arteries such as the aorta, coronary, femoral, and carotid arteries, and especially at predisposed sites such as bifurcations where there is flow disturbance. Plaques form on the basis of fatty streaks that may be present very early in life. Damage to the endothelial lining from high blood pressure, local injury, or poor oxygen supply results in increased permeability, enabling lipoproteins to pass more easily into the subendothelial space. LDL and triglyceride-rich lipoprotein remnants are atherogenic. The influx into the arterial wall depends on both the concentration and the size of the LDL particles in plasma. The higher the concentration of LDL in the plasma, the greater is the degree of influx, and smaller denser LDL3 particles cross the endothelium more easily. LDL in the arterial wall undergoes a number of changes including oxidation with LDL3 particles being more susceptible. The oxidized LDL particles are engulfed by scavenger macrophages. These macrophages are formed from monocytes that have traversed the damaged endothelial wall and are immobilized in response to a number of chemical signals. In response to altered LDL, the macrophages express acetylated LDL receptors and take up LDL to become lipid rich foam cells. These undergo apoptosis producing a lipid-rich extracellular medium. Smooth muscle cells migrate from the arterial media in response to this process. These proliferate and produce a connective tissue matrix rich in collagen, elastin, and proteoglycans forming the plaque cap, as part of a damage-healing process.
What is the atheroma of the heart?
Atheromas are raised lesions that protrude into the vessel lumen and contain a soft, yellow, grumous (thick and lumpy) core consisting mainly of cholesterol and cholesterol esters, covered by a white, fibrous cap. Extracellular lipid enters the atheroma by bulk transport from the vessel lumen, especially when dyslipidemia is present. Lipid is also released into the necrotic core from degenerating foam cells. Cholesterol is frequently present in the atheroma center as crystalline aggregates seen as cholesterol clefts in histological preparation. (Routine tissue processing washes out the cholesterol and leaves behind only empty “clefts.”) Cholesterol accumulation in the plaque reflects an imbalance between lipid influx and efflux. High-density lipoproteins (HDLs) facilitate cholesterol efflux from these accumulations by reverse cholesterol transport (see below). Under the influence of inflammatory mediators, smooth muscle cells migrate to the intima, differentiate into fibroblast-like cells, proliferate, and produce ECM elements, including collagen and proteoglycans as shown below.
What is an aortic atheroma?
Aortic atheromas, also known as “atheromata,” result from an accumulation of lipids, macrophages, connective tissue, and calcium within the intimal layer of the aortic wall. Such collections begin as atherosclerotic plaques that line the wall of the aorta, but they can subsequently grow and bulge into the aortic lumen to form “protruding atheromas” (Fig. 34.21 ). Moreover, on TEE imaging, some atheromas will have mobile components that protrude even further into the lumen (see Fig. 34.21B and Video 34.8); it is believed that these mobile components represent thrombus superimposed on the underlying atherosclerotic plaque. TEE produces high-resolution images of the intimal surface of the thoracic aorta and is therefore the modality of choice to assess the location, size, severity, and mobility of aortic atheromas.
How thick is an atheroma?
The thickness of a healthy intimal layer is normally ≤1 mm; consequently, an irregular intima with a thickness of ≥2 mm is considered to be an atheroma. 1 The presence of aortic atheromas with a thickness of greater than 4 mm is associated with increased risk of embolic events. 10 The presence of superimposed mobile components further increases the risk of embolization. A grading systems exists ( Table 34.3) that classifies atheromas based on maximal thickness and the presence of mobile or ulcerated components, assigning them a grade of 1–5. 1 However, many find it easier to use a descriptive scale, ranging from mild to complex. When significant atheromas are present, the echocardiography report should comment on location, the atheroma thickness, and the presence of mobile segments.
How do atheromas affect the aorta?
Aneurysmatic dilatation: Atheromas may weaken the vessel wall by destroying the elastic tissue and the smooth muscles that maintain the integrity of the normal aorta. Under the influence of blood pressure, such weakened vessel walls will bulge outside and form an aneurysm.
What is the risk of death from aortic atheroma?
In addition, plaque complexity predicts clinical outcome with a 15% annual risk of death or a cerebral embolic event in patients with a complex plaque (thickness greater than or equal to 4 mm or any mobile components) compared to those with a noncomplex plaque.
What is the white, fibrous cap of an atheroma?
Atheromas are raised lesions that protrude into the vessel lumen and contain a soft, yellow, grumous ( thick and lumpy) core consisting mainly of cholesterol and cholesterol esters, covered by a white, fibrous cap.
What is the role of deranged cell proliferation in atheroma?
Traditional thinking accorded a major role to deranged cell proliferation as a determinant of the abnormal cellularity of atheroma. However, studies conducted in several laboratories have documented the occurrence of disordered apoptosis during atherogenesis, leading to the death of lipid-rich foam cells (promoting lipid-core formation) ...
What are the two major participants in the atherosclerotic response?
Beyond lipid accumulation, atherogenesis involves innate and acquired immunity. Two major cellular participants in the immune response, macrophages and T lymphocytes, undergo activation in atheroma. 59 The antigenic substances may include oxidized lipoproteins and some stress proteins, such as heat shock protein-60. The effector of acquired immunity par excellence, the CD8-positive T lymphocyte, can kill cells by apoptosis via the production of perforin, granzyme, and Fas ligand (FasL). 53 However, mediators of innate immunity may also contribute to this process. For example, exposure of human SMCs to a “cocktail” of cytokines found in human atheroma, including interleukin (IL)-1β, TNF-α, and IFN-γ, can induce apoptosis. 7 In addition, “priming” of SMCs with cytokines implicated in innate immunity can sensitize them to killing by Fas engagement. 8 Thus, the effector limbs of innate and acquired immunity may cooperate in causing the demise of cells within atheroma ( Figure 1 ).
How does apoptosis affect vascular remodeling?
Apoptosis probably participates in the progression or regression of atherosclerotic lesions, in vascular remodeling, and in complications of advanced atheroma. Many environmental and endogenous factors can influence apoptosis through various signal transduction or enzymatic pathways. The apoptotic mechanisms illustrated above link risk factors (eg, oxidized lipids) and immune and inflammatory effector mechanisms to disordered cell accumulation, providing a unifying concept situated at the center of current thinking about atherosclerosis. Abnormality of apoptosis may occur in atherosclerosis, favoring the accumulation of intimal cells during some phases of atherogenesis. In advanced atheroma, cell death may contribute to aneurysm formation and to weakening of the fibrous cap, enhance thrombogenicity of the lesion core, and increase the risk of plaque disruption. Future studies will assess whether therapies directed toward apoptosis will modify vascular diseases such as atherosclerosis.
Which system is involved in apoptosis?
Many surface receptors and intracellular proteins or enzyme systems participate in the regulation of apoptosis. Table 3 lists some of these receptors and cellular proteins potentially important for the regulation of vascular cell apoptosis during atherogenesis.
Can apoptotic endothelial cells cause coagulation?
Either apoptotic endothelial cells ( ECs) 26 or SMCs 27 can promote coagulation. Rapid exposure of membrane phosphatidylserine and loss of the anticoagulant membrane components in apoptotic ECs can occur, which may promote a procoagulant environment. Apoptotic vascular SMCs acquire a thrombin-generating capacity due to exposure of phosphatidylserine. Thus, apoptotic cells within atherosclerotic plaques may allow local thrombin activation, thereby contributing to disease progression. 27 Increased tissue factor on the surface of apoptotic cells may also contribute to the procoagulant activities. 28 These findings illustrate how apoptotic cells or bodies, if not promptly removed, may become thrombogenic or proinflammatory.
How does atherosclerosis occur?
When a plaque covers more than 40% of internal elastic layer of the vessel, the arterial channel is considered to be occupied. At the end of the plaque's lifetime, the restrictive obstruction of the blood flow happens. Studies show that atherosclerosis is a result of intima damage with some cellular responses that involve monocytes, SMC, and lymphocytes. The initial soft lesion is composed of foam cells and extracellular fat deposits and a small number of platelets. During the progress of the process, SMC proliferate and in the final steps, intensify bleeding into the plaque[5,6,7,8,9,10] [Figure 1].
Which cell is involved in the primary stages of atherosclerosis?
Leukocyte adhesion molecules are involved in the primary stages of atherosclerosis. Endothelial cells are important sources for producing adhesion molecules on leukocytes.
What causes a plaque to form in the arteries?
Formation of these plaques starts with the deposition of small cholesterol crystals in the intima and its underlying smooth muscle. Then the plaques grow with the proliferation of fibrous tissues and the surrounding smooth muscle and bulge inside the arteries and consequently reduce the blood flow. Connective tissue production by fibroblasts and deposition of calcium in the lesion cause sclerosis or hardening of the arteries. Finally, the uneven surface of the arteries results in clot formation and thrombosis, which leads to the sudden obstruction of blood flow.[5]
What is the role of inflammation in atherosclerosis?
The disease is accompanied by excessive fibrosis of the intima, fatty plaques formation, proliferation of smooth muscle cells, and migration of a group of cells such as monocytes, T cells, and platelets which are formed in response to inflammation. The oxidation of low density lipoprotein (LDL) to Ox-LDL indicates the first step of atherosclerosis in cardiovascular diseases. Malondialdehyde factor shows the level of lipoperoxidation and is a sign of increased oxidative pressure and cardiovascular diseases. In special pathological conditions such as severe hypercholesterolemia, peroxynitrite concentration increases and atherosclerosis and vascular damage are intensified. Medicinal plants have shown to be capable of interacting these or other pathogenesis factors to prevent atherosclerosis.
What is the first sign of atherosclerosis?
Both animal and human studies show that the fatty streaks are the first sign of atherosclerosis. The initial lesions are usually caused by the focal increase in the lipoproteins of the intimal layer of the arteries.[5]
Where is the fatty material located in the plaque?
Fatty material is located in the central core of the plaque , covered by fibrous cap. The term, atherosclerosis consists of two parts; atherosis (accumulation of fat accompanied by several macrophages) and sclerosis (fibrosis layer comprising smooth muscle cells [SMC], leukocyte, and connective tissue).[3,4]
Is atherosclerosis a disease?
Atherosclerosis is the result of hyperlipidemia and lipid oxidation and has always been a major cause of mortality in developed countries. It is a disease of vascular intima, in which all the vascular system from aorta to coronary arteries can be involved and is characterized by intimal plaques.[ 1,2]
Which arteries are most susceptible to atherosclerosis?
All arteries are susceptible to atherosclerosis, but the aorta, coronary and carotid arteries are affected most.
What are the risk factors for atherosclerosis?
Risk factors for atherosclerosis include age, sex (particularly male), family history, hypertension, smoking, obesity, diabetes, stress, high blood cholesterol, and a sedentary lifestyle. A growing body of evidence shows a link between internal inflammation and the formation and rupture of atheroslerotic plaques.
What is the process of smooth muscle cells proliferating and forming fibrous caps?
Smooth muscle cells proliferate and a fibrous cap forms — smooth muscle cells from the tunica media migrate and deposit elastic and collagen fibers thickening the intima and producing lesions with a core of dead and dying foam cells called atheroslerotic plaques. Initially, vessel walls will expand to accommodate the growing plaque, but eventually, the plaque will begin to block parts of the vessel lumen. At this point, the patient would be diagnosed with atherosclerosis.
What are the factors that contribute to thrombus formation?
Two other factors promote thrombus formation: Endothelial cells damaged by plaque release nitric oxide and prostacyclin — these chemical inhibit platelet formation and promote vasodilation, so if cells that release these chemicals are damaged, the internal environment of vessels becomes clot friendly.
Where do lipids accumulate and oxidize?
Lipids accumulate and oxidize in the tunica intima — injured endothelial cells release chemotactic agents and growth factors and begin to transport and modify lipids picked up from blood, particularly low-density lipoproteins (LDL’s) that deliver cholesterol to tissue cells. The built-up LDL oxidizes in the inflammatory environment damaging the neighboring cells. It also acts as a chemotactic agent and attracts macrophages. Some of the macrophages become engorged with LDL’s and end up transforming into lipid-laden foam cells. Built-up foam cells form a fatty streak, the first visible sign of an atheroma.
Is atherosclerosis prevention or treatment?
When it comes to atherosclerosis, prevention is the best treatment. By making a few healthy lifestyle decisions, arteriosclerosis can be prevented and in some cases, completely avoided.
General Information
Causes
- The main factor in the formation of retention cysts is the formation of an obstacle or significant difficulty in the outflow of sebaceous gland secretions against the background of ongoing sebum production. The causes of outflow disorders are diverse, often combined and mutually enhance each other’s effect. The main mechanisms of atheroma formation...
Pathogenesis
- Secretions continue to be produced in the clogged sebaceous gland. The contents accumulate and begin to press on the walls of the cavity, gradually stretching them. An increase in the volume of the gland does not cause unpleasant sensations, itching or pain, since there is no compression of the nerve endings. The skin rises above the growing cyst, a rounded seal of a soft-elastic con…
Classification
- Atheromas are divided into groups according to histological structure and causes of occurrence. Differences in the cellular structure of cysts do not manifest themselves clinically in any way, therefore histological classification is of interest only to researchers. In practical dermatology, classification based on the peculiarities of the formation of atheromas is important. According t…
Symptoms
- Retention cysts can develop on any part of the head, body and limbs where there are sebaceous glands, regardless of whether the ducts of the glands open to the surface of the skin or into the mouths of the hair follicles. In fact, this is any anatomical area, including the armpits and popliteal pits, with the exception of the palms and feet. False atheromas are more common on the head, …
Complications
- The most common complication of atheroma is its suppuration. The addition of infection leads to the development of an inflammatory reaction, a violation of the general condition, hyperthermia. This condition requires urgent medical attention. Abscessing atheroma is also dangerous in cases when its contents are trying to squeeze out or restore the patency of the duct by mechani…
Diagnostics
- The clinical picture of most benign neoplasms of the skin and subcutaneous tissue is largely similar. The dermatologist at the reception is faced with the task of conducting a differential diagnosis, determining the type of pathological formation, and choosing the most effective method of treatment. To do this , it is carried out: 1. General inspection. During palpation, signs …
Treatment
- Approaches to the treatment of epidermal cysts in dermatology and outpatient surgery differ significantly. They are not mutually exclusive and can be effective in different clinical situations, because it is important not only to remove the neoplasm, but to choose treatment and care procedures in order to normalize the production of sebum, to prevent the appearance of new ath…
Prognosis and Prevention
- Timely referral to a dermatologist and cosmetologist about any changes in the condition of the skin and hair allows you to prevent the development of atheromas. Juvenile acne, seborrhea, increased oily skin are conditions that require correction and constant, properly selected supportive treatment. With already developed atheromatosis, it is indicated to conduct an exami…