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Ateroskleroz patogenezi

Year 2012, Volume: 29 Issue: 3s, 101 - 106, 06.02.2013

Abstract

Dünyada ve ülkemizde ateroskleroz ve komplikasyonları en önde gelen ölüm nedenidir. Ateroskleroz, tipik lezyonu ateroma plakları olan orta ve büyük çaplı arterlerin intima tabakalarını etkileyen bir hastalıktır. Aterosklerozun başlamasında endotel disfonksiyonu major rol oynamaktadır. Aterosklerozun risk faktörlerinin ortak noktası endotel disfonksiyonudur. Düşük dansiteli lipoproteinin (LDL) endotel altına geçmesiyle birlikte salınan bir takım sitokinler ve kemotaktanların etkisiyle enflamatuvar hücreler intimada birikmeye başlar. Makrofajların intimada okside LDL’yi fagosite etmesiyle birlikte köpük hücresi oluşur ve intima altında sarı çizgilenmeler olarak gözlenir. Lümende darlık oluşturmayan bu lezyonlar yağlı çizgilenme olarak adlandırılır ve aterosklerozun ilk lezyonudur. Köpük hücrelerinin apopitosisi ile nekrotik lipid çekirdek oluşur. Mediadan intimaya göç eden düz kas hücrelerinin proliferatif özellik kazanması ile birlikte lipid çekirdek etrafında ekstrasellüler bağ dokusu (kapsül) sentezi başlar. Lipit çekirdek ve etrafında fibröz kapsülü olan, lümeni daraltan lezyona fibröz plak denir. Lipit çekirdeğin büyüyüp kapsülün incelmesi ve enflamatuvar hücrelerin çoğalması ile birlikte unstable plak oluşur. Plak kapsülünün yırtılıp plak içeriğinin kan ile teması sonucu plak üzerine trombüs ve fibrinin bindiği komplike lezyon meydana gelir. Ateroskleroz endotel disfonksiyonu, dislipidemi ve enflamatuvar hücrelerin merkezi rol oynadığı, birçok risk faktörünün tetiklediği kronik inflamatuvar bir hastalıktır.

Pathogenesis of atherosclerosis

Atherosclerosis and its complications are the leading cause of death both in our country and the world. Atheroma plaques are the typical lesion of atherosclerosis and affect intimal layers of medium and large arteries. Endothelial dysfunction plays a major role in the initiation of atherosclerosis. Endothelial dysfunction is a common point in risk factors of atherosclerosis. Inflammatory cells begin to accumulate in intima by the effect of cytokines and chemokines secreted with passage of LDL (low-density lipoprotein) through endothelium. Foam cells are formed as a result of phagocytosis of LDL by macrophages and seen as yellow streaks under the intima. Those lesions are first lesions of atherosclerosis and do not cause stenosis and termed as fatty streaks. The necrotic lipid core is formed by apoptosis of foam cells. Extracellular connective tissue (capsule) synthesis begins around the lipid core by proliferation of smooth muscle cells that migrate to intima. Fibrous plaque is a lesion with a fibrous capsule around the lipid core and narrows the lumen. Unstable plaque is formed by proliferation of inflammatory cells and thinning of capsule through enlargement of lipid core. Tear of plaque capsule and contact of plaque content with blood results in formation of a complicated lesion in which thrombus and fibrin bind on plaque. Atherosclerosis is a chronic inflammatory disease in which endothelial dysfunction, dyslipidemia and inflammatory cells play a central role and triggered by many risk factors.

J. Exp. Clin. Med., 2012; 29: S101-S106

References

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  • Erol, Ç., 2004. Klinik Kardiyoloji. Medikal & Nobel Tıp Kitap Sarayı. 3, 9-15.
  • Farugi, R.M., Di Corleto, P.E., 1993. Mechanisms of monocyte recruitment and accumulation. B.H.J. 69, 19-29.
  • Fuster, V., Fayad, A.Z., Badimon, J.J., 1999. Acute coronary sendromes: Biology. Lancet. 353, 5-9.
  • Koeng, W., 1999. Athersclerosis involves more than just lipids: Fcus on inflammation. Eur. Heart. J. 19-26.
  • Li, H., Forsterman, U., 2000. Nitric oxide in pathogenesis of vascular disease. J. Pathol. 190, 244-254.
  • Libby, P., 1995. Molecular bases of the acute coronary syndromes. Circulation. 91, 2844-2850.
  • Nagel, T., Resnick, N., Atkinson, W.J., Dewey, C.F., Gimbrone, M.A., 1994. Shear stress selectively upregulates intercellular adhesion mole- cule-1 expression in cultured human vascular endothelial cells. J. Clin. Invest. 94, 885-891.
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  • Ross, R., 1993. The pathogenesis of atherosclerosis. Nature. 362, 801-809.
  • Topper, J.N., Cai, J., Falb, D., Gimbrone, M.A. Jr., 1996. Identification of vascular endothelial genes differentially responsive to fluid mechani- cal stimuli: Cyclooxygenase-2, manganese superoxide dismutase, and endothelial cell nitric oxide synthase are selectively up-regulated by steady laminar shear stress. Proc. Natl. Acad. Sci. U.S.A. 93, 10417-10422.
  • Vallace, P., 1996. Vascular endothelium, its physiology and pathophysiology. In: Weatherall DJ et al. Oxford text book of medicine, 3rd ed. Oxford Medical Publications. 2, 2295-2300.
  • Williams, K.J., Tabas, I., 1998. The response-to-retention hypothesis of atherogenesis reinforced. Curr. Opin. Lipidol. 9, 471-474.
  • Zipes, D.P., Libby, P., Bonow, R.O., Braunwald, E., 2005. Braunwald’s heart disease: A textbook of cardiovascular medicine. 925.
Year 2012, Volume: 29 Issue: 3s, 101 - 106, 06.02.2013

Abstract

References

  • Avşar, A., Akci, A., Beyter, M.E., 2011. Aterosklerozun patogenezi. Turkiye Klinikleri J. Cordiol. Special Topics. 4, 5.
  • Camejo, G., Hurt-Camejo, E., Wiklund, O., Bondjers, G., 1998. Association of apo B lipoproteins with arterial proteoglycans: Pathological significance and molecular basis. Atherosclerosis. 139, 205-222.
  • Hansson, G.K., Nilsson, J., 2010. Pathogenesis of Atherosclerosis. In: Crawford, M.H., Di Marco, J.P., Paulus, W.J., eds. Cardiology. 3rd Ed. Philadelphia. Mosby Elsevier, 3-15.
  • Erol, Ç., 2004. Klinik Kardiyoloji. Medikal & Nobel Tıp Kitap Sarayı. 3, 9-15.
  • Farugi, R.M., Di Corleto, P.E., 1993. Mechanisms of monocyte recruitment and accumulation. B.H.J. 69, 19-29.
  • Fuster, V., Fayad, A.Z., Badimon, J.J., 1999. Acute coronary sendromes: Biology. Lancet. 353, 5-9.
  • Koeng, W., 1999. Athersclerosis involves more than just lipids: Fcus on inflammation. Eur. Heart. J. 19-26.
  • Li, H., Forsterman, U., 2000. Nitric oxide in pathogenesis of vascular disease. J. Pathol. 190, 244-254.
  • Libby, P., 1995. Molecular bases of the acute coronary syndromes. Circulation. 91, 2844-2850.
  • Nagel, T., Resnick, N., Atkinson, W.J., Dewey, C.F., Gimbrone, M.A., 1994. Shear stress selectively upregulates intercellular adhesion mole- cule-1 expression in cultured human vascular endothelial cells. J. Clin. Invest. 94, 885-891.
  • Onat, A., 2009. TEKHARF çalışması 2009. Figur grafik ve matbaacılık Tic. Ltd. Şti. İstanbul. 24.
  • Ross, R., 1993. The pathogenesis of atherosclerosis. Nature. 362, 801-809.
  • Topper, J.N., Cai, J., Falb, D., Gimbrone, M.A. Jr., 1996. Identification of vascular endothelial genes differentially responsive to fluid mechani- cal stimuli: Cyclooxygenase-2, manganese superoxide dismutase, and endothelial cell nitric oxide synthase are selectively up-regulated by steady laminar shear stress. Proc. Natl. Acad. Sci. U.S.A. 93, 10417-10422.
  • Vallace, P., 1996. Vascular endothelium, its physiology and pathophysiology. In: Weatherall DJ et al. Oxford text book of medicine, 3rd ed. Oxford Medical Publications. 2, 2295-2300.
  • Williams, K.J., Tabas, I., 1998. The response-to-retention hypothesis of atherogenesis reinforced. Curr. Opin. Lipidol. 9, 471-474.
  • Zipes, D.P., Libby, P., Bonow, R.O., Braunwald, E., 2005. Braunwald’s heart disease: A textbook of cardiovascular medicine. 925.
There are 16 citations in total.

Details

Primary Language English
Journal Section Internal Medical Sciences
Authors

Halit Zengin

Publication Date February 6, 2013
Submission Date December 13, 2011
Published in Issue Year 2012 Volume: 29 Issue: 3s

Cite

APA Zengin, H. (2013). Ateroskleroz patogenezi. Journal of Experimental and Clinical Medicine, 29(3s), 101-106. https://doi.org/10.5835/jecm.omu.29.s3.002
AMA Zengin H. Ateroskleroz patogenezi. J. Exp. Clin. Med. February 2013;29(3s):101-106. doi:10.5835/jecm.omu.29.s3.002
Chicago Zengin, Halit. “Ateroskleroz Patogenezi”. Journal of Experimental and Clinical Medicine 29, no. 3s (February 2013): 101-6. https://doi.org/10.5835/jecm.omu.29.s3.002.
EndNote Zengin H (February 1, 2013) Ateroskleroz patogenezi. Journal of Experimental and Clinical Medicine 29 3s 101–106.
IEEE H. Zengin, “Ateroskleroz patogenezi”, J. Exp. Clin. Med., vol. 29, no. 3s, pp. 101–106, 2013, doi: 10.5835/jecm.omu.29.s3.002.
ISNAD Zengin, Halit. “Ateroskleroz Patogenezi”. Journal of Experimental and Clinical Medicine 29/3s (February 2013), 101-106. https://doi.org/10.5835/jecm.omu.29.s3.002.
JAMA Zengin H. Ateroskleroz patogenezi. J. Exp. Clin. Med. 2013;29:101–106.
MLA Zengin, Halit. “Ateroskleroz Patogenezi”. Journal of Experimental and Clinical Medicine, vol. 29, no. 3s, 2013, pp. 101-6, doi:10.5835/jecm.omu.29.s3.002.
Vancouver Zengin H. Ateroskleroz patogenezi. J. Exp. Clin. Med. 2013;29(3s):101-6.