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==Overview==
==Overview==
'''Atherosclerosis''' is a [[disease]] affecting [[artery|arterial]] [[blood vessel]]s. It is a chronic inflammatory response in the walls of arteries, in large part due to the deposition of [[lipoproteins]] (plasma proteins that carry cholesterol and [[triglycerides]]). It is commonly referred to as a "hardening" or "furring" of the arteries. It is caused by the formation of multiple [[atheroma|plaques]] within the [[arteries]].
'''Atherosclerosis''' is a [[disease]] affecting [[artery|arterial]] [[blood vessel]]s. It is a chronic inflammatory response in the walls of arteries, in large part due to the deposition of [[lipoproteins]] (plasma proteins that carry cholesterol and [[triglycerides]]). It is commonly referred to as a "hardening" or "furring" of the arteries. It is caused by the formation of multiple [[atheroma|plaques]] within the [[arteries]].
[[anatomical pathology|Pathologically]], the [[atheroma|atheromatous plaque]] is divided into three distinct components:
*The [[atheroma]] ("lump of porridge", from ''Athera'', porridge in Greek,) is the nodular accumulation of a soft, flaky, yellowish material at the center of large plaques, composed of [[macrophage]]s nearest the [[lumen (anatomy)|lumen]] of the artery.
*Underlying areas of [[cholesterol]] crystals.
*Calcification at the outer base of older/more advanced lesions.
The following terms are similar, yet distinct, in both spelling and meaning, and can be easily confused: arteriosclerosis, arteriolosclerosis and atherosclerosis. Arteriosclerosis is a general term describing any hardening (and loss of elasticity) of medium or large arteries (in Greek, "Arterio" meaning artery and "sclerosis" meaning hardening), arteriolosclerosis is  atherosclerosis mainly affecting the [[arteriole]]s (small arteries), atherosclerosis is a hardening of an artery specifically due to an atheromatous plaque. Therefore, atherosclerosis is a form of arteriosclerosis.
Atherosclerosis causes two main problems. First, the [[atheroma|atheromatous plaques]], though long compensated for by artery enlargement, see [[intima-media thickness|IMT]], eventually lead to plaque ruptures and stenosis (narrowing) of the artery and, therefore, an insufficient blood supply to the organ it feeds. Alternatively, if the compensating artery enlargement process is excessive, then a net [[aneurysm]] results.
These complications are chronic, slowly progressing and cumulative.  Most commonly, soft plaque suddenly ruptures (see [[vulnerable plaque]]), causing the formation of a thrombus that will rapidly slow or stop blood flow, e.g. 5 minutes, leading to death of the tissues fed by the artery. This catastrophic event is called an [[infarction]]. One of the most common recognized scenarios is called [[coronary thrombosis]] of a [[coronary artery]] causing [[myocardial infarction]] (a heart attack). Another common scenario in very advanced disease is [[claudication]] from insufficient blood supply to the legs, typically due to a combination of both stenosis and aneurysmal segments narrowed with [[thrombus|clots]]. Since atherosclerosis is a body wide process, similar events also occur in the arteries to the brain, intestines, kidneys, legs, etc.


==Pathophysiology==
==Pathophysiology==
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===Medical Therapy===
===Medical Therapy===
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.
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.
===Future or Investigational Therapies===
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==
==References==
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[[Category:Primary care]]
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[[Category:Cardiology]]
[[Category:Cardiology]]
[[Category:Disease]]
[[Category:Disease]]

Latest revision as of 20:31, 29 July 2020

https://https://www.youtube.com/watch?v=MjC1-odNY5k%7C350}}

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Overview

Atherosclerosis is a disease affecting arterial blood vessels. It is a chronic inflammatory response in the walls of arteries, in large part due to the deposition of lipoproteins (plasma proteins that carry cholesterol and triglycerides). It is commonly referred to as a "hardening" or "furring" of the arteries. It is caused by the formation of multiple plaques within the arteries.

Pathophysiology

Atherogenesis is the developmental process of atheromatous plaques. It is characterized by a remodeling of arteries involving the concomitant accumulation of fatty substances called plaques. One recent theory suggests that for unknown reasons, leukocytes such as monocytes or basophils begin to attack the endothelium of the artery lumen in cardiac muscle. The ensuing inflammation leads to formation of atheromatous plaques in the arterial tunica intima, a region of the vessel wall located between the endothelium and the tunica media and tunica adventitia. The bulk of these lesions are made of excess fat, collagen, and elastin. Initially, as the plaques grow only wall thickening occurs without any narrowing, stenosis of the artery opening, called the lumen; stenosis is a late event which may never occur and is often the result of repeated plaque rupture and healing responses, not the just atherosclerosis process by itself.

Diagnosis

History and Symptoms

According to United States data for the year 2004, for about 65% of men and 47% of women, the first symptom of atherosclerotic cardiovascular disease is heart attack or sudden cardiac death (death within one hour of onset of the symptom).

Laboratory Findings

Cardiac stress testing, traditionally the most commonly performed non-invasive testing method for blood flow limitations generally only detects lumen narrowing of ~75% or greater, although some physicians advocate that nuclear stress methods can detect as little as 50%.

Treatment

Medical Therapy

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.

Future or Investigational Therapies

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

Template:WH Template:WS CME Category::Cardiology