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Atherosclerosis

From Wikipedia
atherosclerosis
class of disease
Subclass ofarteriosclerotic cardiovascular disease, arteriosclerosis, disease Edit
Has immediate causeatherogenesis Edit
Health specialtycardiology Edit
Symptoms and signsatheroma Edit
Drug or therapy used for treatmentfluvastatin, clopidogrel, rosuvastatin Edit
Genetic associationGRM8, RYR3, MAST4, ABI2, DNAH5 Edit
Risk factorsmoking, binge eating Edit
ICD-9-CM440 Edit
NCI Thesaurus IDC35768, C35771 Edit

Atherosclerosis be a pattern of de disease arteriosclerosis,[1] wey be characterized by development of abnormalities dem call lesions insyd walls of arteries. Dis be a chronic inflammatory disease wey dey involve chaw different cell types wey e be driven by elevated blood levels of cholesterol.[2] Dese lesions fi lead to narrowing of de arterial walls secof buildup of atheromatous plaques.[3][4]

At de onset, der usually be no symptoms, buh if dem develop, symptoms generally dey begin around middle age.[5] Insyd severe cases, e fi result insyd coronary artery disease, stroke, peripheral artery disease, anaa kidney disorders, wey dey depend on de body part(s) insyd wich de affected arteries be located.[5]

De exact cause of atherosclerosis be unknown wey dem propose e be multifactorial.[5] Risk factors dey include abnormal cholesterol levels, elevated levels of inflammatory biomarkers,[6] high blood pressure, diabetes, smoking (both active den passive smoking), obesity, genetic factors, family history, lifestyle habits, den an unhealthy diet.[7] Plaque dey make up of fat, cholesterol, immune cells, calcium, den oda substances dem find insyd de blood.[2][3] De narrowing of arteries dey limit de flow of oxygen-rich blood to parts of de body.[3] Diagnosis dey base upon a physical exam, electrocardiogram, den exercise stress test, among odas, wey dey depend on de affected artery anaa arteries.[8]

Prevention guidelines dey include eating a healthy diet, exercising, no dey smoke, den dey maintain a normal body weight.[9] Treatment of established atherosclerotic disease fi include medications to lower cholesterol such as statins, blood pressure medication, den anticoagulant therapies make dem reduce de risk of blood clot formation.[10] As de disease state dey progress, dem dey apply more invasive strategies, such as percutaneous coronary intervention, coronary artery bypass graft, anaa carotid endarterectomy.[10] Insyd sam individuals, genetic factors sanso be implicated insyd de disease process den dey cause a strongly increased predisposition to development of atherosclerosis.[11]

Atherosclerosis generally dey start wen a person be young wey e dey worsen plus age. Almost all people be affected to sam degree by de age of 65.[12] E be de number one cause of death den disability insyd developed countries.[13][14][15] Though na dem first describe am insyd 1575,[16] der be evidence wey dey suggest say dis disease state be genetically inherent insyd de broader human population, plus ein origins dey trace back to CMAH genetic mutations wey na e fi occur more dan two million years ago during de evolution of hominin ancestors of modern human beings.[17]

References

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  1. ↑ "Arteriosclerosis / atherosclerosis - Symptoms and causes". Mayo Clinic (in English). Retrieved 2021-05-06.
  2. 1 2 Scipione CA, Hyduk SJ, Polenz CK, Cybulsky MI (December 2023). "Unveiling the Hidden Landscape of Arterial Diseases at Single-Cell Resolution". The Canadian Journal of Cardiology. 39 (12): 1781–1794. doi:10.1016/j.cjca.2023.09.009. PMID 37716639.
  3. 1 2 3 "What Is Atherosclerosis? - NHLBI, NIH". www.nhlbi.nih.gov (in English). 22 June 2016. Retrieved 6 November 2017.
  4. ↑ Tsukahara T, Tsukahara R, Haniu H, Matsuda Y, Murakami-Murofushi K (September 2015). "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. PMID 26007326.
  5. 1 2 3 "What Are the Signs and Symptoms of Atherosclerosis? - NHLBI, NIH". www.nhlbi.nih.gov (in English). 22 June 2016. Retrieved 5 November 2017.
  6. ↑ 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.
  7. ↑ "Who Is at Risk for Atherosclerosis?". www.nhlbi.nih.gov (in English). 22 June 2016. Retrieved 5 November 2017.
  8. ↑ "How Is Atherosclerosis Diagnosed? - NHLBI, NIH". www.nhlbi.nih.gov (in English). 22 June 2016. Archived from the original on November 28, 2014. Retrieved 6 November 2017.
  9. ↑ "How Can Atherosclerosis Be Prevented or Delayed? - NHLBI, NIH". www.nhlbi.nih.gov (in English). 22 June 2016. Archived from the original on December 21, 2014. Retrieved 6 November 2017.
  10. 1 2 "How Is Atherosclerosis Treated? - NHLBI, NIH". www.nhlbi.nih.gov (in English). 22 June 2016. Archived from the original on December 6, 2014. Retrieved 6 November 2017.
  11. ↑ "Atherosclerosis". Genes and Disease [Internet]. National Center for Biotechnology Information (US). 1998.
  12. ↑ Aronow WS, Fleg JL, Rich MW (2013). Tresch and Aronow's Cardiovascular Disease in the Elderly, Fifth Edition (in English). CRC Press. p. 171. ISBN 978-1-84214-544-9.
  13. ↑ Roth GA, Mensah GA, Johnson CO, Addolorato G, Ammirati E, Baddour LM, Barengo NC, Beaton AZ, Benjamin EJ, Benziger CP, Bonny A, Brauer M, Brodmann M, Cahill TJ, Carapetis J, Catapano AL, Chugh SS, Cooper LT, Coresh J, Criqui M, DeCleene N, Eagle KA, Emmons-Bell S, Feigin VL, Fernández-Solà J, Fowkes G, Gakidou E, Grundy SM, He FJ, Howard G, Hu F, Inker L, Karthikeyan G, Kassebaum N, Koroshetz W, Lavie C, Lloyd-Jones D, Lu HS, Mirijello A, Temesgen AM, Mokdad A, Moran AE, Muntner P, Narula J, Neal B, Ntsekhe M, Moraes de Oliveira G, Otto C, Owolabi M, Pratt M, Rajagopalan S, Reitsma M, Ribeiro AL, Rigotti N, Rodgers A, Sable C, Shakil S, Sliwa-Hahnle K, Stark B, Sundström J, Timpel P, Tleyjeh IM, Valgimigli M, Vos T, Whelton PK, Yacoub M, Zuhlke L, Murray C, Fuster V (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.
  14. ↑ Song P, Fang Z, Wang H, Cai Y, Rahimi K, Zhu Y, Fowkes FG, Fowkes FJ, Rudan I (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 (in English). 8 (5): e721 – e729. doi:10.1016/S2214-109X(20)30117-0. hdl:10044/1/78967. PMID 32353319.
  15. ↑ Topol EJ, Califf RM (2007). Textbook of Cardiovascular Medicine (in English). Lippincott Williams & Wilkins. p. 2. ISBN 978-0-7817-7012-5.
  16. ↑ Shor A (2007). Chlamydia Atherosclerosis Lesion. p. 8. doi:10.1007/978-1-84628-810-4. ISBN 978-1-84628-809-8.
  17. ↑ "Evolutionary gene loss may help explain why only humans are prone to heart attacks". ScienceDaily. University of California - San Diego. 23 July 2019.
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