Written and peer-reviewed by physicians—but use at your own risk. Read our disclaimer.

banner image

amboss

Trusted medical answers—in seconds.

Get access to 1,000+ medical articles with instant search
and clinical tools.

Try free for 5 days

Atherosclerosis

Last updated: March 29, 2021

Summarytoggle arrow icon

Atherosclerosis is the most common type of arteriosclerosis, or thickening and stiffening of the arterial wall. Major risk factors include smoking, diabetes mellitus, arterial hypertension, dyslipidemia, family history of early heart disease, and advanced age. The pathogenesis is a complicated process precipitated by endothelial damage, which leads to an invasion of inflammatory cells into the tunica intima and adhesion of platelets to the disrupted endothelium. Invading smooth muscle cells (SMCs) and macrophages take up cholesterol from oxidized low-density lipoprotein (LDL) in the vessel wall. They then become foam cells, which accumulate in early atherosclerotic lesions (fatty streaks), triggering the production of extracellular matrix (e.g., collagen). This leads to the formation of fibrous plaques (foam cells, extracellular matrix, free cholesterol, and cellular debris), which may rupture and lead to thrombosis. Common sites of atherosclerosis include the abdominal aorta, coronary arteries, popliteal arteries, and carotid arteries. Depending on the location, atherosclerosis may lead to a variety of conditions, such as arterial aneurysms, dissection, coronary heart disease (CHD), peripheral artery disease (PAD), intestinal ischemia, subcortical vascular dementia (Binswanger's disease), thrombosis (e.g., acute coronary syndrome and stroke), and renovascular hypertension.

The terms “arteriosclerosis” and “atherosclerosis” are often used synonymously!


References:[1][2][3]

  • Leading cause of vascular disease worldwide
  • Sex: >

Epidemiological data refers to the US, unless otherwise specified.

The term metabolic syndrome refers to the presence of at least 3 of the following risk factors: obesity, elevated triglycerides, low high-density lipoprotein (HDL), diabetes mellitus, and arterial hypertension. [5]

Pathogenesis of atherosclerosis

  1. Chronic stress on the endothelium
  2. Endothelial dysfunction, which leads to
  3. Inflammation of the vessel wall
  4. Macrophages and SMCs ingest cholesterol from oxidized LDL and transform into foam cells.
  5. Foam cells accumulate to form fatty streaks (early atherosclerotic lesions).
  6. Lipid-laden macrophages and SMCs produce extracellular matrix (e.g., collagen) → development of a fibrous plaque (atheroma)
  7. Inflammatory cells in the atheroma (e.g., macrophages) secrete matrix metalloproteinases weakening of the fibrous cap of the plaque due to the breakdown of extracellular matrix minor stress ruptures the fibrous cap
  8. Calcification of the intima (the amount and pattern of calcification affect the risk of complications) [8][9]
  9. Plaque rupture exposure of thrombogenic material (e.g., collagen) thrombus formation with vascular occlusion or spreading of thrombogenic material

Common sites (in order of increasing frequency)

To remember the order of vessels affected by atherosclerosis (in increasing order of frequency), think of the “Die hard” plot: Bruce Willis CAtches a Perceptive Criminal named HAns.

Atherosclerotic diseases

References:[1][2][10][11][12]

The most significant therapeutic step patients with vascular disease can take is stopping smoking!
References:[13]

  1. Kumar V, Abbas AK, Aster JC. Robbins & Cotran Pathologic Basis of Disease. Elsevier Saunders ; 2014
  2. Le T, Bhushan V. First Aid for the USMLE Step 1 2015. McGraw-Hill Education ; 2014
  3. Damjanov I. The Blood Vessels. Elsevier ; 2008 : p. 121-136
  4. Martín-Timón I. Type 2 diabetes and cardiovascular disease: Have all risk factors the same strength?. World J Diabetes. 2014; 5 (4): p.444. doi: 10.4239/wjd.v5.i4.444 . | Open in Read by QxMD
  5. Grundy SM, Cleeman JI, Daniels SR, et al. Diagnosis and management of the metabolic syndrome: an American Heart Association/National Heart, Lung, and Blood Institute Scientific Statement. Circulation. 2005; 112 (17): p.2735-2752. doi: 10.1161/CIRCULATIONAHA.105.169404 . | Open in Read by QxMD
  6. Black PH, Garbutt LD. Stress, inflammation and cardiovascular disease. J Psychosom Res. 2002; 52 (1): p.1-23.
  7. Kiechl S, Willeit J, Rungger G, Egger G, Oberhollenzer F, Bonora E. Alcohol consumption and atherosclerosis: what is the relation? Prospective results from the Bruneck Study. Stroke. 1998; 29 (5): p.900-907. doi: 10.1161/01.STR.29.5.900 . | Open in Read by QxMD
  8. Shi X, Gao J, Lv Q, et al. Calcification in Atherosclerotic Plaque Vulnerability: Friend or Foe?. Frontiers in Physiology. 2020; 11 . doi: 10.3389/fphys.2020.00056 . | Open in Read by QxMD
  9. Vasuri F, Fittipaldi S, Pini R, et al. Diffuse Calcifications Protect Carotid Plaques regardless of the Amount of Neoangiogenesis and Related Histological Complications. BioMed Research International. 2015; 2015 : p.1-8. doi: 10.1155/2015/795672 . | Open in Read by QxMD
  10. Zhao XQ. Pathogenesis of atherosclerosis. In: Post TW, ed. UpToDate. Waltham, MA: UpToDate. http://www.uptodate.com/contents/pathogenesis-of-atherosclerosis.Last updated: May 17, 2016. Accessed: March 28, 2017.
  11. Ferrières J. Effects on coronary atherosclerosis by targeting low-density lipoprotein cholesterol with statins. Am J Cardiovasc Drugs. 2009; 9 (2): p.109-115. doi: 10.2165/00129784-200909020-00005 . | Open in Read by QxMD
  12. Endemann DH, Schiffrin EL. Endothelial dysfunction. J Am Soc Nephrol. 2004; 15 (8): p.1983-1992. doi: 10.1097/01.ASN.0000132474.50966.DA . | Open in Read by QxMD
  13. Eckel RH, Jakicic JM, Ard JD, et al. 2013 AHA/ACC guideline on lifestyle management to reduce cardiovascular risk: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. Circulation. 2013; 129 (25 Suppl 2): p.S76-99. doi: 10.1161/01.cir.0000437740.48606.d1 . | Open in Read by QxMD