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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 clearly 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, always the initiating cells in the newest sections of atheroma, to more complex structures including living cells, cellular debris of cells which have died and extracelluar deposits of fibrous tissue & calcified crystals, within the oldest, outer portions of atheroma structures.
Atheroma typically progress silently for decades and remain undetected by most clinical diagnostic approaches, including cardiac stress testing and angiography. Eventually, their presence is revealed by production of disastrous clinical events and permanent disability, such as heart attack or stroke, with the majority of people 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.
In first world countries, with improved public health, infection control and increasing life spans, atheroma processes have become an increasingly important problem and burden for society. They continue to be the number one underlying basis for disability and deathThis page deals with death, the cessation of life. For other meanings of death, see death (disambiguation). Death is a term that can refer to either the termination of life in a living system, or the state of that organism after that event. A common perce, despite a trend for gradual improvement since the early 1960sCenturies: 19th century 20th century 21st century Decades: 1900s 1910s 1920s 1930s 1940s 1950s 1960s 1970s 1980s 1990s 2000s 2010s Years: 1960 1961 1962 1963 1964 1965 1966 1967 1968 1969 Events and trends The 1960s was a turbulent decade of change around (adjusted for patient age). Thus, increasing efforts towards better understanding, treating and preventing the problem are continuing to evolve.
In the mid-twentieth century, it was assumed that atheromata simply expanded into the lumenIn anatomy, the lumen is the cavity or channel within a tube or tubular structure, such as the vascular lumen of a blood vessel, along which blood flows. In astronomy, 141 Lumen is the name of an asteroid discovered by the French astronomer Paul Henry in and produced stenosesA stenosis is an abnormal narrowing in a blood vessel or other tubular organ or structure. Commonly, atherosclerosis causes stenotic lesions in arteries. Stenoses can also be due to birth defects or disease processes including ischaemia, infection, neopla as they grew, since the disease always developed between the inner endothelialThe endothelium is the layer of thin, flat cells that lines the interior surface of blood vessels, forming an interface between circulating blood in the lumen and the rest of the vessel wall. Endothelial cells line the entire circulatory system, from the lining and the muscular wall. This belief was based on the angiography view of the blood column within arteries and a belief that the smooth muscleSmooth muscle is a type of non- striated muscle, found within the " walls" of hollow organs; such as blood vessels, bladders, uteri. gastrointestinal tracts, Smooth muscle is used to move matter withintraction|contraction]]; it generally operates " involu wall of an artery (the thickest and strongest portion of the artery wall in a healthy artery) would not change overtime. This belief continued despite contradicting evidence that this was an overly simplistic attempt to explain empirical findings. Most artists' illustrations of atheromata and the atherosclerosis process in 2004 still portray this concept incorrectly. By the late 1980s and early 1990s, careful pathology work and research using intravascular ultrasound (IVUS) showed clearly that this angiographic assumption was incorrect.
Since the early to mid 1990s, better research has led to a wide recognition that one of two overall changes typically occurs in the artery wall structure as an atheroma develops and progresses: (a) wall thickening and external enlargement with associated lumen preservation until late in the process; or (b) wall thickening and both external size and lumen enlargement. These processes probably have survival value, as they reduce and hide some of the effects of the atheroma process in terms of both symptoms and detection by most conventional diagnostic tests (e.g., cardiac stress tests) until advanced stages.