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An Atheroma (plural: atheromata) is unhealthy tissue growth which develops within the walls of arteries over time. Veins do not develop atheroma, unless surgically moved to function as an artery, as in bypass surgery.
Collectively, the process of atheroma development within an individual is called atherogenesis and the overall result of the disease process is termed atherosclerosis.
In humans, atheroma usually begin in later childhood, about ages 5-9, as fatty streaks. These, and older, larger atheroma lesions have long been observed in autopsy examinations of people who have died for unrelated reasons; they are so common, more so with increasing age, they were long considered normal, even though unhealthy.
More advanced atheroma develop multiple different internal tissue characteristics within the same atheroma. By light microscopy visualization, pathologists have characterized as many as 10 different tissues subtypes within a single atheroma. Generally, these range from collections of macrophage cells, the initiating structure in the newest sections of atheroma, to extracelluar deposits of calcified crystals, within the oldest, outer portions of atheroma structures.
Atheroma typically reveal their presence by producing disastrous clinical events and permanent disability, such as heart attack or stroke, with the majority assuming they are healthy until proven otherwise. For some individuals, warning symptoms do occur before the onset of major debility or death, however these are the minority. Historically physicians, who are trained to treat symptoms and avoid treatment before onset of clear enough symptoms and physical abnormalities, have just considered the processes a normal part of aging, even though unhealthy.
Most people first develop clinical symptoms and debility from atheroma activity within the heart arteries. However, the heart arteries, because (a) they are small (from about 5 mm down to invisible), (b) hidden deep within the chest and (c) never stop moving, have been a difficult target organ to track, especially clinically in individuals who are still asymptomatic. Additionally all mass applied clinical strategies focus on both minimal cost, if not "free", and great safety. Therefor existing diagnostic strategies for detecting atheroma and tracking response to treatment have been extremely limited.
For many years, based on the angiography view of the blood column within arteries and a belief that the smooth muscle wall of an artery would not change overtime, it was believed that atheroma simply pushed into the lumen as they grew, producing stenoses; despite long established contradicting evidence that this was a too simplistic view to explain many long know clinical realities. Most artists illustrations of atheroma and the atherosclerosis process still portray this incorrect concept. By the later 1980s and early 1990s, it had become evident, based on more carefully done pathology work and arterial research using IVUS that this angiographic biased view was very incorrect.
In first world countries, with improved public health, infection control and increasing life spans, the atheroma processes have become a increasingly important problem and burden for society; it remains the number one underlying basis for disability and death, despite improvements since the early 1960s. Thus increasing efforts to understand and better treat and prevent the problem are evolving.
Since the early to mid 1990s, it has become more widely recognized, based on better research, that as atheroma develop and progress, either of two overall charges in the overall artery wall structure typically occur: (a) wall thickening and external enlargement is the norm (with associated lumen preservation) until late in the process or (b) wall thickening and both external size and lumen enlargement. These processes probably have survivial value; they do hide the effects of the atheroma process in terms of symptoms and detection by most conventional diagnostic tests, until very advanced.
Over time, atheroma usually progress in size and thickness and induce the surrounding muscular wall of the artery to stretch out, termed remodeling, typically just enough to compensate for their size such that the opening of the artery remains unchanged until typically over 40-50% of the artery wall cross sectional area consists of atheromatous tissue.
If the muscular wall enlargement eventually fails to keep up with the enlargement of the atheroma volume, then the lumen of the artery begins to narrow, commonly as a result of repeated ruptures of the covering tissues separating the atheroma from the blood stream. This becomes a more common event after decades of living, increasingly more common after people are over 40 years old.
If a rupture occurs, a rupture of the endothelium and covering tissue, termed fibrous cap, which separates an atheroma from the blood in the lumen, then a platelet and clotting response over the rupture rapidly develops. Additionally, the rupture may result in a shower of debris. Platelet and clot accumulation over the rupture may produce narrowing/closure of the lumen and tissue damage may occur due to either closure of the lumen and loss of blood flow beyond the ruptured atheroma and/or by occlusion of smaller downstream vessels by debris. See vulnerable plaque.
This is the principle mechanism of heart attack, stroke or other related cardiovascular disease problems. As research has shown, this process is not a result of stenosis. Prior to the rupture, there may have been no lumen narrowing, even aneurysmal enlargement, at the atheroma. On average, by clinical research using IVUS, there is a minor stenosis, about 20%, present over those unstable atheroma which rupture and result in major disability or death. Comparatively, stenoses of about 75% are required to produce detectable abnormalities during cardiac stress tests.
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 can also rupture and shower of 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 sudden hemorrhage, major symptoms and debility; often rapid death.
The sudden nature of the complications of pre-existing atheroma, vulnerable plaque, have led, since the 1950s, to the development of intensive care units and complex medical and surgical interventions. Angiography and later stress testing was begun to either visualize or indirectly detect stenosis. Next came bypass surgery, to plumb transplanted veins, sometimes arteries, around the stenoses and more recently angioplasty, now including stents, most 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 flow, atheroma 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. By clinical trials, bypass surgery and angioplasty procedures have had only a minimal effect, some would argue no effect, on improving overall survival. Additionally, these treatments are often done only after an individual is symptomatic, often already partially disabled, as a result of the disease.
The older methods for understanding atheroma, dating to before WWII, relied on autopsy data. Autopsy data has long shown initiation of fatty streaks in later childhood with slow asymptomatic progession over decades.
Since the later 1980s, the best way to see atheroma and better understand atheroma behaviour in living individuals has been IVUS technology. Angiography does not visualize atheroma; it only makes the blood flow within blood vessels visible. Alterative methods, non or less physically invasive and less expensive per individual test, using CT, lead by the EBT form given its greater speed, and MRI (magnetic resonance imaging) have been and are continuing in development. The most promising since the early 1990s has been EBT, typically detecting and recognizing advanced calcification within the base of atheroma about 10 years before most individuals start having clinically recognized symptoms and debility. However, these methods, though used in research, are not widely available to most patients, still have mild to 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 the more effective focus of treatment is slowing, stopping and even partially reversing the atheroma growth process. However, this effort has been slow, partly because atheroma are hidden within, create no symptoms and people don't complain about things they cannot see or feel. Additionally understanding what drives atheroma development is complex with multiple different factors involved, some known, some not.
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