Ateroesclerosis

  1. Lorente Ros, A. 1
  2. Rajjoub Al-Mahdi, E.A. 1
  3. Monteagugo Ruiz, J.M. 1
  4. Zamorano Gómez, J.L. 1
  1. 1 Servicio de Cardiología, Hospital Universitario Ramón y Cajal, Madrid, España
Revista:
Medicine: Programa de Formación Médica Continuada Acreditado

ISSN: 0304-5412

Año de publicación: 2021

Título del ejemplar: Enfermedades cardiovasculares (II)

Serie: 13

Número: 36

Páginas: 2063-2070

Tipo: Artículo

DOI: 10.1016/J.MED.2021.06.010 DIALNET GOOGLE SCHOLAR

Otras publicaciones en: Medicine: Programa de Formación Médica Continuada Acreditado

Resumen

La ateroesclerosis es el proceso patogénico que subyace a las diferentes manifestaciones clínicas de la enfermedad cardiovascular. Mediante la reducción progresiva del diámetro de la luz del vaso o el desarrollo brusco de un trombo, se provoca una obstrucción al flujo sanguíneo normal a los diferentes tejidos, pudiendo afectar al corazón (cardiopatía isquémica), cerebro (ictus) o extremidades (enfermedad arterial periférica). Actualmente la ateroesclerosis se considera un proceso inflamatorio crónico que precede a las manifestaciones clínicas en varias décadas. El proceso inicial que promueve el desarrollo de la placa es la disrupción de la integridad del endotelio y su función. La formación de la placa se produce por la acumulación de partículas lipídicas en zonas predispuestas y está facilitado por procesos de inflamación, necrosis, fibrosis y calcificación. Su desarrollo está muy ligado a la exposición prolongada a determinados factores de riesgo, que interactúan con otros factores ambientales, los genes y la susceptibilidad de cada organismo. Durante la vida del individuo, la enfermedad suele evolucionar de forma indolente, hasta que la progresión de la placa provoca su desestabilización y rotura, dando lugar a una situación de isquemia del órgano afectado.

Referencias bibliográficas

  • Moran AE, Forouzanfar MH, Roth GA, Mensah GA, Ezzati M, Murray CJL. Temporal trends in ischemic heart disease mortality in 21 world regions, 1980 to 2010: the Global Burden of Disease 2010 study. Circulation. 2014;129(14):1483-92.
  • Bentzon JF, Otsuka F, Virmani R, Falk E. Mechanisms of plaque formation and rupture. Circ Res. 2014;114(12):1852-66.
  • Faxon DP, Fuster V, Libby P, Beckman JA, Hiatt WR, Thompson RW. Atherosclerotic Vascular Disease Conference: Writing Group III: Pathophysiology. Circulation. 2004;109(21):2617-25.
  • Giannelou M, Mavragani CP. Cardiovascular disease in systemic lupus erythematosus: A comprehensive update. J Autoimmun. 2017;82:1-12.
  • Mundi S, Massaro M, Scoditti E, Carluccio MA, van Hinsbergh VWM, Iruela Arispe ML. Endothelial permeability, LDL deposition, and cardiovascular risk factors a review. Cardiovasc Res. 2018 01;114(1):35-52.
  • Kelly RF, Snow HM. Characteristics of the response of the iliac artery to wall shear stress in the anaesthetized pig. J Physiol. 2007;582(Pt 2):731-43.
  • Becker BF, Chappell D, Jacob M. Endothelial glycocalyx and coronary vascular permeability: the fringe benefit. Basic Res Cardiol. 2010;105(6):687-701.
  • Nieuwdorp M, van Haeften TW, Gouverneur MCLG, Mooij HL, van Lieshout MHP, Levi M. Loss of endothelial glycocalyx during acute hyperglycemia coincides with endothelial dysfunction and coagulation activation in vivo. Diabetes. 2006;55(2):480-6.
  • Ridker PM, Hennekens CH, Buring JE, Rifai N. C-reactive protein and other markers of inflammation in the prediction of cardiovascular disease in women. N Engl J Med. 2000;342(12):836-43.
  • Heo KS, Fujiwara K, Abe J. Shear stress and atherosclerosis. Mol Cells. 2014;37(6):435-40.
  • Tarbell JM. Shear stress and the endothelial transport barrier. Cardiovasc Res. 2010;87(2):320-30.
  • Stary HC, Chandler AB, Dinsmore RE, Fuster V, Glagov S, Insull W. A definition of advanced types of atherosclerotic lesions and a histological classification of atherosclerosis. A report from the Committee on Vascular Lesions of the Council on Arteriosclerosis, American Heart Association. Circulation. 1995;92(5):1355-74.
  • Virmani R, Kolodgie FD, Burke AP, Farb A, Schwartz SM. Lessons from sudden coronary death: a comprehensive morphological classification scheme for atherosclerotic lesions. Arterioscler Thromb Vasc Biol. 2000;20(5):1262-75.
  • Velican D, Velican C. Atherosclerotic involvement of the coronary arteries of adolescents and young adults. Atherosclerosis. 1980;36(4):449-60.
  • McGill HC, McMahan CA, Zieske AW, Tracy RE, Malcom GT, Herde-rick EE. Association of Coronary Heart Disease Risk Factors with microscopic qualities of coronary atherosclerosis in youth. Circulation. 2000;102(4):374-9.
  • Tabas I, Williams KJ, Borén J. Subendothelial lipoprotein retention as the initiating process in atherosclerosis: update and therapeutic implications. Circulation. 2007;116(16):1832-44.
  • Bentzon JF, Weile C, Sondergaard CS, Hindkjaer J, Kassem M, Falk E. Smooth muscle cells in atherosclerosis originate from the local vessel wall and not circulating progenitor cells in ApoE knockout mice. Arterioscler Thromb Vasc Biol. 2006;26(12):2696-702.
  • Stone GW, Maehara A, Lansky AJ, de Bruyne B, Cristea E, Mintz GS. A prospective natural history study of coronary atherosclerosis. N Engl J Med. 2011;364(3):226-35.
  • Burke AP, Kolodgie FD, Farb A, Weber DK, Malcom GT, Smialek J. Healed plaque ruptures and sudden coronary death: evidence that subclinical rupture has a role in plaque progression. Circulation. 2001;103(7):934-40.
  • Burke AP, Farb A, Malcom GT, Liang Y, Smialek J, Virmani R. Effect of risk factors on the mechanism of acute thrombosis and sudden coronary death in women. Circulation. 1998;97(21):2110-6.
  • Fayad ZA, Fuster V. Clinical imaging of the high risk or vulnerable atherosclerotic plaque. Circ Res. 2001;89(4):305-16.
  • Janoudi A, Shamoun FE, Kalavakunta JK, Abela GS. Cholesterol crystal induced arterial inflammation and destabilization of atherosclerotic plaque. Eur Heart J. 2016;37(25):1959-67.
  • Burke AP, Kolodgie FD, Farb A, Weber D, Virmani R. Morphological predictors of arterial remodeling in coronary atherosclerosis. Circulation. 2002;105(3):297-303.
  • Van der Wal AC, Becker AE, van der Loos CM, Das PK. Site of intimal rupture or erosion of thrombosed coronary atherosclerotic plaques is characterized by an inflammatory process irrespective of the dominant plaque morphology. Circulation. 1994;89(1):36-44.
  • Kubo T, Imanishi T, Takarada S, Kuroi A, Ueno S, Yamano T. Assessment of culprit lesion morphology in acute myocardial infarction. J Am Coll Cardiol. 2007;50(10):933-9.
  • Crea F, Libby P. Acute coronary syndromes: the way forward from mechanisms to precision treatment. Circulation. 2017; 136(12):1155-66.
  • Liuzzo G, Biasucci LM, Gallimore JR, Grillo RL, Rebuzzi AG, Pepys MB. The prognostic value of C-reactive protein and serum amyloid a protein in severe unstable angina. N Engl J Med. 1994;331(7):417-24.
  • Ridker PM, Everett BM, Thuren T, MacFadyen JG, Chang WH, Ballantyne C. Antiinflammatory therapy with canakinumab for atherosclerotic disease. N Engl J Med. 2017;377(12):1119-31.
  • Nidorf SM, Fiolet ATL, Mosterd A, Eikelboom JW, Schut A, Opstal TSJ. Colchicine in patients with chronic coronary disease. N Engl J Med. 2020;383(19):1838-47.
  • Nakamura S, Inami S, Murai K, Takano M, Takano H, Asai K. Relationship between cholesterol crystals and culprit lesion characteristics in patients with stable coronary artery disease: an optical coherence tomography study. Clin Res Cardiol. 2014;103(12):1015-21.
  • Virmani R, Burke AP, Farb A, Kolodgie FD. Pathology of the vulnerable plaque. J Am Coll Cardiol. 2006;47(8):C13-8.
  • Hansson GK, Libby P, Tabas I. Inflammation and plaque vulnerability. J Intern Med. 2015;278(5):483-93.
  • Quillard T, Araújo HA, Franck G, Shvartz E, Sukhova G, Libby P. TLR2 and neutrophils potentiate endothelial stress, apoptosis and detachment: implications for superficial erosion. Eur Heart J. 2015;36(22):1394-404.
  • Jia H, Dai J, Hou J, Xing L, Ma L, Liu H. Effective antithrombotic therapy without stenting: intravascular optical coherence tomography based management in plaque erosion (the EROSION study). Eur Heart J. 2017;38(11):792-800.
  • Ong P, Athanasiadis A, Borgulya G, Voehringer M, Sechtem U. 3 year follow up of patients with coronary artery spasm as cause of acute coronary syndrome: the CASPAR (coronary artery spasm in patients with acute coronary syndrome) study follow up. J Am Coll Cardiol. 2011;57(2):147-52.
  • Masumoto A, Mohri M, Shimokawa H, Urakami L, Usui M, Takeshita A. Suppression of coronary artery spasm by the Rho-kinase inhibitor fasudil in patients with vasospastic angina. Circulation. 2002;105(13):1545-7.