跳转到内容

动脉粥样硬化

本页使用了标题或全文手工转换
维基百科,自由的百科全书
(重定向自動脈硬化
动脉粥样硬化
Atherosclerosis
又称Arteriosclerotic vascular disease (ASVD)
动脉粥样硬化的病程 (血管狹窄化的放大圖)
症状[1]
併發症冠狀動脈疾病中風周邊動脈阻塞腎功能衰竭[1]
起病年龄青年 (並且隨著年紀增加而惡化)[2]
类型動脈硬化性心血管疾病[*]动脉硬化疾病
病因未知[1]
风险因素高血壓糖尿病吸煙肥胖症、家族史、不健康的飲食[3]
預防健康飲食、規律運動、不抽菸、維持正常體重[4]
藥物Statin抗高血压药阿司匹林[5]
患病率~100% (高於65歲)[6]
分类和外部资源
醫學專科心臟病學血管學
ICD-9-CM440
DiseasesDB1039
MedlinePlus000171
eMedicine1950759
[编辑此条目的维基数据]

动脉粥样硬化(英語:atherosclerosis)或粥样硬化,是动脉内膜因多种原因损伤后,内膜下积聚脂质复合糖类并引发出血、血栓形成、纤维组织增生,使动脉管壁增厚、管腔缩小、血流受阻、管壁变硬和弹性减退的现象[7][8]

粥样斑块(atheromatous plaque)或粥瘤[9](atheroma)则是动脉粥样硬化的典型病变,结构由中央含脂肪和钙的无定形粥样脂肪核(fatty core)及外覆的纤维帽(fibrous cap)组成[10]。在显微镜下,动脉内膜呈现黄色粥样改变,引而得名。粥样斑块除脂质和钙质沉着外,另含巨噬细胞、T淋巴细胞、细胞外基质以及坏死碎片聚集,进而导致动脉壁增厚,是心血管疾病的主要病因。

動脈粥樣硬化的早期通常沒有症狀[1],嚴重時視其影響的動脈所在,可能造成冠狀動脈疾病中風周邊動脈疾病以及腎功能衰竭[1]。一般而言,動脈粥樣硬化的相關症狀在中年之後才會出現[3]

目前造成動脈粥樣硬化的原因尚不明朗[1]。相關的風險因子包括血中膽固醇異常高血壓糖尿病吸菸肥胖、動脈粥樣硬化的家族史、以及不健康的飲食習慣[3]。血管壁的斑塊由脂肪膽固醇血栓結締組織、以及其他血中物質組成。斑塊使得血管變得狹窄,含氧血的運送也因此被干擾[8]。動脈粥樣硬化的診斷常包括理學檢查心電圖心臟壓力測試等等 [11]

預防動脈粥樣硬化的方式一般包括健康飲食、運動、戒菸、以及維持正常體重[4]、用以降低血中膽固醇他汀類藥物抗高血压药,或是阿斯匹靈抗凝血劑都常用來治療動脈粥狀硬化。除了藥物之外,經皮冠狀動脈介入治療冠狀動脈繞道手術、以及頸動脈內膜切除手術等手術也可以用來治療動脈粥樣硬化[5]

動脈粥樣硬化這個疾病最早在1575年就有記載,但疾病本身的歷史遠久於此,在超過5000年前的考古證據中就已經有動脈粥樣硬化的蹤跡[12]。動脈粥樣硬化一般在年輕時便已經發生,然後隨著年齡而惡化[2],大多數的老年人(65歲以上)都患有不同程度的動脈粥樣硬化[6]。動脈粥樣硬化是已開發國家排名第一的致死與致殘疾病[13]

病理

在过去很长时间裡动脉硬化始终是医学生物化学研究的重点。其原因是因为它的普及性。许多人有动脉硬化,但是这个状态可以数年、数十年在人体内存在,却不显示出任何病态,然后它会突然以局部缺血、心绞痛心肌梗塞中风心力衰竭等致命病爆发。在发展国家中动脉硬化后果是最常见的死因。[14]

动脉硬化的特征是动脉的慢性退化及动脉壁的逐渐变化。由于结缔组织的增长、细胞内外胆固醇脂肪酸以及碳酸钙的沉积、膠原蛋白蛋白聚糖的聚集动脉壁变硬变厚,动脉变细,整个动脉失去弹性。[15]

当胆固醇等物质堆积到了足够程度时,血管内皮细胞会诱导单核细胞分化为巨噬细胞。巨噬细胞会吞噬血管壁之间的脂肪并使它们堆积于细胞内,脂肪使细胞成为泡沫细胞[16]

主动脉外,常累及心脏的冠状动脉和脑、肾动脉,可以引起动脉粥样斑块破裂、血栓形成,管腔狭窄至闭塞,从而使有关器官的血液供应发生障碍。

由于动脉硬化过程非常复杂,参加的细胞和组织(上皮细胞平滑肌单核细胞巨噬细胞血小板)、分子(脂蛋白生长激素、胆固醇、脂肪、膠原蛋白和细胞因子等)多样,其中关系错综,因此至今为止在医学上没有良好的可以预言动脉硬化的模型和技术。

视频字幕

致病風險因素

通过众多病史学和临床研究至少可以总结出一定的、有利于动脉硬化形成的因素。

後天可變的

後天不可變的

機率偏低未被完全確認

預防

大量流行病學研究和隨機對照臨床試驗證實,低密度膽固醇的升高是引發動脈粥狀硬化的的一個重要因素[34],因此推動終身的健康生活方式與飲食能幫助管理血液中的膽固醇。即使是基因遺傳導致動脈粥狀硬化風險較高的人也可通過改變生活方式來降低多達50%的風險。除此之外,保持正常的體重和血糖、減少單醣和精製碳水化合物攝入量與增加運動頻率均可改善血脂水平並促進健康。[35]

治療

臨床試驗證實可以透過以下藥物減少血液中低密度膽固醇含量進而減少動脈粥狀硬化心臟病的風險:

  • 他汀類藥物HMG-CoA reductase的競爭性抑制劑,可影響膽固醇合成過程中的速率決定步驟。對HMG-CoA reductase的抑制會使肝臟合成更多LDL受體,使LDL更容易從血液循環內清除。其為降低低密度膽固醇之首選用藥然而需注意其肌痛的不良反應。[36]

參見

參考資料

  1. ^ 1.0 1.1 1.2 1.3 1.4 1.5 What Are the Signs and Symptoms of Atherosclerosis?. NHLBI, NIH. 2016-06-22 [2017-11-05]. (原始内容存档于2017-10-05) (英语). 
  2. ^ 2.0 2.1 What Causes Atherosclerosis? - NHLBI, NIH. NHLBI, NIH. 2016-06-22 [2017-11-06]. (原始内容存档于2015-04-23) (英语). 
  3. ^ 3.0 3.1 3.2 Who Is at Risk for Atherosclerosis? - NHLBI, NIH. NHLBI, NIH. 2016-06-22 [2017-11-05]. (原始内容存档于2017-10-05) (英语). 
  4. ^ 4.0 4.1 How Can Atherosclerosis Be Prevented or Delayed? - NHLBI, NIH. NHLBI, NIH. 2016-06-22 [2017-11-06]. (原始内容存档于2017-11-07) (英语). 
  5. ^ 5.0 5.1 How Is Atherosclerosis Treated?. NHLBI, NIH. 2016-06-22 [2017-11-06]. (原始内容存档于2017-11-07) (英语). 
  6. ^ 6.0 6.1 Aronow, Wilbert S.; Fleg, Jerome L.; Rich, Michael W. Tresch and Aronow's Cardiovascular Disease in the Elderly, Fifth Edition. CRC Press. 2013: 171 [2018-05-11]. ISBN 9781842145449. (原始内容存档于2021-08-03) (英语). 
  7. ^ Insull Jr, William. "The pathology of atherosclerosis: plaque development and plaque responses to medical treatment." The American journal of medicine 122.1 (2009): S3-S14.
  8. ^ 8.0 8.1 What Is Atherosclerosis? - NHLBI, NIH. NHLBI, NIH. 2016-06-22 [2017-11-06]. (原始内容存档于2017-12-02) (英语). 
  9. ^ 國家教育研究院. 醫學名詞. 元照出版公司. 2015: 43. 
  10. ^ (2011). Atherosclerosis/Atheroma. In: Khan, M.G. (eds) Encyclopedia of Heart Diseases. Humana Press. https://doi.org/10.1007/978-1-60761-219-3_21
  11. ^ How Is Atherosclerosis Diagnosed? - NHLBI, NIH. NHLBI, NIH. 2016-06-22 [2017-11-06]. (原始内容存档于2017-10-05) (英语). 
  12. ^ Shor A. Chlamydia Atherosclerosis Lesion: Discovery, Diagnosis and Treatment. Springer Science & Business Media. 2008: 8 [2019-02-12]. ISBN 9781846288104. (原始内容存档于2021-08-03) (英语). 
  13. ^ Topol EJ, Califf RM. Textbook of Cardiovascular Medicine. Lippincott Williams & Wilkins. 2007: 2 [2019-02-12]. ISBN 9780781770125. (原始内容存档于2021-08-03) (英语). 
  14. ^ Ross, Russell. The pathogenesis of atherosclerosis: a perspective for the 1990s. Nature. 1993-04, 362 (6423): 801–809 [2022-01-17]. ISSN 0028-0836. PMID 8479518. doi:10.1038/362801a0. (原始内容存档于2021-10-27) (英语). 
  15. ^ Finn, Aloke V.; Nakano, Masataka; Narula, Jagat; Kolodgie, Frank D.; Virmani, Renu. Concept of vulnerable/unstable plaque. Arteriosclerosis, Thrombosis, and Vascular Biology. 2010-07, 30 (7): 1282–1292 [2022-01-17]. ISSN 1524-4636. PMID 20554950. doi:10.1161/ATVBAHA.108.179739. (原始内容存档于2021-12-07). 
  16. ^ Manning, Robert. Livestrong.com. What Is A Foam Cell?. Demand Media Inc. [5 March 2013]. (原始内容存档于2017-09-08). 
  17. ^ 17.00 17.01 17.02 17.03 17.04 17.05 17.06 17.07 17.08 17.09 17.10 17.11 17.12 17.13 17.14 17.15 17.16 17.17 Atherosclerosis. NHLBI, NIH. [2018-05-11]. (原始内容存档于2017-10-05). 
  18. ^ Enas EA, Kuruvila A, Khanna P, Pitchumoni CS, Mohan V. Benefits & risks of statin therapy for primary prevention of cardiovascular disease in Asian Indians - a population with the highest risk of premature coronary artery disease & diabetes. Indian J Med Res. October 2013, 138 (4): 461–491 [2018-05-14]. PMC 3868060可免费查阅. PMID 24434254. (原始内容存档于2021-05-18). 
  19. ^ Indian Heart Association Why South Asians Facts Web. 30 April 2015. http://indianheartassociation.org/why-indians-why-south-asians/overview/页面存档备份,存于互联网档案馆
  20. ^ Borissoff JI, Spronk HM, Heeneman S, ten Cate H. Is thrombin a key player in the 'coagulation-atherogenesis' maze?. Cardiovasc. Res. June 2009, 82 (3): 392–403 [2018-05-14]. PMID 19228706. doi:10.1093/cvr/cvp066. (原始内容存档于2011-03-21). 
  21. ^ Borissoff JI, Heeneman S, Kilinç E, et al. Early atherosclerosis exhibits an enhanced procoagulant state. Circulation. August 2010, 122 (8): 821–30 [2018-05-14]. PMID 20697022. doi:10.1161/CIRCULATIONAHA.109.907121. (原始内容存档于2011-02-12). 
  22. ^ Borissoff JI, Spronk HM, ten Cate H. The hemostatic system as a modulator of atherosclerosis. N. Engl. J. Med. May 2011, 364 (18): 1746–60 [2018-05-14]. PMID 21542745. doi:10.1056/NEJMra1011670. (原始内容存档于2020-05-18). 
  23. ^ Food and nutrition board, institute of medicine of the national academies. Dietary Reference Intakes for Energy, Carbohydrate, Fiber, Fat, Fatty Acids, Cholesterol, Protein, and Amino Acids (Macronutrients). National Academies Press. 2005: 481–484 [2018-05-14]. (原始内容存档于2015-09-06). 
  24. ^ Mozaffarian D, Rimm EB, Herrington DM. Dietary fats, carbohydrate, and progression of coronary atherosclerosis in postmenopausal women. Am. J. Clin. Nutr. November 2004, 80: 1175–84. PMC 1270002可免费查阅. PMID 15531663. doi:10.1093/ajcn/80.5.1175. 
  25. ^ Bhatt DL, Topol EJ. Need to test the arterial inflammation hypothesis. Circulation. July 2002, 106 (1): 136–40 [2018-05-14]. PMID 12093783. doi:10.1161/01.CIR.0000021112.29409.A2. (原始内容存档于2007-03-11). 
  26. ^ Griffin M, Frazer A, Johnson A, Collins P, Owens D, Tomkin GH. Cellular cholesterol synthesis—the relationship to post-prandial glucose and insulin following weight loss. Atherosclerosis. 1998, 138 (2): 313–8. PMID 9690914. doi:10.1016/S0021-9150(98)00036-7. 
  27. ^ King, Cr; Knutson, Kl; Rathouz, Pj; Sidney, S; Liu, K; Lauderdale, Ds. Short sleep duration and incident coronary artery calcification. JAMA: The Journal of the American Medical Association. December 2008, 300 (24): 2859–66. PMC 2661105可免费查阅. PMID 19109114. doi:10.1001/jama.2008.867. 
  28. ^ Provost, EB; Madhloum, N; Int Panis, L; De Boever, P; Nawrot, TS. Carotid intima-media thickness, a marker of subclinical atherosclerosis, and particulate air pollution exposure: the meta-analytical evidence. PLoS ONE. 2015, 10 (5): e0127014. PMC 4430520可免费查阅. PMID 25970426. doi:10.1371/journal.pone.0127014. 
  29. ^ Adar, Sara D.; Lianne Sheppard; Sverre Vedal; Joseph F. Polak; Paul D. Sampson; Ana V. Diez Roux; Matthew Budoff; David R. Jacobs Jr; R. Graham Barr; Karol Watson; Joel D. Kaufman. Fine Particulate Air Pollution and the Progression of Carotid Intima-Medial Thickness: A Prospective Cohort Study from the Multi-Ethnic Study of Atherosclerosis and Air Pollution. PLoS Medicine. April 23, 2013, 10 (4): e1001430 [May 4, 2013]. PMC 3637008可免费查阅. PMID 23637576. doi:10.1371/journal.pmed.1001430. (原始内容存档于2014-12-27). This early analysis from MESA suggests that higher long-term PM2.5 concentrations are associated with increased IMT progression and that greater reductions in PM2.5 are related to slower IMT progression. 
  30. ^ Chih-Hao Wang. Biological Gradient Between Long-Term Arsenic Exposure and Carotid Atherosclerosis. ahajournals.org. [2018-05-14]. (原始内容存档于2017-03-09). 
  31. ^ Treating Hypothyroidism Reduces Atherosclerosis Risk. American Family Physician. 2004-02-01, 69 (3) [2018-05-14]. ISSN 0002-838X. (原始内容存档于2019-06-17) (英语). 
  32. ^ Bale, BF; Doneen, AL; Vigerust, DJ. High-risk periodontal pathogens contribute to the pathogenesis of atherosclerosis.. Postgraduate medical journal. April 2017, 93 (1098): 215–220. PMID 27899684. doi:10.1136/postgradmedj-2016-134279. 
  33. ^ Jie Yang; Juan Wu; Rui Zhang; Min Yao; Yu Liu; Leiying Miao; Weibin Sun. Porphyromonas gingivalis oral infection promote T helper 17/Treg imbalance in the development of atherosclerosis. Dental Sciences. 2016-12-14, 12 (1): 60–69. 
  34. ^ Efficacy and safety of more intensive lowering of LDL cholesterol: a meta-analysis of data from 170 000 participants in 26 randomised trials. The Lancet. 2010-11, 376 (9753): 1670–1681. ISSN 0140-6736. doi:10.1016/s0140-6736(10)61350-5. 
  35. ^ Brinton, Eliot A. Management of Hypertriglyceridemia for Prevention of Atherosclerotic Cardiovascular Disease. Cardiology Clinics. 2015-05, 33 (2): 309–323. ISSN 0733-8651. doi:10.1016/j.ccl.2015.02.007. 
  36. ^ Thompson, Paul D. What to Believe and Do About Statin-Associated Adverse Effects. JAMA. 2016-11-15, 316 (19): 1969. ISSN 0098-7484. doi:10.1001/jama.2016.16557. 
  37. ^ Aronow, Wilbert. Faculty of 1000 evaluation for Ezetimibe Added to Statin Therapy after Acute Coronary Syndromes.. F1000 - Post-publication peer review of the biomedical literature. 2015-06-21 [2019-12-31]. 
  38. ^ Abifadel, Marianne; Varret, Mathilde; Rabès, Jean-Pierre; Allard, Delphine; Ouguerram, Khadija; Devillers, Martine; Cruaud, Corinne; Benjannet, Suzanne; Wickham, Louise. Mutations in PCSK9 cause autosomal dominant hypercholesterolemia. Nature Genetics. 2003-05-05, 34 (2): 154–156. ISSN 1061-4036. doi:10.1038/ng1161. 
  39. ^ JE, Manson; NR, Cook; IM, Lee; W, Christen; SS, Bassuk; S, Mora; H, Gibson; CM, Albert; D, Gordon. Marine n-3 fatty acids and prevention of cardiovascular disease and cancer. Yearbook of Paediatric Endocrinology. 2019-09-12. ISSN 1662-4009. doi:10.1530/ey.16.12.13. 

外部链接