Plaque, arterial

ALSO KNOWN AS: Atheroma, atheromatous plaque

ANATOMY OR SYSTEM AFFECTED: Blood vessels, circulatory system, heart

DEFINITION: Fatty deposits within arterial walls

CAUSES: Hypercholesterolemia, hypertension, inflammation

SYMPTOMS: None in early stages; in later stages, when blood flow is impaired, then unusual fatigue, light-headedness, palpitations, feeling of pressure on chest (angina)

DURATION: Chronic

TREATMENTS: Lifestyle changes, statins, blood pressure medication

Causes and Symptoms

Arterial plaques are caused by a buildup of cholesterol and cell debris within arterial walls. This process occurs over a period of decades, starting at local sites of arterial inflammation. Low-density carrying (LDL-C) that infiltrate these sites are highly susceptible to oxidation, which activates another inflammatory response that summons macrophages (part of the immune system). The macrophages engulf the oxidized LDL-C and accumulate as bloated foam cells along with some other cells to become a fatty streak. A tug-of-war ensues in which cholesterol continues to accumulate while other processes remove it. When too much cholesterol accumulates, a scablike cap is formed, while other processes slowly calcify the from the bottom up. This strategy works well as long as the cap does not crack; a cracked cap leaks debris into the artery, which triggers thrombosis (clotting). Blockage of a large coronary artery causes a heart attack; blockage of feeding the causes a stroke. Clots that are not fully occlusive get degraded, but repeated rounds of plaque rupturing and recapping eventually cause stenosis (narrowing of the artery) and ischemia (oxygen starvation).

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Treatment and Therapy

Treatment begins with lifestyle changes—exercising, managing stress, stopping smoking, lowering blood pressure, eating more fruits and vegetables. The next step is reducing high levels of LDL-C using statins, which also provide antioxidant, anti-inflammatory, and plaque-stabilizing benefits. Bile acid sequestrants and cholesterol absorption inhibitors are sometimes used as well. Fibrates and niacin are used to counteract LDL-C by boosting HDL-C, the high-density lipoprotein or “good” cholesterol. High is typically treated using diuretics, beta blockers, or angiotensin-converting enzyme (ACE) inhibitors. Thrombosis risk is reduced using low-dose aspirin or drugs such as warfarin, clopidogrel, and prasugrel. Stenosis can be treated using nitroglycerin, ranolazine, and calcium-channel inhibitors to help arteries dilate. A common surgical procedure is to physically open the artery using a catheter, often done in conjunction with implanting a stent to keep the artery propped open. Surgery can also be used to scrape out arteries or replace them.

Perspective and Prospects

Once plaques reach their later stages of development, they are extremely difficult, if not impossible, to remove. Prospects are best when lifestyle changes are initiated early in adulthood. Blood tests for assessing are invaluable; the most useful ones measure fasting levels of glucose, total cholesterol, LDL-C, HDL-C, triglycerides, homocysteine, and C-reactive protein (a marker of inflammation). Monitoring and controlling blood pressure is also vitally important.

Bibliography

Alpert, Joseph S. "New Coronary Heart Disease Risk Factors." The American Journal of Medicine, vol. 135, no. 4, Apr. 2023, pp. 331-332, doi.org/10.1016/j.amjmed.2022.08.002. Accessed 7 Apr. 2024.

"Coronary Artery Disease (CAD)." Centers for Disease Control and Prevention (CDC), 19 July 2021, www.cdc.gov/heartdisease/coronary‗ad.htm. Accessed 7 Apr. 2024.

Crowley, Leonard V. An Introduction to Human Disease, Pathology, and Pathophysiology Correlations. 9th ed. Boston: Jones and Bartlett, 2013.

Mittal, Satish. Coronary Heart Disease in Clinical Practice. London: Springer, 2005.

Rosenblum, Laurie. "Atherosclerosis." Health Library, May 8, 2013.