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| {{Atherosclerosis}} | | {{Atherosclerosis}} |
| {{CMG}}
| | '''For patient information, click [[Atherosclerosis (patient information)|here]]''' |
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| ==Physiologic factors that increase risk==
| | {{CMG}} {{AOEIC}} [[User:Maheep Sangha|Maheep Singh Sangha, M.B.B.S.]]{{NE}} |
| Various anatomic, physiological & behavioral risk factors for atherosclerosis are known. These can be divided into various categories: congenital ''vs'' acquired, modifiable or not, classical or non-classical. The points labelled '+' in the following list form the core components of "[[metabolic syndrome]]":
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| * [[Senescence|Advanced age]]
| | {{SK}} Plaque buildup - arteries; hardening of the arteries |
| * [[Male]] sex
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| * Having [[Diabetes]] or [[Impaired glucose tolerance]] (IGT) +
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| * [[lipoprotein|Dyslipoproteinemia]] (unhealthy patterns of serum proteins carrying fats & [[cholesterol]]): +
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| ** High serum concentration of [[low density lipoprotein]] (LDL, "bad if elevated concentrations and small"), [[Lipoprotein(a)]] (a variant of LDL), and / or [[very low density lipoprotein]] (VLDL) particles, i.e. "lipoprotein subclass analysis"
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| ** Low serum concentration of functioning [[high density lipoprotein]] (HDL "protective if large and high enough" particles), i.e. "lipoprotein subclass analysis"
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| * [[Tobacco smoking]]
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| * Having [[hypertension|high]] [[blood pressure]] +
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| * Being [[obesity|obese]] (in particular [[central obesity]], also referred to as ''abdominal'' or ''male-type'' obesity) +
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| * A [[sedentary lifestyle]]
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| * Having close relatives who have had some complication of atherosclerosis (eg. [[coronary heart disease]] or [[stroke]])
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| * Elevated serum levels of [[homocysteine]]
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| * Elevated serum levels of [[uric acid]] (also responsible for gout)
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| * Elevated serum [[fibrinogen]] concentrations +
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| * Chronic systemic [[inflammation]] as reflected by upper normal WBC concentrations, elevated [[C reactive protein|hs-CRP]] and many other blood chemistry markers, most only research level at present, not clinically done.<ref name=Bhatt> [http://circ.ahajournals.org/cgi/content/full/circulationaha;106/1/136 Deepak L. Bhatt, MD; Eric J. Topol, MD] ''Need to Test the Arterial Inflammation Hypothesis'', 2002, referenced on 4/1/06 </ref>
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| * [[Stress (medicine)|Stress]] or symptoms of [[clinical depression]]
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| * [[Hypothyroidism]] (a slow-acting [[thyroid]])
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| * High intake of trans-fats and saturated fats in diet
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| ==Treatment== | | ==[[Atherosclerosis overview|Overview]]== |
| If atherosclerosis leads to symptoms, some symptoms such as [[angina pectoris]] can be treated. Non-pharmaceutical means are usually the first method of treatment, such as cessation of smoking and practicing regular exercise. If these methods do not work, medicines are usually the next step in treating cardiovascular diseases, and with improvements, have increasingly become the most effective method over the long term. However, medicines are criticized for their expense, patented control and occasional undesired effects.
| | ==[[Historical Perspective]]== |
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| [[dyslipidemia|Lipoprotein imbalances]], upper normal and especially elevated blood sugar, i.e. [[diabetes]], high blood pressure, [[homocysteine]], stopping smoking, taking [[anticoagulant]]s (anti-clotting agents) which target clotting factors, taking omega 3 oils from fatty fish or plant oils such as flax or canola oils, exercising and losing weight are the usual focus of treatments which have proved to be helpful in clinical trials. The target serum cholesterol level is ideally equal or less than 4mmol/L (160 mg/dL) and triglycerides equal or less than 2mmol/L 180 (mg/dL). | | ==[[Atherosclerosis classification|Classification]]== |
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| In general, the group of medications referred to as statins has seen popularity yet they are not approved in most jurisdictions for treating atherosclerosis. They have relatively few short-term undesirable side-effects and have shown some effect in reducing atherosclerotic disease 'events' in some but not all studies such as [http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12479764&dopt=Abstract ALLHAT].
| | ==[[Atherosclerosis pathophysiology|Pathophysiology]]== |
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| The newest statin, [[rosuvastatin]], has been the first to demonstrate regression of atherosclerotic plaque within the [[coronary arteries]] by [[IVUS]] evaluation,<ref name=Nissen "JAMA">[http://jama.ama-assn.org/cgi/reprint/jama;295/13/1556.pdf?ijkey=Md42dlk7z9TzyL8&keytype=finite], "Effect of Very High-Intensity Statin Therapy on Regression of Coronary Atherosclerosis".</ref> see the ''Effect of Very High-Intensity Statin Therapy'' reference below. The study was not set up to demonstrate clinical benefit or harm. However, for most people, changing their physiologic behaviors, from the usual high risk to greatly reduced risk, requires a combination of several compounds, taken on a daily basis and indefinitely. More and more human treatment trials have been done and are ongoing which demonstrate improved outcome for those people using more complex and effective treatment regimens which change physiologic behaviour patterns to more closely resemble those humans exhibit in childhood at a time before [[fatty streaks]] begin forming.
| | ==[[Atherosclerosis causes|Causes]]== |
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| Lowering lipoprotein little a, a genetic variant of LDL, can be achieved with large daily doses of vitamin B3, niacin. Niacin also tends to shift LDL particle distribution to larger particle size and improve HDL functioning. Work on increasing HDL particle concentration and function, beyond the niacin effect, perhaps even more important, is slowly advancing. Combinations of [[statin]]s, [[niacin]], intestinal cholesterol absorption inhibiting supplements ([[ezetimibe]] and others, and to a much lesser extent [[fibrate]]s have been the most successful in changing [[dyslipidemia]] patterns and but, in the case of inhibitors and fibrates without improving clinical outcomes in secondary prevention. In primary prevention, cholesterol lowering agents have not reduced the mortality rates, for example the AFCAPS/TexCAPS and EXCEL trials and the 2 main trials with atorvastatin, Lipitor, as in the ASCOT and SPARCL studies. Dietary changes to achieve benefit have been more controversial, generally far less effective and less widely adhered to with success.
| | ==[[Atherosclerosis differential diagnosis|Differentiating Atherosclerosis from other Diseases]]== |
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| Evidence has increased that people with [[diabetes]], despite not having clinically detectable atherosclotic disease, have more severe debility from atherosclerotic events over time than even non-diabetics who have already suffered atherosclerotic events. Thus [[diabetes]] has been upgraded to be viewed as an advanced atherosclerotic disease equivalent.
| | ==[[Atherosclerosis epidemiology and demographics|Epidemiology and Demographics]]== |
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| Lowering [[homocysteine]] levels, including within the normal range and dietary supplements of Omega 3 oils, especially those from the muscle of some deep salt water living fish species, also have clinical evidence of significant protective effects as confirmed by 6 [[double blind]] [[placebo]] [[scientific control|controlled]] human clinical trials.
| | ==[[Atherosclerosis risk factors|Risk Factors]]== |
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| Medical treatments often focus predominantly on the symptoms. However, over time, the treatments which focus on decreasing the underlying atherosclerosis processes, as opposed to simply treating the symptoms resulting from the atherosclerosis, have been shown by clinical trials to be more effective.
| | ==[[Atherosclerosis screening]]== |
| | ==Overview== |
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| Other physical treatments, helpful in the short term, include minimally invasive [[angioplasty]] procedures to physically expand narrowed arteries and major invasive surgery, such as [[Coronary artery bypass surgery|bypass surgery]], to create additional blood supply connections which go around the more severely narrowed areas.
| | There is insufficient evidence to recommend routine screening for [disease/malignancy]. |
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| High dose supplements of vitamin E or C, with the goal of improving [[antioxidant]] protection, have failed to produce any beneficial trends in human, double blind, clinical research trials. However, these trials have consistently used lower doses than those claimed to be effective and have ignored the short half life of high intakes of [[vitamin C]] in the body.
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| On the other hand, the [[statin]]s, and some other medications have been shown to have [[antioxidant]] effects, possibly part of their basis for some of their therapeutic success in reducing cardiac 'events'.
| | According to the [guideline name], screening for [disease name] is not recommended. |
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| The success of statin drugs in clinical trials is based on some reductions in mortality rates, however never in women or people over the age of 70 [http://www.cmaj.ca/cgi/content/full/173/10/1207-a CMAJ]. For example, in 4S, the first large placebo controlled, randomized clinical trial of a statin in people with advanced disease who had already suffered a heart attack, the overall mortality rate reduction for those taking the statin, vs. placebo, was 30%. For the subgroup of people in the trial who had Diabetes Mellitus, the mortality rate reduction between statin and placebo was 54%. 4S was a 5.4 year trial which started in 1989 and was published in 1995 after completion. There were 3 more dead women at trial's end on statin than in the group on placebo drug. The [http://jama.ama-assn.org/cgi/reprint/jama;295/13/1556.pdf?ijkey=Md42dlk7z9TzyL8&keytype=finite |ASTEROID] trial, mentioned above and in reference 3, has been the first to show actual disease volume regression (see page 8 of the paper which shows cross-sectional areas of the total heart artery wall at start and 2 years of rosuvastatin 40 mg/day treatment); however, its design was not able to "prove" the mortality reduction issue since it has no placebo group.
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| In summary, the key to the more effective approaches has been better understanding of the widespread and insidious nature of the disease and to combine multiple different treatment strategies, not rely on just one or a few approaches. Additionally, for those approaches, such as lipoprotein transport behaviors, which have been shown to produce the most success, adopting more aggressive combination treatment strategies has generally produced better results, both before and especially after people are symptomatic. However, treating asymptomatic people remains controversial in the medical community.
| | According to the [guideline name], screening for [disease name] by [test 1] is recommended every [duration] among patients with [condition 1], [condition 2], and [condition 3]. |
| | ==Screening== |
| | There is insufficient evidence to recommend routine screening for [disease/malignancy]. |
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| Patients at risk for atherosclerosis-related diseases are increasingly being treated [[prophylaxis|prophylactically]] with low-dose [[aspirin]] and a [[statin]]. The high incidence of cardiovascular disease led Wald and Law<ref name="Polypill">Wald NJ, Law MR. A strategy to reduce cardiovascular disease by more than 80%. ''[[British Medical Journal|BMJ]]'' 2003;326:1419. PMID.</ref> to propose a ''[[Polypill]]'', a once-daily pill containing these two types of drugs in addition to an [[ACE inhibitor]], [[diuretic]] and [[beta blocker]] and [[folic acid]]. They maintain that high uptake by the general population by such a ''Polypill'' would reduce cardiovascular mortality by 80%. It must be emphasized however that this is purely theoretical, as the Polypill has never been tested in a clinical trial.
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| == Recent research ==
| | According to the [guideline name], screening for [disease name] is not recommended. |
| Methods to increase [[high density lipoprotein]] (HDL) particle concentrations, which in some animal studies largely reverses and remove atheromas, are being developed and researched. [[Niacin]] has HDL raising effects (by 10 - 30%) and showed clinical trial benefit in the Coronary Drug Project, however, the drug [[torcetrapib]] most effectively raising HDL (by 60%) also raised deaths by 60% and all studies regarding this drug were halted in December 2006.[http://www.nlm.nih.gov/medlineplus/news/fullstory_42459.html]
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| An indication of the role of HDL on atherosclerosis has been with the rare Apo-A1 Milano human genetic variant of this HDL protein. Ongoing work starting in the 1990s may lead to human clinical trials probably by about 2008, on using either synthesized Apo-A1 Milano HDL directly or by gene-transfer methods to pass the ability to synthesize the Apo-A1 Milano HDL protein.
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| The ASTEROID trial used a high-dose of a powerful statin, [[rosuvastatin]], and found plaque (intima + media volume) reduction; see the ''Effect of Very High-Intensity Statin Therapy'' reference below. No attempt has yet been made to compare this drug with placebo regarding clinical benefit.
| | According to the [guideline name], screening for [disease name] by [test 1] is recommended every [duration] among patients with: |
| | *[Condition 1] |
| | *[Condition 2] |
| | *[Condition 3] |
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| Since about 2002, progress in understanding and developing techniques for modulating immune system function so as to significantly suppress the action of macrophages to drive atherosclerotic plaque progression are being developed with considerable success in reducing plaque development in both mice and rabbits. Plans for human trials, hoped for by about 2008, are in progress. Generally these techniques are termed immunomodulation of atherosclerosis.
| | ==References== |
| | {{Reflist|2}} |
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| Genetic expression and control mechanism research, including (a) the PPAR [[peroxisome proliferator activated receptors]] known to be important in blood sugar and variants of lipoprotein production and function and (b) of the multiple variants of the proteins which form the lipoprotein transport particles, is progressing.
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| Some controversial research has suggested a link between atherosclerosis and the presence of several different [[nanobacterium|nanobacteria]] in the arteries, e.g. [[Chlamydophila pneumoniae]], though trials of current antibiotic treatments known to be usually effective in suppressing growth or killing these bacteria have not been successful in improving outcomes.
| | ==[[Atherosclerosis natural history, complications and prognosis|Natural History, Complications and Prognosis]]== |
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| The immunomodulation approaches mentioned above, because they deal with innate responses of the host to promote atherosclerosis, have far greater prospects for success. <ref>Stevens, Karen M.J. Douglas, Athanasios N. Saratzis and George D. Kitas Inflammation and atherosclerosis in rheumatoid arthritis Robert J. Expert Rev. Mol. Med. Vol. 7, Issue 7</ref> <ref>Mol, A 2002 _The Body Multiple: Ontology in medical practice_ London: Duke University Press</ref>
| | ==Diagnosis== |
| | [[Atherosclerosis history and symptoms|History and Symptoms]] | [[Atherosclerosis physical examination|Physical Examination]] | [[Atherosclerosis laboratory findings|Laboratory Findings]] | [[Atherosclerosis other diagnostic studies|Other Diagnostic Studies]] |
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| ==Pathological Findings== | | ==Treatment== |
| | | [[Atherosclerosis medical therapy|Medical Therapy]] | [[Atherosclerosis primary prevention|Primary Prevention]] | [[Atherosclerosis secondary prevention|Secondary Prevention]] | [[Atherosclerosis cost-effectiveness of therapy|Cost-Effectiveness of Therapy]] | [[Atherosclerosis future or investigational therapies|Future or Investigational Therapies]] |
| [http://www.peir.net Images courtesy of Professor Peter Anderson DVM PhD and published with permission © PEIR, University of Alabama at Birmingham, Department of Pathology] | |
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| <gallery>
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| Image:Atherosclerosis 1.jpg|Atherosclerosis: Gross, close-up of fatty streak and intimal thickening
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| Image:Atherosclerosis 2.jpg|Atherosclerosis: Gross, very good example of fibrous plaques with ulceration and thrombosis
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| Image:Atherosclerosis 3.jpg|Atherosclerosis: Gross, proximal left anterior descending artery showing faint fatty streaks and penetrating arteries
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| Image:Atherosclerosis 4.jpg|Atherosclerosis: Gross, close-up view of aorta. A plaque with ulceration and thrombosis
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| </gallery>
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| <gallery>
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| Image:Atherosclerosis 5.jpg|Atherosclerosis: Gross, good example of plaques in aorta
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| Image:Atherosclerosis 6.jpg|Atherosclerosis: Coronary artery: Gross, close-up view of excellent plaque lesion causing more than 90% occlusion
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| Image:Atherosclerosis 7.jpg|Atherosclerosis: Gross, good example of advanced calcific atherosclerosis in aorta.
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| Image:Atherosclerosis 8.jpg|Atherosclerosis: Gross, very good example of calcified and ulcerated atheromatous plaques in aorta
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| </gallery>
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| <gallery>
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| Image:Atherosclerosis with dissecting aneurysm 1.jpg|Atherosclerosis: Dissecting Aortic Aneurysm: Gross, shows dilated aorta with extensive atherosclerosis dissection is seen. A small abdominal aorta, atherosclerotic aneurysm is present. A good picture for association of dilation with dissection
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| Image:Atherosclerosis 10.jpg|Atherosclerosis: Gross, close-up, an excellent view but appearance much like that of syphilitic aortitis
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| Image:Atherosclerosis 11.jpg|Atherosclerosis: Gross, an excellent example of ulcerated lesions with many mural thrombi
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| Image:Atherosclerosis 12.jpg|Atherosclerosis: Gross, very good example of plaque lesion and small mural thrombi
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| </gallery>
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| <gallery>
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| Image:Atherosclerosis coronary artery 111.jpg|Atherosclerosis: Coronary artery: Gross, an excellent example of plaque, 80% occlusion, uncomplicated lesion.
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| Image:Atherosclerosis coronary artery in situ 1.jpg|Atherosclerosis: Coronary artery: Atherosclerosis and thrombotic occlusion: Gross, (an excellent example) in situ on heart
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| Image:Atherosclerosis 15.jpg|Atherosclerosis: Coarctation: Gross, adult lesion with dramatic demonstration of accelerated atherosclerosis
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| Image:Atherosclerosis 16.jpg|Atherosclerosis: Coronary artery: Gross, cross section well shown hemorrhage into plaque and thrombosis
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| </gallery>
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| <gallery>
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| Image:Atherosclerosis 17.jpg|Atherosclerosis: Aorta: Gross, good example of fibrous plaques
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| Image:Atherosclerosis 18.jpg|Atherosclerosis: Aorta: Gross, an excellent example of fibrous plaques and mural thrombi
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| Image:Atherosclerosis 19.jpg|Atherosclerosis: Aorta: Gross, thrombi at the origin of celiac axis and superior mesenteric arteries
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| Image:Atherosclerosis 20.jpg|Atherosclerosis: Aorta: Gross, thrombotic occlusion extending from just below renal arteries into iliac artery
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| </gallery>
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| <gallery>
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| Image:Atherosclerosis 21.jpg|Atherosclerosis: Abdominal Aneurysm Ruptured: Gross, a good example, opened kidneys in marked place. Atherosclerosis in lower thoracic aorta
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| Image:Atherosclerosis 22.jpg|Atherosclerosis: Adult type coarctation with atherosclerosis in aortic arch
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| Image:Atherosclerosis 23.jpg|Atherosclerosis: Abdominal Aneurysm Graft Repair: Gross natural color, close-up, an excellent example of Dacron graft that has been in place for years with pseudointima and atherosclerosis
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| Image:Atherosclerosis 24.jpg|Atherosclerosis: Renal Transplant: Gross, natural color, a close-up view of severe atherosclerosis in abdominal segment of aorta and fatty streaks in descending thoracic much advanced lesions for a 22 years old male with chronic glomerulonephritis
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| </gallery>
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| ===Saphenous Vein Graft===
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| <gallery>
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| Image:Atherosclerosis 29.jpg|Saphenous vein coronary bypass graft: Atherosclerosis: Micro, an excellent demonstration of myofibroblastic type cells in thickened intima
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| Image:Atherosclerosis 30.jpg|Saphenous vein coronary bypass graft: Atherosclerosis: Micro, trichrome low mag, advanced plaque with hemorrhage into atheroma and complete lumen occlusion with fresh thrombus
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| Image:Atherosclerosis 31.jpg|Saphenous vein coronary bypass graft: Atherosclerosis: Micro, low mag, early atheromata consisting of subendothelial foam cells, whole graft and fibrous intimal thickening, (102 months after CABG)
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| Image:Atherosclerosis 32.jpg|Saphenous vein coronary bypass graft: Atherosclerosis: Micro, high mag, subendothelial foam cells
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| </gallery>
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| <gallery>
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| Image:Atherosclerosis 32a.jpg|Saphenous vein coronary bypass graft: Atherosclerosis: Micro, trichrome, low mag, large athero plaque and recanalized thrombus in lumen
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| Image:Atherosclerosis 32b.jpg|Saphenous vein coronary bypass graft: Atherosclerosis: Micro, H&E, low mag, large and ruptured atheromatous plaque with focal hemorrhage and calcification
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| Image:Atherosclerosis 32c.jpg|Saphenous vein coronary bypass graft: Atherosclerosis: Micro, trichrome, low mag, very complicated hemorrhagic and necrotic plaque with lumen occlusion. A recanalized thrombus and a large aneurysm at side filled with old blood and atheroma crystals
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| Image:Atherosclerosis 32d.jpg|Saphenous vein coronary bypass graft: Atherosclerosis: Micro, ald. fusch., complicated occlusive lesion with organized and recanalized thrombus and old hemorrhage into atheroma
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| </gallery>
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| ===Coronary Arteries===
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| [http://www.peir.net Images courtesy of Professor Peter Anderson DVM PhD and published with permission © PEIR, University of Alabama at Birmingham, Department of Pathology]
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| <gallery>
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| Image:Atherosclerosis 33.jpg|Coronary artery: Atherosclerosis: Micro, H&E, low mag, injected artery, good demonstration of organized and recanalized thrombus
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| Image:Atherosclerosis 34.jpg|Coronary artery: Atherosclerosis: Micro, H&E, low mag, injected artery, very good example of marked lumen stenosis due to typical fibrous plaque with some calcifications
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| Image:Atherosclerosis 35.jpg|Coronary artery: Atherosclerosis: Micro, H&E, injected artery, marked large plaque with thin fibrous cap has eroded to adventitia, the start of an aneurysm
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| Image:Atherosclerosis 36.jpg|Coronary artery: Atherosclerosis: Micro, H&E, low mag, an excellent example of plaque with calcification and marked narrowing of lumen. 90% lumen is occluded by thrombus
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| </gallery>
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| <gallery>
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| Image:Atherosclerosis 37.jpg|Coronary artery: Atherosclerosis: Micro, low mag, an excellent example of atheromatous plaque causing marked lumen obstruction. An uncomplicated plaque
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| Image:Atherosclerosis 38.jpg|Coronary artery: Atherosclerosis: Micro, H&E, low mag, an excellent example of athero plaque. the lumen is completely occluded
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| Image:Atherosclerosis 39.jpg|Coronary artery: Atherosclerosis: Micro, H&E, low mag, a plaque with hemorrhage and organizing mural thrombus in lumen
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| Image:Atherosclerosis 40.jpg|Coronary artery: Atherosclerosis: Micro, H&E, low mag, a good example of plaque with old hemorrhage and marked lumen compensation
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| </gallery>
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| <gallery>
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| Image:Atherosclerosis 41.jpg|Coronary artery: Atherosclerosis: Micro, H&E, med mag, plaque rupture with thrombosis
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| Image:Atherosclerosis 42.jpg|Coronary artery: Atherosclerosis: Micro, H&E, low mag, injected artery, a good example of atheromatous plaque that appears to owe much of its mass to an organized mural thrombus
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| Image:Atherosclerosis 43.jpg|Coronary artery: Atherosclerosis: Micro, H&E, low mag, typical uncomplicated fibrous plaque
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| Image:Atherosclerosis 44.jpg|Coronary artery: Atherosclerosis: Micro, H&E, low mag, a good example of athero plaque with marked lumen narrowing. A small mural thrombus in lumen
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| </gallery>
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| <gallery>
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| Image:Atherosclerosis 44a.jpg|Coronary artery: Atherosclerosis: Micro, low mag, hemorrhage into plaque and thrombosis
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| Image:Atherosclerosis 44b.jpg|Coronary artery: Atherosclerosis: Recanalized Thrombus: Micro, low mag, H&E, lesion is nearly completely organized, small adventitial dissection probably related to bypass surgery about 24 hours before death (a good example)
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| Image:Atherosclerosis 44c.jpg|Coronary artery: Atherosclerosis: Plaque Hemorrhage and Thrombosis: Micro, low mag, H&E, quite good photo, large plaque with hemorrhage, organizing thrombus in lumen
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| Image:Atherosclerosis 44d.jpg|Coronary artery: Atherosclerosis, Severe: Micro, low mag, H&E, more than 90% stenosis, also shown a side branch
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| </gallery>
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| ===Aorta===
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| [http://www.peir.net Images courtesy of Professor Peter Anderson DVM PhD and published with permission © PEIR, University of Alabama at Birmingham, Department of Pathology]
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| <gallery>
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| Image:Atherosclerosis Aorta 1.jpg|Kidney: Atheromatous Embolus: Gross, natural color, external view of kidney with typical scarring pattern of repeated infarction and aorta with severe atherosclerosis (quite good example)
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| Image:Atherosclerosis Aorta 2.jpg|Aorta, Atherosclerosis: Gross, natural color, opened thoracic segment showing sessile plaques covering intima with several mural thrombi
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| Image:Atherosclerosis Aorta 3.jpg|Aorta, Atherosclerosis: Gross natural color view of descending thoracic and abdominal segments with expected distribution of atherosclerotic lesions in subject over 60 years old. Not much in thoracic segment and extensive plaques in abdominal segment, some with ulceration
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| Image:Atherosclerosis aorta, renal and iliac 1.jpg|Thrombus: Gross natural color aorta with kidneys showing thrombotic occlusion due to atherosclerosis beginning just below renal arteries and extending into common iliac (very good example)
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| </gallery>
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| ===Carotid Artery===
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| [http://www.peir.net Images courtesy of Professor Peter Anderson DVM PhD and published with permission © PEIR, University of Alabama at Birmingham, Department of Pathology]
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| <gallery>
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| Image:Atherosclerosis carotid artery 2.jpg|Carotid artery: Atherosclerosis: Gross, internal carotid plaque with thrombosis
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| Image:Atherosclerosis carotid artery 3.jpg|Carotid artery: Atherosclerosis: Gross, plaque with hemorrhage in carotid bulb
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| Image:Atherosclerosis carotid artery 4.jpg|Carotid artery bifurcation, atherosclerosis
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| Image:Atherosclerosis carotid artery 5.jpg|Carotid artery, atherosclerosis and thrombosis
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| Image:Atherosclerosis carotid artery 6.jpg|Carotid artery: Atherosclerosis: Gross, good example of carotid bulb plaque with thrombus
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| </gallery>
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| ===Lung===
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| [http://www.peir.net Images courtesy of Professor Peter Anderson DVM PhD and published with permission © PEIR, University of Alabama at Birmingham, Department of Pathology]
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| <gallery>
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| Image:Atherosclerosis lung 1.jpg|Lung: Pulmonary fibrosis and atherosclerosis of pulmonary artery
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| Image:Atherosclerosis lung 2.jpg|Lung: Pulmonary fibrosis and atherosclerosis of pulmonary artery
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| Image:Atherosclerosis lung 3.jpg|Lung: Pulmonary fibrosis and atherosclerosis of pulmonary artery
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| Image:Atherosclerosis lung 4.jpg|Lung: Atherosclerosis: Gross, natural color, arteries show atherosclerotic plaque lesions
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| </gallery>
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| ===Pulmonary Artery===
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| [http://www.peir.net Images courtesy of Professor Peter Anderson DVM PhD and published with permission © PEIR, University of Alabama at Birmingham, Department of Pathology] | |
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| <gallery>
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| Image:Atherosclerosis 57.jpg|Pulmonary artery atherosclerosis in patient with pulmonary hypertension
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| Image:Atherosclerosis 58.jpg|Pulmonary Artery Atherosclerosis: Gross, essentially natural color, artery stained by hemolysis, small plaque lesions
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| Image:Atherosclerosis pulmonary artery 1.jpg|Atherosclerosis: Gross, natural color, close-up fatty plaques in large pulmonary artery
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| Image:Atherosclerosis 60.jpg|Atherosclerosis: Micro, low mag, van Gieson, thickened intima with fatty streak type lesion and preservation of fetal medial structure, a large pulmonary artery, 4yo male with primary pulmonary hypertension
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| </gallery>
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| ===Brain===
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| [http://www.peir.net Images courtesy of Professor Peter Anderson DVM PhD and published with permission © PEIR, University of Alabama at Birmingham, Department of Pathology] | |
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| <gallery>
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| Image:Atherosclerosis brain 1.jpg|Brain: Atherosclerosis: Gross, a good example of atherosclerosis in vessels at base of brain.
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| Image:Atherosclerosis brain 2.jpg|Brain: Basilar Artery Atherosclerosis: Gross, fixed tissue, an external view of base of brain (typical lesion)
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| Image:Atherosclerosis brain 3.jpg|Brain: Old Cystic Encephalomalacia: Gross, fixed tissue, frontal lobe lesion with frontal artery atherosclerosis
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| Image:Atherosclerosis brain 4.jpg|Brain: Watershed Infarct and Carotid Atherosclerosis
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| </gallery>
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| ===Liver===
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| [http://www.peir.net Images courtesy of Professor Peter Anderson DVM PhD and published with permission © PEIR, University of Alabama at Birmingham, Department of Pathology]
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| <gallery>
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| Image:Atherosclerosis 65.jpg|
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| Image:Atherosclerosis 66.jpg|
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| Image:Atherosclerosis 67.jpg|
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| Image:Atherosclerosis 68.jpg|
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| </gallery>
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| ===Kidney===
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| [http://www.peir.net Images courtesy of Professor Peter Anderson DVM PhD and published with permission © PEIR, University of Alabama at Birmingham, Department of Pathology]
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| <gallery>
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| Image:Atherosclerosis renal 1.jpg|Atherosclerosis: Kidney: Atheromatous Embolus: Gross, natural color, kidney with typical scarring pattern of repeated embolism and aorta with severe atherosclerosis (a quite good example)
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| Image:Atherosclerosis renal 2.jpg|Atherosclerosis: Kidney: Atrophy secondary to renal artery atherosclerosis: Gross, natural color, both kidneys one very atrophic the large left kidney weighed 220 grams and the small left one 90 gram
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| </gallery>
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| ===Spleen=== | | ==Case Studies== |
| | | [[Atherosclerosis case study one|Case #1]] |
| [http://www.peir.net Images courtesy of Professor Peter Anderson DVM PhD and published with permission © PEIR, University of Alabama at Birmingham, Department of Pathology] | |
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| <gallery>
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| Image:Atherosclerosis spleen 1.jpg|
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| Image:Atherosclerosis spleen 2.jpg|
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| Image:Atherosclerosis spleen 3.jpg|
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| Image:Atherosclerosis spleen 4.jpg|
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| </gallery>
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| ==References==
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| {{reflist|2}}
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| ==See also== | | ==Related Chapters== |
| <div style="-moz-column-count:2; column-count:2;"> | | <div style="-moz-column-count:2; column-count:2;"> |
| *[[Monckeberg's arteriosclerosis]] | | *[[Monckeberg's arteriosclerosis]] |
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| [[Category:Primary care]] | | [[Category:Primary care]] |