Back Aterosclerosi AN تصلب عصيدي Arabic آتروسکلروزیس AZB Атеросклероз Bashkir Атэрасклероз Byelorussian Атэрасклероз BE-X-OLD Ateroesclerosi Catalan ڕەقبوونی خوێنبەر CKB Ateroskleróza Czech Atherosklerose German

Atherosclerosis

Not to be confused with Arteriosclerosis.
For the journal, see Atherosclerosis (journal).
Atherosclerosis
Other namesArteriosclerotic vascular disease (ASVD)
The progression of atherosclerosis (narrowing exaggerated)
SpecialtyCardiology, angiology
SymptomsNone[1]
ComplicationsCoronary artery disease, stroke, peripheral artery disease, kidney problems[1]
Usual onsetYouth (worsens with age)[2]
CausesAccumulation of saturated fats, smoking, high blood pressure and diabetes
Risk factorsHigh blood pressure, diabetes, smoking, obesity, family history, unhealthy diet (notably trans fat), chronic Vitamin C deficiency[3][4]
PreventionHealthy diet, exercise, not smoking, maintaining a normal weight[5]
MedicationStatins, blood pressure medication, aspirin[6]
Frequency≈100% (>65 years old)[7]

Atherosclerosis[a] is a pattern of the disease arteriosclerosis,[8] characterized by development of abnormalities called lesions in walls of arteries. This is a chronic inflammatory disease involving many different cell types, and driven by elevated levels of cholesterol in the blood.[9] These lesions may lead to narrowing of the arterial walls due to buildup of atheromatous plaques.[10][11] At onset there are usually no symptoms, but if they develop, symptoms generally begin around middle age.[1] In severe cases, it can result in coronary artery disease, stroke, peripheral artery disease, or kidney disorders, depending on which body part(s) the affected arteries are located in the body.[1]

The exact cause of atherosclerosis is unknown and is proposed to be multifactorial.[1] Risk factors include abnormal cholesterol levels, elevated levels of inflammatory biomarkers,[12] high blood pressure, diabetes, smoking (both active and passive smoking), obesity, genetic factors, family history, lifestyle habits, and an unhealthy diet.[4] Plaque is made up of fat, cholesterol, immune cells, calcium, and other substances found in the blood.[10][9] The narrowing of arteries limits the flow of oxygen-rich blood to parts of the body.[10] Diagnosis is based upon a physical exam, electrocardiogram, and exercise stress test, among others.[13]

Prevention guidelines include, eating a healthy diet, exercising, not smoking, and maintaining normal body weight.[5] Treatment of established disease may include medications to lower cholesterol such as statins, blood pressure medication, and anticoagulant therapies to reduce the risk of blood clot formation.[6] As the disease state progresses more invasive strategies are applied such as percutaneous coronary intervention, coronary artery bypass graft, or carotid endarterectomy.[6] Genetic factors are also strongly implicated in the disease process; it is unlikely to be entirely based on lifestyle choices.[14]

Atherosclerosis generally starts when a person is young and worsens with age.[2] Almost all people are affected to some degree by the age of 65.[7] It is the number one cause of death and disability in developed countries.[15][16][17] Though it was first described in 1575,[18] there is evidence suggesting that this disease state is genetically inherent in the broader human population, with its origins tracing back to genetic mutations that may have occurred more than two million years ago during the evolution of hominin ancestors of modern human beings.[19]

  1. ^ a b c d e "What Are the Signs and Symptoms of Atherosclerosis? - NHLBI, NIH". www.nhlbi.nih.gov. 22 June 2016. Retrieved 5 November 2017.
  2. ^ a b "What Causes Atherosclerosis? - NHLBI, NIH". www.nhlbi.nih.gov. 22 June 2016. Retrieved 6 November 2017.
  3. ^ "New Concept of Heart Disease Posits Vitamin C Deficiency as Culprit". DAIC (Diagnostic and Interventional Cardiology). 27 April 2015. Retrieved 2022-02-06.
  4. ^ a b "Who Is at Risk for Atherosclerosis?". www.nhlbi.nih.gov. 22 June 2016. Retrieved 5 November 2017.
  5. ^ a b "How Can Atherosclerosis Be Prevented or Delayed? - NHLBI, NIH". www.nhlbi.nih.gov. 22 June 2016. Retrieved 6 November 2017.
  6. ^ a b c "How Is Atherosclerosis Treated? - NHLBI, NIH". www.nhlbi.nih.gov. 22 June 2016. Retrieved 6 November 2017.
  7. ^ a b Aronow WS, Fleg JL, Rich MW (2013). Tresch and Aronow's Cardiovascular Disease in the Elderly, Fifth Edition. CRC Press. p. 171. ISBN 978-1-84214-544-9.
  8. ^ "Arteriosclerosis / atherosclerosis - Symptoms and causes". Mayo Clinic. Retrieved 2021-05-06.
  9. ^ a b Scipione, Corey A.; Hyduk, Sharon J.; Polenz, Chanele K.; Cybulsky, Myron I. (December 2023). "Unveiling the Hidden Landscape of Arterial Diseases at Single-Cell Resolution". Canadian Journal of Cardiology. 39 (12): 1781–1794. doi:10.1016/j.cjca.2023.09.009.
  10. ^ a b c "What Is Atherosclerosis? - NHLBI, NIH". www.nhlbi.nih.gov. 22 June 2016. Retrieved 6 November 2017.
  11. ^ Tsukahara, Tamotsu; Tsukahara, Ryoko; Haniu, Hisao; Matsuda, Yoshikazu; Murakami-Murofushi, Kimiko (2015-09-05). "Cyclic phosphatidic acid inhibits the secretion of vascular endothelial growth factor from diabetic human coronary artery endothelial cells through peroxisome proliferator-activated receptor gamma". Molecular and Cellular Endocrinology. 412: 320–329. doi:10.1016/j.mce.2015.05.021. hdl:10069/35888. ISSN 0303-7207. PMID 26007326. S2CID 10454566.
  12. ^ Lind L (August 2003). "Circulating markers of inflammation and atherosclerosis". Atherosclerosis. 169 (2): 203–214. doi:10.1016/s0021-9150(03)00012-1. PMID 12921971.
  13. ^ "How Is Atherosclerosis Diagnosed? - NHLBI, NIH". www.nhlbi.nih.gov. 22 June 2016. Retrieved 6 November 2017.
  14. ^ Information (US), National Center for Biotechnology (1998), "Atherosclerosis", Genes and Disease [Internet], National Center for Biotechnology Information (US), retrieved 2023-11-21
  15. ^ Roth GA, Mensah GA, Johnson CO, Addolorato G, Ammirati E, Baddour LM, et al. (December 2020). "Global Burden of Cardiovascular Diseases and Risk Factors, 1990-2019: Update From the GBD 2019 Study". Journal of the American College of Cardiology. 76 (25): 2982–3021. doi:10.1016/j.jacc.2020.11.010. PMC 7755038. PMID 33309175.
  16. ^ Song P, Fang Z, Wang H, Cai Y, Rahimi K, Zhu Y, et al. (May 2020). "Global and regional prevalence, burden, and risk factors for carotid atherosclerosis: a systematic review, meta-analysis, and modelling study". The Lancet. Global Health. 8 (5): e721–e729. doi:10.1016/S2214-109X(20)30117-0. hdl:10044/1/78967. PMID 32353319. S2CID 218474949.
  17. ^ Topol EJ, Califf RM (2007). Textbook of Cardiovascular Medicine. Lippincott Williams & Wilkins. p. 2. ISBN 978-0-7817-7012-5.
  18. ^ Shor A (2008). Chlamydia Atherosclerosis Lesion: Discovery, Diagnosis and Treatment. Springer Science & Business Media. p. 8. ISBN 978-1-84628-810-4.
  19. ^ "Evolutionary gene loss may help explain why only humans are prone to heart attacks". ScienceDaily. Retrieved 2023-11-21.


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