RESEARCH STARTER

Plaque, arterial

Arterial plaque, also known as atheroma or atheromatous plaque, refers to fatty deposits that accumulate within the walls of arteries, impacting the circulatory system and heart. This condition is primarily caused by hypercholesterolemia, hypertension, and chronic inflammation, which lead to the gradual buildup of cholesterol and cellular debris over several decades. Initially, there may be no symptoms; however, as the plaque progresses, individuals may experience unusual fatigue, light-headedness, palpitations, or chest pressure (angina) due to impaired blood flow.

Treatment approaches generally begin with lifestyle changes, including increased physical activity, healthier eating habits rich in fruits and vegetables, stress management, and smoking cessation. Medications like statins are commonly prescribed to lower low-density lipoprotein cholesterol (LDL-C) levels and provide additional heart health benefits. In cases of severe narrowing of arteries (stenosis) or the risk of thrombosis, further interventions such as medications to promote artery dilation, catheter-based procedures, or surgery may be necessary. Early intervention through lifestyle modification and regular blood testing can significantly improve health outcomes and reduce the risk of serious complications, such as heart attacks or strokes.

Full Article

  • ALSO KNOWN AS: Atheroma, atheromatous plaque
  • ANATOMY OR SYSTEM AFFECTED: Blood vessels, circulatory system, heart
  • 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

DEFINITION: Fatty deposits within arterial walls

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 lipoproteins carrying cholesterol (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 plaque 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 arteries feeding the brain 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).

Treatment and Therapy

Treatment begins with lifestyle changes—exercising, managing stress, stopping smoking, lowering blood pressure, and 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 (fenofibrate, gemfibrozil), some statins (simvastatin, rosuvastatin), and niacin may be used to counteract LDL-C by boosting HDL-C, the high-density lipoprotein or “good” cholesterol. PCSK9 inhibitors (evolocumab, alirocumab) also aid in decreasing bad cholesterol, particularly in patients who do not respond to other treatments. High blood pressure is typically treated using diuretics, beta blockers, angiotensin II receptor blockers (ARBs), calcium channel blockers (CBCs), or angiotensin-converting enzyme (ACE) inhibitors. Thrombosis risk is reduced using drugs such as warfarin, clopidogrel, and prasugrel. Stenosis can be treated using nitroglycerin, ranolazine, and CBCs 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 risk factors 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

"About Coronary Artery Disease (CAD) ." Centers for Disease Control and Prevention (CDC), 15 May 2024, www.cdc.gov/heart-disease/about/coronary-artery-disease.html. Accessed 9 Sept. 2025.

Alpert, Joseph S. "New Coronary Heart Disease Risk Factors." The American Journal of Medicine, vol. 135, no. 4, Apr. 2023, pp. 331-32, doi:10.1016/j.amjmed.2022.08.002. Accessed 9 Sept. 2025.

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

Ohayon, Jacques, et al. Biomechanics of Coronary Atherosclerotic Plaque: From Model to Patient. Academic Press, 2020.

Reisner, Emily, and Howard Reisner. Crowley's An Introduction to Human Disease: Pathology and Pathophysiology Correlations. 11th ed., Jones and Bartlett, 2022.

"What Is Atherosclerosis?" The National Heart, Lung, and Blood Institute, National Institutes of Health, 28 Oct. 2024, www.nhlbi.nih.gov/health/atherosclerosis. Accessed 9 Sept. 2025.

Full Article

  • ALSO KNOWN AS: Atheroma, atheromatous plaque
  • ANATOMY OR SYSTEM AFFECTED: Blood vessels, circulatory system, heart
  • 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

DEFINITION: Fatty deposits within arterial walls

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 lipoproteins carrying cholesterol (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 plaque 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 arteries feeding the brain 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).

Treatment and Therapy

Treatment begins with lifestyle changes—exercising, managing stress, stopping smoking, lowering blood pressure, and 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 (fenofibrate, gemfibrozil), some statins (simvastatin, rosuvastatin), and niacin may be used to counteract LDL-C by boosting HDL-C, the high-density lipoprotein or “good” cholesterol. PCSK9 inhibitors (evolocumab, alirocumab) also aid in decreasing bad cholesterol, particularly in patients who do not respond to other treatments. High blood pressure is typically treated using diuretics, beta blockers, angiotensin II receptor blockers (ARBs), calcium channel blockers (CBCs), or angiotensin-converting enzyme (ACE) inhibitors. Thrombosis risk is reduced using drugs such as warfarin, clopidogrel, and prasugrel. Stenosis can be treated using nitroglycerin, ranolazine, and CBCs 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 risk factors 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

"About Coronary Artery Disease (CAD) ." Centers for Disease Control and Prevention (CDC), 15 May 2024, www.cdc.gov/heart-disease/about/coronary-artery-disease.html. Accessed 9 Sept. 2025.

Alpert, Joseph S. "New Coronary Heart Disease Risk Factors." The American Journal of Medicine, vol. 135, no. 4, Apr. 2023, pp. 331-32, doi:10.1016/j.amjmed.2022.08.002. Accessed 9 Sept. 2025.

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

Ohayon, Jacques, et al. Biomechanics of Coronary Atherosclerotic Plaque: From Model to Patient. Academic Press, 2020.

Reisner, Emily, and Howard Reisner. Crowley's An Introduction to Human Disease: Pathology and Pathophysiology Correlations. 11th ed., Jones and Bartlett, 2022.

"What Is Atherosclerosis?" The National Heart, Lung, and Blood Institute, National Institutes of Health, 28 Oct. 2024, www.nhlbi.nih.gov/health/atherosclerosis. Accessed 9 Sept. 2025.

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