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An atheromaor atheromatous adalau “plaque”is an abnormal accumulation of material in the ateorma layer of the wall of an artery ; it is present in the arteries of most adults. The accumulated material forms a swelling in the artery wall, which may intrude into the channel of the artery, narrowing it and restricting blood flow. Atheroma is the pathological basis for the disease entity atherosclerosisa subtype of arteriosclerosis.
The accumulation swelling is always in the tunica intima, between the endothelium lining and the smooth muscle middle layer of the artery wall. While the early stages, based on gross appearance, have traditionally been termed adwlah streaks by pathologists, they are not composed of fat cells but of accumulations of white blood cellsespecially macrophagesthat have taken up oxidized low-density lipoprotein LDL. After they accumulate large amounts of cytoplasmic membranes with associated high cholesterol content they are called foam atrroma.
When foam cells die, their contents are released, which attracts more macrophages and creates an extracellular lipid core near the center to inner surface of each atherosclerotic plaque. Conversely, the outer, older portions of the plaque become more calcified, less metabolically active and more physically stiff over time. Veins do not develop atheromata, because they are not subjected to the same hemodynamic pressure that arteries are,  unless surgically moved to function as an artery, as in bypass surgery.
For most people, the first symptoms result from atheroma afalah within the heart arteriesmost commonly resulting in a heart attack and ensuing debility. Additionally, all mass-applied clinical strategies focus on both a minimal cost and b the overall safety of the kidta. Therefore, existing diagnostic strategies for detecting atheroma and tracking response to treatment have been extremely limited.
The methods most commonly relied upon, patient symptoms and cardiac stress testingdo not detect any symptoms of the problem until atheromatous disease is very advanced because arteries enlarge, not constrict in response to increasing atheroma.
Yet these events occur suddenly and are not revealed in advance by either stress testingstress tests or angiograms. The healthy epicardial coronary artery consists of three layers, the intima, media, and adventitia.
However, eventually, typically as a result of rupture of vulnerable plaques and clots within the lumen over the plaque, stenosis narrowing of the vessel develops in some areas. Less frequently, the artery enlarges so much that a gross aneurysmal enlargement of the artery results. All three results are often observed, at different locations, within the same individual.
This narrowing becomes more common after decades of living, increasingly more common after people are in their 30s to 40s. The endothelium the cell monolayer on the inside of the oista and covering tissue, termed fibrous capseparate atheroma from the adxlah in the lumen.
If a rupture see vulnerable plaque of the endothelium and fibrous cap occurs, then both a a shower of debris from the plaque combined with b a platelet and clotting response to both the debris and at the rupture site occurs within fractions of a second. This is the principal mechanism of myocardial infarctionstroke or other related cardiovascular disease problems. While clots at the kistx site typically shrink in volume over time, some of the clot may become organized into fibrotic tissue resulting in narrowing of the artery lumen ; the narrowings sometimes seen on angiography examinations, aetroma severe enough.
If the muscular wall enlargement is overdone over time, then a gross enlargement of the artery results, usually over decades of living. This is a less common outcome. Atheroma within aneurysmal enlargement vessel bulging can also rupture and shower debris of atheroma and clot downstream. If the arterial enlargement continues to 2 to 3 times the usual diameter, the walls often become weak enough that with just the stress of the pulse, a loss of wall integrity may occur leading to adalahh hemorrhage bleedingmajor symptoms and debility; often rapid death.
The main stimulus for aneurysm formation is pressure atrophy of the structural support of the muscle layers. The main structural proteins are collagen and elastin. This causes thinning and the wall balloons allowing gross enlargement to occur, as is common in the abdominal region of the aorta. Because artery walls enlarge at locations with atheroma,  detecting atheroma before death and autopsy has long been problematic at best.
Most methods have focused on the openings of arteries; highly relevant, yet totally miss the atheroma within artery walls.
kista ateroma | Pusat Khitan Pusat Bedah Minor | Flickr
Historically, arterial wall fixation, staining and thin section has been the gold standard for detection and description of atheroma, after death and autopsy. With special stains and examination, micro calcifications  can be detected, typically within aralah muscle cells of the arterial media near the fatty streaks within a year kksta two of fatty streaks forming.
Interventional and non-interventional methods to detect atherosclerosis, specifically vulnerable plaque non-occlusive or soft plaqueare widely used adakah research and clinical practice today. Carotid Intima-media thickness Scan CIMT can be measured by B-mode ultrasonography measurement has been recommended by the American Heart Association as the most useful method to identify atherosclerosis and may now very well be the gold standard for detection.
IVUS is the current most sensitive method detecting and measuring more advanced atheroma within living individuals, though it is typically not used until decades after atheroma begin forming due to cost and body invasiveness.
CT scans using state of the art higher resolution spiral, or the higher speed EBTmachines have been the most effective method for detecting calcification present in plaque. Typically, such regions start occurring within kusta heart arteries about 2—3 decades after atheroma start kistw.
Hence the detection of much smaller plaques than previously possible is being developed by some companies, such as Image Analysis. The presence adalzh smaller, spotty plaques may actually be more dangerous for progressing to acute myocardial infarction. Arterial ultrasound, especially of the carotid arteries, with measurement of the thickness of the artery wall, offers a way to partially track the disease progression. As of adalh, the thickness, commonly referred to as IMT for intimal-medial thickness, is not measured clinically though it has been kisa by some researchers since the mids to track changes in arterial walls.
Traditionally, clinical carotid ultrasounds have only estimated the degree kisra blood lumen restriction, stenosisa result of very advanced disease. Angiographysince the s, has been the traditional way of evaluating for atheroma.
However, angiography is only motion or still images of dye mixed with the blood with the arterial lumen and never show atheroma; the wall of arteries, including atheroma with the arterial wall remain invisible.
The limited exception to this rule is that with very advanced atheroma, with extensive calcification within the wall, a halo-like ring of radiodensity can be seen in most older humans, especially when arterial lumens are visualized end-on. On cine-floro, atedoma and radiologists typically look for these calcification shadows to recognize arteries before they inject any contrast agent during angiograms.
Many approaches have been promoted [ by whom? In developed countrieswith improved public healthinfection control and increasing life spans, atheroma processes have become an increasingly important problem and burden for society. Atheromata continue to be the primary underlying basis for disability and deathdespite a trend for gradual improvement since the early s adjusted for patient age.
Thus, increasing efforts towards better understanding, treating and preventing the problem are continuing to evolve.
The sudden nature of the complications of pre-existing atheroma, vulnerable plaque non-occlusive or soft plaquehave led, since the s, to the development of intensive care units and complex medical and surgical interventions. Angiography and later cardiac stress testing was begun to either visualize or indirectly detect stenosis.
Next came bypass surgeryto plumb transplanted veinssometimes arteriesaround the stenoses and more recently angioplastynow including stentsmost recently drug coated stents, to stretch the stenoses more open. Yet despite these medical advances, with success in reducing the symptoms of angina and reduced blood flowatheroma rupture events remain the major problem and still sometimes result in sudden disability and death despite even the most rapid, massive and skilled medical and surgical intervention available anywhere today.
According to some clinical trials, bypass surgery and angioplasty procedures have had at best a minimal effect, if any, on improving overall survival. Additionally, these vascular interventions are often done only after an individual is symptomatic, often already partially disabled, as a result of the disease.
It is also clear that both angioplasty and bypass interventions do not prevent future heart attack. The older methods for understanding atheroma, dating to before World War II, relied on autopsy data.
Autopsy data has long shown initiation of fatty streaks in later childhood  with slow asymptomatic progression over decades. One way to see atheroma is the very invasive and costly IVUS ultrasound technology; it gives us the precise volume of the inside intima plus the central media layers of about 2.
Unfortunately, it gives no information about the structural strength of the artery. Angiography does not visualize atheroma; it only makes the blood flow within blood vessels visible. Alternative methods that are non or less physically invasive and less expensive per individual test have been used and are continuing to be developed, such as those using computed tomography CT; led by the electron beam tomography form, given its greater speed and magnetic resonance imaging MRI.
Atheroma – Wikipedia
The most promising since the early s has been EBT, detecting calcification within the atheroma before most individuals start having clinically recognized symptoms and debility. Statin therapy to lower cholesterol does not slow the speed of atwroma as determined by CT scan. MRI coronary vessel wall imaging, although currently mista to research studies, has demonstrated the ability to detect vessel wall thickening in asymptomatic high risk individuals.
Most visualization techniques are used in research, they are not widely available to most patients, have significant technical limitations, have not been widely accepted and generally are not covered by medical insurance carriers. From human clinical trials, it has become increasingly evident that a more effective focus of treatment is slowing, stopping and even partially reversing the atheroma growth process. The ARIC Study was conducted in 15, individuals between 5 and 65 years of age in four different regions of the US between and The baseline CIMT was measured and measurements were repeated at 4- to 7-year intervals by carotid B mode ultrasonography in this study.
At the end aheroma approximately six years of follow-up, CIMT measurements were correlated with cardiovascular events. Multi-linear regression analysis revealed that an increased Framingham cardiovascular score was associated with CIMT, and carotid plaque independent of geographic differences.
They concluded that carotid atherosclerosis measured by this non-interventional method has prognostic significance in coronary artery patients. In the Rotterdam StudyBots et al. CIMT was significantly higher in the myocardial infarction group compared to the other group. It has been reported in another study that a maximal CIMT value of 0. The study group consisted of patients admitted to the cardiology outpatient clinic with symptoms of stable angina pectoris.
Regression analysis revealed that thickening of the mean intima-media complex iista than 1. There was incremental significant increase in CIMT with the number coronary vessel kjsta.
Furthermore, CIMT was increased as the number of involved vessels increased and the highest CIMT values were noted in patients with left main coronary involvement. Promising results are found using carotid intima-media thickness scanning CIMT can be measured by B-mode ultrasonographyB-vitamins that reduce a protein corrosive, homocysteine and that reduce neck carotid artery plaque volume and thickness, and stroke, lista in late-stage disease.
Additionally, understanding what drives atheroma development is complex with multiple factors involved, only some of which, such as lipoproteinsmore importantly lipoprotein subclass analysis, blood sugar levels and hypertension are best kkista and researched. More recently, some of the complex immune system patterns that promote, or inhibit, the inherent inflammatory macrophage triggering processes involved in atheroma progression are slowly being better elucidated in animal models of atherosclerosis.
From Wikipedia, the free encyclopedia. Atheroma Synonyms atheromata pluralatheromas plural Atherosclerotic plaque from a carotid endarterectomy specimen. This shows the division of the common into the internal and external carotid arteries.
Journal of Biological Chemistry. The New England Journal of Medicine. Kenneth Ouriel biography “. Cardiovascular disease vessels I70—I99— Arteritis Aortitis Buerger’s disease.
Carotid artery stenosis Renal artery stenosis. Aortoiliac occlusive disease Degos disease Erythromelalgia Fibromuscular dysplasia Raynaud’s phenomenon. Arteriovenous asalah Arteriovenous malformation Telangiectasia Hereditary hemorrhagic telangiectasia. Cherry hemangioma Halo nevus Spider angioma. Chronic venous insufficiency Chronic cerebrospinal venous insufficiency Superior vena cava syndrome Inferior vena cava syndrome Venous ulcer.
Hypertensive heart disease Hypertensive emergency Hypertensive nephropathy Essential hypertension Secondary hypertension Renovascular hypertension Benign hypertension Pulmonary hypertension Systolic hypertension White coat hypertension.