Koroner Arter Ektazi ve Genetik Yatkınlık
Yıl 2020,
Cilt: 3 Sayı: 1, 27 - 32, 31.01.2020
Kübra Çiğdem Pekkoç Uyanık
,
Onur Kılıçarslan
,
Özgür Ser
,
Oğuz Öztürk
,
Hülya Yılmaz Aydoğan
Öz
Koroner arter ektazi (KAE), koroner arterlerin lokal veya yaygın dilatasyonu olarak tanımlanır. Etiyolojisinde büyük oranda ateroskleroz yer alan koroner ektazide, aterosklerotik plak büyümesine cevap olarak aşırı yeniden şekillenme oluşmaktadır. Bu nedenle aterosklerozda etken genetik risk faktörlerinin koroner ektazi gelişimindeki etkilerinin araştırılması son yıllarda araştırmacıların ilgi odağı haline gelmiştir. Koroner ektazide yer alan moleküler süreçlerin daha iyi anlaşılması, hastalığın etiyolojisi hakkında daha fazla fikir sahibi olmamızı sağlayacak ve tedavi stratejilerinin geliştirilmesi açısından faydalı olacaktır. Bu derleme, koroner ektazi ve moleküler temelde etiyolojisinde rol oynayan genetik mekanizmaları özetlemektedir.
Kaynakça
- 1) Turkmen M., Bitigen A., Esen A. M. Koroner Arter Ektazileri, Turkiye Klinikleri J Med Sci. 2006, 26(1):68-72.
- 2) Uyarel H., Okmen E., Tartan Z. et al. The role of angiotensin converting enzyme genotype in coronary artery ectasia Int Heart J. 2005, (46) 89-96.
- 3) Oliveros R.A., Falsetti H.L., Carroll R.J., Heinle R.A., Ryan G.F. Atherosclerotic coronary artery aneurysm: Report of five cases and a review of the literature. Arch. Intern. Med. 1974, 134, 1072–1076.
- 4) Swaye P.S., Fisher L.D., Litwin P., Vignola P.A., Judkins M.P., Kemp H.G., Mudd J.G., Gosselin A.J. Aneurysmal coronary artery disease. Circulation 1983, 67, 134–138.
- 5) Hartnell G.G., Parnell B.M., Pridie R.B. Coronary artery ectasia. Its prevalence and clinical significance in 4993 patients. Br. Heart. J. 1985, 54, 392–395.
- 6) Yilmaz H., Sayar N., Yilmaz M., Tangürek B., Cakmak N., Gürkan U., Gül M., Simşek D., Bolca O. Coronary artery ectasia: clinical and angiographical evaluation. Turk. Kardiyol. Dern. Ars. 2008, 36, 530–535.
- 7) Sharma S.N., Kaul U., Sharma S., Wasir H.S., Manchanda S.C., Bahl V.K., Talwar K.K., Rajani M., Bhatia M.L. Coronary arteriographic profile in young and old Indian patients with ischaemic heart disease: A comparative study. Indian Heart J. 1990, 42, 365–369.
- 8) Özkan B, Örsçelik Ö, Yıldırım Yaroğlu H, Balcı Ş, Özcan MK, Çelik A, Özcan IT. Association between serum adropin levels and isolated coronary artery ectasia in patients with stable angina pectoris. Anatol J Cardiol. 2019 Nov;22(5):250-255.
- 9) Ekmekçi A., Ozcan K.S., Abaci N., Güngör B., Osmonov D., Tosu R., Toprak E., Güleç C., Ustek D., Oz D., Eren M. The relationship between coronary artery ectasia and eNOS intron 4a/b gene polymorphisms. Acta Cardiol. 2013 Feb;68(1):19-22.
- 10) İçli A., Altınbaş A. Beta Fibrinogen -455 G>A Gene Polymorphism in Coronary Artery Ectasia. JACC Vol 62/18/Suppl October 26–29, 2013, TSC Abstracts/Orals.
- 11) Ozbay Y., Akbulut M., Balin M., Kayancicek H., Baydas A., Korkmaz H. The level of hs-CRP in coronary artery ectasia and its response to statin and angiotensin-converting enzyme inhibitor treatment. Mediators Inflamm. 2007, 2007, 89649.
- 12) Li J.J., Nie S.P., Qian X.W., Zeng H.S., Zhang C.Y. Chronic inflammatory status in patients with coronary artery ectasia. Cytokine. 2009, 46, 61–64.
- 13) Sezen Y., Bas M., Polat M., Yildiz A., Buyukhatipoglu H.., Kucukdurmaz Z., Kaya Z., Demirbag R. The relationship between oxidative stress and coronary artery ectasia. Cardiol. J. 2010, 17, 488–494.
- 14) Singh U., Jialal I. Oxidative stress and atherosclerosis. Pathophysiology 2006, 13, 129–142. Int. J. Mol. Sci. 2014, 15.
- 15) Vogiatzi G., Tousoulis D., Stefanadis C. The role of oxidative stress in atherosclerosis. Hellenic. J. Cardiol. 2009, 50, 402–409
- 16) Croteau, D.L.; Bohr, V.A. Repair of oxidative damage to nuclear and mitochondrial DNA in mammalian cells. J. Biol. Chem. 1997, 272, 25409–25412.
- 17) Bruner S.D., Norman D.P., Verdine G.L. Structural basis for rec ognition and repair of the endogenous mutagen 8-oxoguanine in DNA. Nature 2000, 403, 859–866.
- 18) Li H., Hao X., Zhang W., Wei Q., Chen K. The hOGG1 Ser326Cys polymorphism and lung cancer risk: a meta-analysis. Cancer. Epidemiol. Biomarkers Prev. 2008, 17, 1739–1745.
- 19) Wang C.L., Hsieh M.C., Hsin S.C., Lin H.Y., Lin K.D., Lo C.S., Chen Z.H., Shin S.J. The hOGG1 Ser326Cys gene polymorphism is associated with decreased insulin sensitivity in subjects with normal glucose tolerance. J. Hum. Genet. 2006, 51, 124–128.
- 20) Hsu P.C., Wang C.L., Su H.M., Juo S.H., Lin T.H., Voon W.C., et al. The hOGG1 Ser326Cys gene polymorphism and the risk of coronary ectasia in the Chinese population. Int J Mol Science. 2014, 15(1):1671-82.
- 21) Singh B.M., Mehta J.L. Interactions between the renin-angiotensin system and dyslipidemia: relevance in the therapy of hypertension and coronary heart disease Arch Intern Med, 2003, ( 163), 1296-1304.
- 22) Akbulut T., Bilsel T., Uyarel H., Terzi S., Sayar N., Aydın A., ve diğerleri.Anjiyotensin Dönüştürücü Enzim Gen Polimorfizminin Erken Koroner Arter Hastalığı Gelişimindeki Rolü. Türk Kardiyol Dern Arş. 2004, 32: 23-27.
- 23) Antoniadis A.P., Chatzizisis Y.S., Giannoglou G.D. Pathogenetic mechanisms of coronary ectasia. Int J Cardiol. 2008, Nov 28;130(3):335-43.
- 24) Hayek T., Attias J,. Coleman R. et al. The angiotensin-converting enzyme inhibitor, fosinopril, and the angiotensin II receptor antagonist, losartan, inhibit LDL oxidation and attenuate atherosclerosis independent of lowering blood pressure in apolipoprotein E deficient mice. Cardiovasc Res. 1999, 44579- 587.
- 25) Leif S.J., Karin P., Gunnar A., Rolf G. G.A., Bengt E. K., Anders G.O. Antiatherosclerotic effects of the angiotensin-converting enzyme inhibitors captopril and fosinopril in hypercholesterolemic minipigs. J Cardiovasc Pharmacol. 1994, 24670- 677.
- 26) Daugherty A., Manning M.W., Cassis L.A. Angiotensin II promotes atherosclerotic lesions and aneurysms in apolipoprotein E-deficient mice. J Clin Invest. 2000, 105,1605- 1612.
- 27) Schieffer B., Schieffer E., Hilfiker-Kleiner D. et al. Expression of angiotensin II and interleukin 6 in human coronary atherosclerotic plaques: potential implications for inflammation and plaque instability Circulation. 2000, (101),1372-1378.
- 28) Samani N.J., Thompson J.R., O’Toole L., Channer K., Woods K.L. A meta-analysis of the association of the deletion allele of the angiotensin-converting enzyme gene with myocardial infarction. Circulation. 1996, 94:708-712.
- 29) Griendling K.K., Murphy T.J., Alexander R.W. Molecular biology of the renin-angiotensin system. Circulation. 1993, 87 1816- 1828.
- 30) Chen H., Li D., Sawamura T., Inoue K., Mehta J.L. Upregulation of LOX-1 expression in aorta of hypercholesterolemic rabbits: modulation by losartan. Biochem Biophys Res Commun. 2000, 276 1100- 1104.
- 31) Devabhaktuni S., Mercedes A., Diep J., Ahsan C. Coronary Artery Ectasia-A Review of Current Literature. Curr Cardiol Rev. 2016;12(4):318-323.
- 32) Johanning J.M., Franklin D.P., Han D.C., Carey D.J., Elmore J.R. Inhibition of inducible nitric oxide synthase limits nitric oxide production and experimental aneurysm expansion. J Vasc Surg. 2001, Mar;33(3):579-86.
- 33) Arif Yalcin A., Faruk Akturk I., Celik O., Erturk M., Sabri Hancer V., Yalcin B. et al. Coronary artery ectasia is associated with the c.894G>T (Glu298Asp) polymorphism of the endothelial nitric oxide synthase gene. Tohoku J Exp Med. 2014, 232(2):137-44.
- 34) Lu T.P., Chuang N.C., Cheng C.Y., Hsu C.A., Wang Y.C., Lin Y.H. et al. Genomewide methylation profiles in coronary artery ectasia. Clin Sci (Lond). 2017, 131(7):583-94.
- 35) Danesh J., Lewington S., Thompson S.G., Lowe G.D., Collins R. et al Plasma fibrinogen level and the risk of major cardiovascular diseases and nonvascular mortality: an individual participant meta-analysis. JAMA. 2005, 294:1799–1809.
36) Kannel W.B., Wolf P.A., Castelli W.P., D'Agostino R.B. Fibrinogen and risk of cardiovascular disease. The Framingham Study. JAMA. 1987, Sep 4;258(9):1183-6.
- 37) Folsom A.R., Aleksic N., Ahn C., Boerwinkle E., Wu K.K. Beta-fibrinogen gene -455G/A polymorphism and coronary heart disease incidence:the Atherosclerosis Risk in Communities (ARIC) Study. Ann Epidemiol. 2001, Apr;11(3):166-70.
- 38) Thomas A., Lamlum H., Humphries S., Green F. Linkage disequilibrium across the fibrinogen locus as shown by five genetic polymorphisms, G/A−455 (HAEIII), C/T148 (HindIII/AluI), T/G+1689 (AvaIII), and BclI (β-Fibrinogen) and TaqI (α-Fibrinogen), and their detection by PCR Human Mutation. 1994, (3) 79-81.
- 39) Ser Ö.S. Aterosklerotik Koroner Arter Ektazi Hastalarında Tgfbeta Geninde Yer Alan Fonksiyonel Varyasyonların Klinik Fenotiple İlşkilerinin İncelenmesi. İstanbul Üniversitesi, Uzmanlık Tezi; Kardiyoloji Enstitüsü, İstanbul, 2018.
- 40) Mäki J.M., Räsänen J., Tikkanen H., Sormunen R., Mäkikallio K., Kivirikko K.I., Soininen R. Inactivation of the lysyl oxidase gene Lox leads to aortic aneurysms, cardiovascular dysfunction, and perinatal death in mice. Circulation. 2002, Nov 5;106(19):2503-9.
- 41) Kılıcarslan O. Aterosklerotik Koroner Arter Ektazi Hastalarında Lizil Oksidaz Fonksiyonel Gen Varyasyonlarının İnflamatuar Sitokin Paneli İle Birlikte Değerlendirilmesi. İstanbul Üniversitesi, Uzmanlık Tezi; Kardiyoloji Enstitüsü, İstanbul, 2019.
Yıl 2020,
Cilt: 3 Sayı: 1, 27 - 32, 31.01.2020
Kübra Çiğdem Pekkoç Uyanık
,
Onur Kılıçarslan
,
Özgür Ser
,
Oğuz Öztürk
,
Hülya Yılmaz Aydoğan
Kaynakça
- 1) Turkmen M., Bitigen A., Esen A. M. Koroner Arter Ektazileri, Turkiye Klinikleri J Med Sci. 2006, 26(1):68-72.
- 2) Uyarel H., Okmen E., Tartan Z. et al. The role of angiotensin converting enzyme genotype in coronary artery ectasia Int Heart J. 2005, (46) 89-96.
- 3) Oliveros R.A., Falsetti H.L., Carroll R.J., Heinle R.A., Ryan G.F. Atherosclerotic coronary artery aneurysm: Report of five cases and a review of the literature. Arch. Intern. Med. 1974, 134, 1072–1076.
- 4) Swaye P.S., Fisher L.D., Litwin P., Vignola P.A., Judkins M.P., Kemp H.G., Mudd J.G., Gosselin A.J. Aneurysmal coronary artery disease. Circulation 1983, 67, 134–138.
- 5) Hartnell G.G., Parnell B.M., Pridie R.B. Coronary artery ectasia. Its prevalence and clinical significance in 4993 patients. Br. Heart. J. 1985, 54, 392–395.
- 6) Yilmaz H., Sayar N., Yilmaz M., Tangürek B., Cakmak N., Gürkan U., Gül M., Simşek D., Bolca O. Coronary artery ectasia: clinical and angiographical evaluation. Turk. Kardiyol. Dern. Ars. 2008, 36, 530–535.
- 7) Sharma S.N., Kaul U., Sharma S., Wasir H.S., Manchanda S.C., Bahl V.K., Talwar K.K., Rajani M., Bhatia M.L. Coronary arteriographic profile in young and old Indian patients with ischaemic heart disease: A comparative study. Indian Heart J. 1990, 42, 365–369.
- 8) Özkan B, Örsçelik Ö, Yıldırım Yaroğlu H, Balcı Ş, Özcan MK, Çelik A, Özcan IT. Association between serum adropin levels and isolated coronary artery ectasia in patients with stable angina pectoris. Anatol J Cardiol. 2019 Nov;22(5):250-255.
- 9) Ekmekçi A., Ozcan K.S., Abaci N., Güngör B., Osmonov D., Tosu R., Toprak E., Güleç C., Ustek D., Oz D., Eren M. The relationship between coronary artery ectasia and eNOS intron 4a/b gene polymorphisms. Acta Cardiol. 2013 Feb;68(1):19-22.
- 10) İçli A., Altınbaş A. Beta Fibrinogen -455 G>A Gene Polymorphism in Coronary Artery Ectasia. JACC Vol 62/18/Suppl October 26–29, 2013, TSC Abstracts/Orals.
- 11) Ozbay Y., Akbulut M., Balin M., Kayancicek H., Baydas A., Korkmaz H. The level of hs-CRP in coronary artery ectasia and its response to statin and angiotensin-converting enzyme inhibitor treatment. Mediators Inflamm. 2007, 2007, 89649.
- 12) Li J.J., Nie S.P., Qian X.W., Zeng H.S., Zhang C.Y. Chronic inflammatory status in patients with coronary artery ectasia. Cytokine. 2009, 46, 61–64.
- 13) Sezen Y., Bas M., Polat M., Yildiz A., Buyukhatipoglu H.., Kucukdurmaz Z., Kaya Z., Demirbag R. The relationship between oxidative stress and coronary artery ectasia. Cardiol. J. 2010, 17, 488–494.
- 14) Singh U., Jialal I. Oxidative stress and atherosclerosis. Pathophysiology 2006, 13, 129–142. Int. J. Mol. Sci. 2014, 15.
- 15) Vogiatzi G., Tousoulis D., Stefanadis C. The role of oxidative stress in atherosclerosis. Hellenic. J. Cardiol. 2009, 50, 402–409
- 16) Croteau, D.L.; Bohr, V.A. Repair of oxidative damage to nuclear and mitochondrial DNA in mammalian cells. J. Biol. Chem. 1997, 272, 25409–25412.
- 17) Bruner S.D., Norman D.P., Verdine G.L. Structural basis for rec ognition and repair of the endogenous mutagen 8-oxoguanine in DNA. Nature 2000, 403, 859–866.
- 18) Li H., Hao X., Zhang W., Wei Q., Chen K. The hOGG1 Ser326Cys polymorphism and lung cancer risk: a meta-analysis. Cancer. Epidemiol. Biomarkers Prev. 2008, 17, 1739–1745.
- 19) Wang C.L., Hsieh M.C., Hsin S.C., Lin H.Y., Lin K.D., Lo C.S., Chen Z.H., Shin S.J. The hOGG1 Ser326Cys gene polymorphism is associated with decreased insulin sensitivity in subjects with normal glucose tolerance. J. Hum. Genet. 2006, 51, 124–128.
- 20) Hsu P.C., Wang C.L., Su H.M., Juo S.H., Lin T.H., Voon W.C., et al. The hOGG1 Ser326Cys gene polymorphism and the risk of coronary ectasia in the Chinese population. Int J Mol Science. 2014, 15(1):1671-82.
- 21) Singh B.M., Mehta J.L. Interactions between the renin-angiotensin system and dyslipidemia: relevance in the therapy of hypertension and coronary heart disease Arch Intern Med, 2003, ( 163), 1296-1304.
- 22) Akbulut T., Bilsel T., Uyarel H., Terzi S., Sayar N., Aydın A., ve diğerleri.Anjiyotensin Dönüştürücü Enzim Gen Polimorfizminin Erken Koroner Arter Hastalığı Gelişimindeki Rolü. Türk Kardiyol Dern Arş. 2004, 32: 23-27.
- 23) Antoniadis A.P., Chatzizisis Y.S., Giannoglou G.D. Pathogenetic mechanisms of coronary ectasia. Int J Cardiol. 2008, Nov 28;130(3):335-43.
- 24) Hayek T., Attias J,. Coleman R. et al. The angiotensin-converting enzyme inhibitor, fosinopril, and the angiotensin II receptor antagonist, losartan, inhibit LDL oxidation and attenuate atherosclerosis independent of lowering blood pressure in apolipoprotein E deficient mice. Cardiovasc Res. 1999, 44579- 587.
- 25) Leif S.J., Karin P., Gunnar A., Rolf G. G.A., Bengt E. K., Anders G.O. Antiatherosclerotic effects of the angiotensin-converting enzyme inhibitors captopril and fosinopril in hypercholesterolemic minipigs. J Cardiovasc Pharmacol. 1994, 24670- 677.
- 26) Daugherty A., Manning M.W., Cassis L.A. Angiotensin II promotes atherosclerotic lesions and aneurysms in apolipoprotein E-deficient mice. J Clin Invest. 2000, 105,1605- 1612.
- 27) Schieffer B., Schieffer E., Hilfiker-Kleiner D. et al. Expression of angiotensin II and interleukin 6 in human coronary atherosclerotic plaques: potential implications for inflammation and plaque instability Circulation. 2000, (101),1372-1378.
- 28) Samani N.J., Thompson J.R., O’Toole L., Channer K., Woods K.L. A meta-analysis of the association of the deletion allele of the angiotensin-converting enzyme gene with myocardial infarction. Circulation. 1996, 94:708-712.
- 29) Griendling K.K., Murphy T.J., Alexander R.W. Molecular biology of the renin-angiotensin system. Circulation. 1993, 87 1816- 1828.
- 30) Chen H., Li D., Sawamura T., Inoue K., Mehta J.L. Upregulation of LOX-1 expression in aorta of hypercholesterolemic rabbits: modulation by losartan. Biochem Biophys Res Commun. 2000, 276 1100- 1104.
- 31) Devabhaktuni S., Mercedes A., Diep J., Ahsan C. Coronary Artery Ectasia-A Review of Current Literature. Curr Cardiol Rev. 2016;12(4):318-323.
- 32) Johanning J.M., Franklin D.P., Han D.C., Carey D.J., Elmore J.R. Inhibition of inducible nitric oxide synthase limits nitric oxide production and experimental aneurysm expansion. J Vasc Surg. 2001, Mar;33(3):579-86.
- 33) Arif Yalcin A., Faruk Akturk I., Celik O., Erturk M., Sabri Hancer V., Yalcin B. et al. Coronary artery ectasia is associated with the c.894G>T (Glu298Asp) polymorphism of the endothelial nitric oxide synthase gene. Tohoku J Exp Med. 2014, 232(2):137-44.
- 34) Lu T.P., Chuang N.C., Cheng C.Y., Hsu C.A., Wang Y.C., Lin Y.H. et al. Genomewide methylation profiles in coronary artery ectasia. Clin Sci (Lond). 2017, 131(7):583-94.
- 35) Danesh J., Lewington S., Thompson S.G., Lowe G.D., Collins R. et al Plasma fibrinogen level and the risk of major cardiovascular diseases and nonvascular mortality: an individual participant meta-analysis. JAMA. 2005, 294:1799–1809.
36) Kannel W.B., Wolf P.A., Castelli W.P., D'Agostino R.B. Fibrinogen and risk of cardiovascular disease. The Framingham Study. JAMA. 1987, Sep 4;258(9):1183-6.
- 37) Folsom A.R., Aleksic N., Ahn C., Boerwinkle E., Wu K.K. Beta-fibrinogen gene -455G/A polymorphism and coronary heart disease incidence:the Atherosclerosis Risk in Communities (ARIC) Study. Ann Epidemiol. 2001, Apr;11(3):166-70.
- 38) Thomas A., Lamlum H., Humphries S., Green F. Linkage disequilibrium across the fibrinogen locus as shown by five genetic polymorphisms, G/A−455 (HAEIII), C/T148 (HindIII/AluI), T/G+1689 (AvaIII), and BclI (β-Fibrinogen) and TaqI (α-Fibrinogen), and their detection by PCR Human Mutation. 1994, (3) 79-81.
- 39) Ser Ö.S. Aterosklerotik Koroner Arter Ektazi Hastalarında Tgfbeta Geninde Yer Alan Fonksiyonel Varyasyonların Klinik Fenotiple İlşkilerinin İncelenmesi. İstanbul Üniversitesi, Uzmanlık Tezi; Kardiyoloji Enstitüsü, İstanbul, 2018.
- 40) Mäki J.M., Räsänen J., Tikkanen H., Sormunen R., Mäkikallio K., Kivirikko K.I., Soininen R. Inactivation of the lysyl oxidase gene Lox leads to aortic aneurysms, cardiovascular dysfunction, and perinatal death in mice. Circulation. 2002, Nov 5;106(19):2503-9.
- 41) Kılıcarslan O. Aterosklerotik Koroner Arter Ektazi Hastalarında Lizil Oksidaz Fonksiyonel Gen Varyasyonlarının İnflamatuar Sitokin Paneli İle Birlikte Değerlendirilmesi. İstanbul Üniversitesi, Uzmanlık Tezi; Kardiyoloji Enstitüsü, İstanbul, 2019.