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Severe Aortic Atherosclerosis
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Severe Aortic Atherosclerosis

View of inner surface of aorta and bifurcaton, opened lengthwise along the posterior midline.
Note: irregular variegated lining due to diffuse disease, with red thrombi (black arrow); ostia of celiac and superior mesenteric arteries and right renal artery (white arrows); deceptive narrower caliber of abdominal aorta below celiac artery due to rigidity of calcified atheroma in the typically more severely diseased lower aorta, which maintains its shape after being cut.
(Description By:J. Hasson, M.D. )
(Image Contrib. by: Saint Francis Hospital )
Atherosclerosis
Etiology

Unknown. Although the role of risk factors contributing to the pathogenesis is clear, the problem is that there are a few privileged individuals and experimental animals that are resistant when challenged by risk factors. Knowledge of the resistant factor(s) and their mechanism(s) of action would lead to a solution of the etiology.
Pathogenesis

Hypotheses: Endothelial damage (dysfunction) with increased permeability, monocyte adhesion, and endothelial proliferation; hyperlipidemia with invasion of intima by foamy macrophages; macrophage derived cytokines (IL-1, TNF) and growth factors (PDGF, FGF) cause inflammatory response and proliferation of smooth muscle with sclerosis; plaque thickened by organization of superimposed thrombi.,
Epidemiology

Causes 50% of all deaths in the U.S. due to coronary, cerebral, peripheral, and mesenteric vascular disease, and aortic aneurysms.
A disease of Western civilization. Absent in certain third world ethnic groups.
Major risk factors are high animal fat diets, hyperlipidemias, hypertension, cigarette smoking, and diabetes.
Other important risk factors are obesity, male gender, family history, and physical inactivity.
General Gross Description

Lesions in childhood appear as "fatty streaks".
Adult plaques are discrete, yellow white random elevations, more prominent around ostia of large branches, abdominal aorta, and coronary, popliteal, internal carotid, and cerebral arteries.
Plaques may have sclerotic firm surfaces, or ulcerate with soft exposed grumous material.
Plaques may become confluent with thrombosis.
Severity increases with age, into very old age.
General Microscopic Description

An intimal lesion, made up of a deposition of neutral fats, cholesterol esters, necrotic debris and foam cells, with a variable chronic fibrotic inflammatory response forming a superficial fibrous cap containing smooth muscle and foam cells and lymphocytes.
Complications are ulcers with thrombi, bleeding into plaque, embolization of thrombi and/or atheromas, calcifications, and atrophy of media with formation of aneurysms.
Clinical Correlation

Important clinical syndromes due to occlusive disease are ischemic heart disease (angina pectoris, myocardial infarction, congestive heart failure), cerebral infarcts, peripheral vascular disease with gangrene of legs, ischemic bowel disease with infarction. Ruptured abdominal aortic aneurysm also a significant cause of death.
Advanced age not an indicator of immunity to atherosclerosis. Highest death rates by age are in those over 85 years old:, 50 % or higher.
References

Cotran RS, Kumar V, Robbins SL. Robbins Pathologic Basis of Disease. 5th edition. Philadelphia, W.B. Saunders, 1994, pp. 473-484.
Atherosclerosis
Synopsis by: J. Hasson M.D. (T42000M52110)[160]
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