动脉粥样硬化
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| 动脉粥样硬化 Atherosclerosis | |
|---|---|
| 同義詞 | Arteriosclerotic vascular disease (ASVD) |
 | |
动脉粥样硬化的病程 (血管狹窄化的放大圖) | |
| 醫學專科 | 心臟病學、血管學 |
| 症状 | 無[1] |
| 併發症 | 冠狀動脈疾病、中風、周邊動脈阻塞、腎功能衰竭[1] |
| 常見始發於 | 青年 (並且隨著年紀增加而惡化)[2] |
| 肇因 | 未知[1] |
| 風險因子 | 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] |
| 盛行率 | ~100% (高於65歲)[6] |
| 动脉粥样硬化 | |
|---|---|
| 分类和外部资源 | |
| 醫學專科 | 心臟內科 |
ICD-10 | I70 |
ICD-9-CM | 440, 414.0 |
| DiseasesDB | 1039 |
| MedlinePlus | 000171 |
| eMedicine | med/182 |
| Patient UK | 动脉粥样硬化 |
| MeSH | D050197 |
提示：本条目的主题不是血管硬化。动脉粥样硬化（英语：Atherosclerosis）是由于脂肪、血栓、结缔组织和碳酸钙在血管（主要是动脉）沉积所造成的一种对人体有害的状态。[7]
目录
1 病理
2 致病風險因素
2.1 後天可變的
2.2 後天不可變的
2.3 機率偏低未被完全確認
3 參見
4 參考來源
病理
在过去很长时间裡动脉硬化始终是医学和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、中风或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。[8]
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、膠原蛋白和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。[9]
当胆固醇等物质堆积到了足够程度时，血管的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。[10]
除主动脉外，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。
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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
糖尿病[11]
Dyslipidemia[11]
吸菸[11]：吸烟可破坏血管壁，诱导平滑肌细胞（SMC）增生；
反式脂肪[11]- 高脂血症：公认的危险因素，主要是血浆总胆固醇和甘油三酯的增高，其中尤其胆固醇起关键作用；
腹部肥胖[11]
西方飲食[11]
胰岛素抵抗[11]
高血壓[11]：高血压病人易发生，并且早而严重，好发于血管分叉、弯曲处；
後天不可變的
年紀變大[11]
雄性[11]
- 家族史[11]
染色体畸变[11]
機率偏低未被完全確認
- 遗传因素：冠心病具有家族聚集现象，约200种基因可能对脂质的摄取、代谢、排泄产生影响。
- 其他：肥胖症、性别（男性）、高龄、病毒感染、饮食结构（比如高热量和高脂肪的食物；如肉類或油炸食物）被确定为动脉硬化的可能因素。
南亚後裔[12][13]
Thrombophilia[14][15][16]
飽和脂肪[11][17]
- 過多[糖类]]攝取[11][18]
- 偏高的 三酸甘油酯[11]
Systemic inflammation[19]
高胰島素血症[20]
睡眠剥夺[21]
空氣污染[22][23]
久坐的習慣[11]
砷中毒[24]
Alcohol[11]
Chronic stress[11]
甲狀腺機能低下症[25]
牙周炎[26]：感染导致牙龈发炎、损伤，病菌进入血管可导致动脉粥样硬化。[27]
參見
- 动脉
- 泡沫细胞
- 血管年齡
- atheroma
參考來源
^ 1.01.11.2 What Are the Signs and Symptoms of Atherosclerosis? - NHLBI, NIH. www.nhlbi.nih.gov. 22 June 2016 [5 November 2017] （英语）.
^ What Causes Atherosclerosis? - NHLBI, NIH. www.nhlbi.nih.gov. 22 June 2016 [6 November 2017] （英语）.
^ Who Is at Risk for Atherosclerosis? - NHLBI, NIH. www.nhlbi.nih.gov. 22 June 2016 [5 November 2017] （英语）.
^ How Can Atherosclerosis Be Prevented or Delayed? - NHLBI, NIH. www.nhlbi.nih.gov. 22 June 2016 [6 November 2017] （英语）.
^ How Is Atherosclerosis Treated? - NHLBI, NIH. www.nhlbi.nih.gov. 22 June 2016 [6 November 2017] （英语）.
^ Aronow, Wilbert S.; Fleg, Jerome L.; Rich, Michael W. Tresch and Aronow's Cardiovascular Disease in the Elderly, Fifth Edition. CRC Press. 2013: 171. ISBN 9781842145449 （英语）.
^ Maton, Anthea; Roshan L. Jean Hopkins, Charles William McLaughlin, Susan Johnson, Maryanna Quon Warner, David LaHart, Jill D. Wright. Human Biology and Health. Englewood Cliffs, New Jersey, USA: Prentice Hall. 1993. ISBN 0-13-981176-1. OCLC 32308337. 引文使用过时参数coauthors (帮助)
^ Ross R. The pathogenesis of atherosclerosis: a perspective for the 1990s. Nature. April 1993, 362 (6423): 801–9. PMID 8479518. doi:10.1038/362801a0.
^ Finn AV, Nakano M, Narula J, Kolodgie FD, Virmani R. Concept of vulnerable/unstable plaque. Arterioscler Thromb Vasc Biol. 2010 Jul;30(7):1282-92. Review. PubMed PMID 20554950.
^ Manning, Robert. Livestrong.com. What Is A Foam Cell?. Demand Media Inc. [5 March 2013].
^ 11.0011.0111.0211.0311.0411.0511.0611.0711.0811.0911.1011.1111.1211.1311.1411.1511.1611.17 https://www.nhlbi.nih.gov/health/health-topics/topics/atherosclerosis/atrisk
^ 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. PMC 3868060. PMID 24434254.
^ Indian Heart Association Why South Asians Facts Web. 30 April 2015. http://indianheartassociation.org/why-indians-why-south-asians/overview/
^ 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. PMID 19228706. doi:10.1093/cvr/cvp066.
^ Borissoff JI, Heeneman S, Kilinç E, 等. Early atherosclerosis exhibits an enhanced procoagulant state. Circulation. August 2010, 122 (8): 821–30. PMID 20697022. doi:10.1161/CIRCULATIONAHA.109.907121.
^ 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. PMID 21542745. doi:10.1056/NEJMra1011670.
^ 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.
^ 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.
^ 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）.
^ 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.
^ 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.
^ 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.
^ 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.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.
^ Chih-Hao Wang. Biological Gradient Between Long-Term Arsenic Exposure and Carotid Atherosclerosis. ahajournals.org.
^ Treating Hypothyroidism Reduces Atherosclerosis Risk. American Family Physician. 1 February 2004, 69 (3). ISSN 0002-838X （英语）.
^ 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.
^ 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. December 24, 2016, 12 (1): 60–69.
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