动脉粥样硬化

(重定向自動脈粥狀硬化

动脉粥样硬化(英语:Atherosclerosis)是一种粥样斑块英语Atheroma沉积在血管壁并造成动脉狭窄的疾病[7]。动脉粥样硬化的早期通常没有症状[1],严重时视其影响的动脉所在,可能造成冠状动脉疾病中风周边动脉疾病以及肾功能衰竭[1]。一般而言,动脉粥样硬化的相关症状在中年之后才会出现[3]

动脉粥样硬化
Atherosclerosis
同义词Arteriosclerotic vascular disease (ASVD)
动脉粥样硬化的病程 (血管狭窄化的放大图)
症状[1]
并发症冠状动脉疾病中风周边动脉阻塞肾功能衰竭[1]
常见始发于青年 (并且随着年纪增加而恶化)[2]
类型动脉硬化性心血管疾病[*]动脉硬化疾病
肇因未知[1]
风险因子高血压糖尿病吸烟肥胖症、家族史、不健康的饮食[3]
预防健康饮食、规律运动、不抽烟、维持正常体重[4]
药物Statin抗高血压药阿司匹林[5]
盛行率~100% (高于65岁)[6]
分类和外部资源
医学专科心脏病学血管学
ICD-9-CM440
DiseasesDB1039
MedlinePlus000171
eMedicine1950759
[编辑此条目的维基数据]

目前造成动脉粥样硬化的原因尚不明朗[1]。相关的风险因子包括血中胆固醇异常高血压糖尿病吸烟肥胖、动脉粥样硬化的家族史、以及不健康的饮食习惯[3]。血管壁的斑块由脂肪胆固醇血栓结缔组织、以及其他血中物质组成。斑块使得血管变得狭窄,含氧血的运送也因此被干扰[7]。动脉粥样硬化的诊断常包括理学检查心电图心脏压力测试等等 [8]

预防动脉粥样硬化的方式一般包括健康饮食、运动、戒烟、以及维持正常体重[4]、用以降低血中胆固醇他汀类药物抗高血压药,或是阿司匹林抗凝血剂都常用来治疗动脉粥样硬化。除了药物之外,经皮冠状动脉介入治疗冠状动脉绕道手术、以及颈动脉内膜切除手术等手术也可以用来治疗动脉粥样硬化[5]

动脉粥样硬化这个疾病最早在1575年就有记载,但疾病本身的历史远久于此,在超过5000年前的考古证据中就已经有动脉粥样硬化的踪迹[9]。动脉粥样硬化一般在年轻时便已经发生,然后随着年龄而恶化[2],大多数的老年人(65岁以上)都患有不同程度的动脉粥样硬化[6]。动脉粥样硬化是发达国家排名第一的致死与致残疾病[10]

病理 编辑

在过去很长时间里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、心绞痛心肌梗死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。[11]

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、胶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。[12]

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[13]

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、胶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

致病风险因素 编辑

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。

后天可变的 编辑

后天不可变的 编辑

几率偏低未被完全确认 编辑

预防 编辑

大量流行病学研究和随机对照临床试验证实,低密度胆固醇的升高是引发动脉粥样硬化的的一个重要因素[31],因此推动终身的健康生活方式与饮食能帮助管理血液中的胆固醇。即使是基因遗传导致动脉粥样硬化风险较高的人也可通过改变生活方式来降低多达50%的风险。除此之外,保持正常的体重和血糖、减少单糖和精制碳水化合物摄入量与增加运动频率均可改善血脂水平并促进健康。[32]

治疗 编辑

临床试验证实可以透过以下药物减少血液中低密度胆固醇含量进而减少动脉粥样硬化心脏病的风险:

  • 他汀类药物HMG-CoA reductase的竞争性抑制剂,可影响胆固醇合成过程中的速率决定步骤。对HMG-CoA reductase的抑制会使肝脏合成更多LDL受体,使LDL更容易从血液循环内清除。其为降低低密度胆固醇之首选用药然而需注意其肌痛的不良反应。[33]

参见 编辑

参考资料 编辑

  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. ^ 7.0 7.1 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). 
  8. ^ 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). 
  9. ^ 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). 
  10. ^ 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). 
  11. ^ 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). 
  12. ^ 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). 
  13. ^ 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). 
  14. ^ 14.00 14.01 14.02 14.03 14.04 14.05 14.06 14.07 14.08 14.09 14.10 14.11 14.12 14.13 14.14 14.15 14.16 14.17 Atherosclerosis. NHLBI, NIH. [2018-05-11]. (原始内容存档于2017-10-05). 
  15. ^ 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 . PMID 24434254. (原始内容存档于2021-05-18). 
  16. ^ 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
  17. ^ 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). 
  18. ^ 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). 
  19. ^ 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). 
  20. ^ 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). 
  21. ^ 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 . PMID 15531663. doi:10.1093/ajcn/80.5.1175. 
  22. ^ 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). 
  23. ^ 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. 
  24. ^ 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 . PMID 19109114. doi:10.1001/jama.2008.867. 
  25. ^ 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 . PMID 25970426. doi:10.1371/journal.pone.0127014. 
  26. ^ 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 . 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. 
  27. ^ 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). 
  28. ^ 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). 
  29. ^ 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. 
  30. ^ 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. 
  31. ^ 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. 
  32. ^ 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. 
  33. ^ 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. 
  34. ^ 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]. 
  35. ^ 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. 
  36. ^ 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 编辑