Jornal Vascular Brasileiro
https://www.jvascbras.org/article/doi/10.1590/jvb.2014.027
Jornal Vascular Brasileiro
Review Article

Inflammatory mediators of coronary artery ectasia

Os mediadores inflamatórios de ectasia coronária

Shi-Min Yuan

http://dx.doi.org/10.1590/jvb.2014.027 J Vasc Bras, vol.13, n3, p.198-207, 2014
PDF
SciELO
Downloads: 0
Views: 831

Abstract

The exact mechanisms underlying coronary artery ectasia (CAE) remain uncertain. This study aims to investigate whether and how inflammatory mediators play a role in the pathogenesis of CAE. The data sources of this study were located by literature searches on MEDLINE, Highwire Press and Google search engine for the year range 2000-2013. The most sensitive of the four types of plasma inflammatory mediators were cell adhesion molecules and systemic inflammatory markers followed by cytokines, while proteolytic substances were the least sensitive indicators of CAE. Hypersensitive C-reaction protein, homocysteine, intercellular adhesion molecule 1, vascular cell adhesion molecule 1, matrix metalloproteinase-9, tissue inhibitor of metalloproteinase-2, vascular endothelial growth factor and neopterin levels were significantly higher in CAE and coronary artery disease (CAD) patients than in controls without CAE. The percentage of granulocytes was higher in CAE, in comparison with individuals with normal coronary arteries. Polymerase chain reaction determination of angiotensin converting enzyme genotypes showed that the DD genotype was more prevalent in CAE patients than in CAD patients, while prevalence of the I allele was higher in CAD than in CAE patients. CAE is more a result of inflammatory processes than of extracellular matrix degradation, as demonstrated by investigations of plasma inflammatory mediators, activation markers and angiotensin converting enzyme genotypes. Contemporary theories are unable to explain CAE's predilection for the right coronary artery or the occurrence of multi-vessel and multi-segment involvement.

Keywords

coronary aneurysm, extracellular matrix, inflammation mediators

Resumo

Os mecanismos exatos da ectasia de artérias coronárias (EAC) não são completamente compreendidos. Este estudo busca verificar, em detalhes, se e como os mediadores inflamatórios funcionam na pathogenesis de EAC. A fonte de dados do presente estudo veio da recuperação de literatura das investigações relevantes em MEDLINE, na Prensa de Highwire e na ativação de pesquisa do Google, do ano 2000 para 2013. Dos quatro tipos de mediadores inflamatórios do plasma, as moléculas de adesão de célula e os marcadores inflamatórios sistêmicos foram os mais sensíveis, sendo que cytokines foram mais sensíveis e substâncias de protease foram menos sensíveis na indicação da presença de EAC. A proteína C reativa hipersensível, o homocysteine, a molécula de adesão intercelular 1, a molécula de adesão de célula vascular 1, a matriz metalloproteinase-9, o nervo inibidor de tecido de metalloproteinase-2, o fator de crescimento endothelial vascular e os níveis de neopterin foram mais altos nos pacientes com EAC do que nos controles sem EAC. A porcentagem de granulocytes foi mais alta no grupo EAC, comparando-se com os indivíduos com a artéria coronária normal. A determinação de genótipo de enzima do angiotensin-conversão utilizando-se a técnica de reação em cadeia da polimerase revelou que o genótipo DD foi prevalecente na EAC, mas não nos pacientes de DAC, enquanto a presença do alelo I foi maior na DAC do que no EAC. O EAC é mais um resultado do processo inflamatório do que da degradação da matriz extracelular, como evidenciado por investigações dos mediadores inflamatórios de plasma, marcadores de ativação e genótipos de enzima do angiotensin a conversão. A predileção de EAC na artéria coronária direita e nos envolvimentos de multinavio e de multissegmento não é apurada por teorias contemporâneas.

Palavras-chave

aneurisma coronário;, matriz extracelular;, mediadores de inflamação

References

Swaye PS, Fisher LD, Litwin P. Aneurysmal coronary artery disease. Circulation. 1983;67(1):134-8.

Falsetti HL, Carrol RJ. Coronary artery aneurysm. A review of the literature with a report of 11 new cases. Chest. 1976;69(5):630-6.

Pinar-Bermúdez E, López Palop R, Lozano Martínez-Luengas I. Coronary ectasia: prevalence, and clinical and angiographic characteristics. Rev Esp Cardiol. 2003;56(5):473-9.

Mavrogeni S. Coronary artery ectasia: diagnosis and treatment. E-Journal of Cardiology Practice. 2009;8(15).

Li JJ, He JG, Nan JL, He ZX, Zhu CG, Li J. Is systemic inflammation responsible for coronary artery ectasia?. Int J Cardiol. 2008;130(2):69-70.

Zografos TA, Haliassos A, Korovesis S, Giazitzoglou E, Serelis J, Katritsis DG. Serum cathepsin levels in coronary artery ectasia. Int J Cardiol. 2010;145(3):606-7.

Turhan H, Erbay AR, Yasar AS. Plasma homocysteine levels in patients with isolated coronary artery ectasia. Int J Cardiol. 2005;104(2):158-62.

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(1):89649.

Tuttolomondo A, Di Raimondo D, Pecoraro R, Arnao V, Pinto A, Licata G. Atherosclerosis as an inflammatory disease. Curr Pharm Des. 2012;18(28):4266-88.

Wang X, Nie SP. The coronary slow flow phenomenon: characteristics, mechanisms and implications. Cardiovasc Diagn Ther. 2011;1(1):37-43.

Tokgozoglu L, Ergene O, Kinay O, Nazli C, Hascelik G, Hoscan Y. Plasma interleukin-6 levels are increased in coronary artery ectasia. Acta Cardiol. 2004;59(5):515-9.

Adiloglu AK, Can R, Nazli C. Ectasia and severe atherosclerosis: relationships with chlamydia pneumoniae, helicobacterpylori, and inflammatory markers. Tex Heart Inst J. 2005;32(1):21-7.

Adiloglu AK, Ocal A, Tas T, Onal S, Kapan S, Aridogan B. Increased expression of CD11a and CD45 on leukocytes and decreased serum TNF-alpha levels in patients with isolated coronary artery ectasia. Clin Lab. 2011;57(9-10):703-9.

Aydin M, Tekin IO, Dogan SM, Yildirim N, Arasli M, Sayin MR. The levels of tumor necrosis factor-alpha and interleukin-6 in patients with isolated coronary artery ectasia. Mediators Inflamm. 2009;2009:106-45.

Daoud EM, Abdelaziz AA, Hassan NA. Isolated coronary artery ectasia debate: Inflammation versus atherosclerosis. Egypt Heart J. 2012;64(4):185-90.

Dogan A, Tuzun N, Turker Y, Akcay S, Kaya S, Ozaydin M. Matrix metalloproteinases and inflammatory markers in coronary artery ectasia: their relationship to severity of coronary artery ectasia. Coron Artery Dis. 2008;19(8):559-63.

Finkelstein A, Michowitz Y, Abashidze A, Miller H, Keren G, George J. Temporal association between circulating proteolytic, inflammatory and neurohormonal markers in patients with coronary ectasia. Atherosclerosis. 2005;179(2):353-9.

Kosar F, Sincer I, Aksoy Y, Ozerol I. Elevated plasma homocysteine levels in patients with isolated coronary artery ectasia. Coron Artery Dis. 2006;17(1):23-7.

Ateia MY, Azmy AM, El-Shafy SA, El-Naggar WM, Abdel-Latif I. Evaluation of serum levels of C-reactive protein (CRP) and interleukin-6 (Il-6) in coronary artery ectasia. Heart Mirror J. 2007;1(2):75-81.

Sahin M, Varol E, Ozaydin M. Comparison of neopterin levels in patients with coronary artery ectasia versus patients with obstructive coronary artery disease. South Med J. 2008;101(5):476-9.

Turhan H, Erbay AR, Yasar AS. Plasma soluble adhesion molecules; intercellular adhesion molecule-1, vascular cell adhesion molecule-1 and E-selectin levels in patients with isolated coronary artery ectasia. Coron Artery Dis. 2005;16(1):45-50.

Turhan H, Erbay AR, Yasar AS, Balci M, Bicer A, Yetkin E. Comparison of C-reactive protein levels in patients with coronary artery ectasia versus patients with obstructive coronary artery disease. Am J Cardiol. 2004;94(10):1303-6.

Yasar AS, Erbay AR, Ayaz S. Increased platelet activity in patients with isolated coronary artery ectasia. Coron Artery Dis. 2007;18(6):451-4.

Yilmaz H, Tayyareci G, Sayar N. Plasma soluble adhesion molecule levels in coronary artery ectasia. Cardiology. 2006;105(3):176-81.

Savino M, Parisi Q, Biondi-Zoccai GG, Pristipino C, Cianflone D, Crea F. New insights into molecular mechanisms of diffuse coronary ectasiae: a possible role for VEGF. Int J Cardiol. 2006;106(3):307-12.

Yildirim N, Tekin IO, Arasli M, Aydin M. Further increase in the expression of activation markers on monocyte-derived dendritic cells in coronary artery disease patients with ectasia compared to patients with coronary artery disease alone. Mediators Inflamm. 2010;2010:748-919.

Yildirim N, Tekin IO, Dogan SM. Expression of monocyte and lymphocyte adhesion molecules is increased in isolated coronary artery ectasia. Coron Artery Dis. 2007;18(1):49-53.

Uyarel H, Okmen E, Tartan Z. The role of angiotensin converting enzyme genotype in coronary artery ectasia. Int Heart J. 2005;46(1):89-95.

Gülec S, Aras O, Atmaca Y. Deletion polymorphism of the angiotensin I converting enzyme gene is a potent risk factor for coronary artery ectasia. Heart. 2003;89(2):213-4.

Chauhan LS. Inflammation mediators: a review. .

Halfman CJ. Mediators of Inflammation. .

Chronic inflammation and mediators. .

Balin M, Celik A, Kobat MA. The association between soluble lectin-like oxidized low-density lipoprotein receptor-1 levels and patients with isolated coronary artery ectasia. J Thromb Thrombolysis. 2012;33(3):239-45.

Díaz-Zamudio M, Bacilio-Pérez U, Herrera-Zarza MC. Coronary artery aneurysms and ectasia: role of coronary CT angiography. Radiographics. 2009;29(7):1939-54.

Manginas A, Cokkinos DV. Coronary artery ectasias: imaging, functional assessment and clinical implications. Eur Heart J. 2006;27(9):1026-31.

Sudhir K, Ports TA, Amidon TM. Increased prevalence of coronary ectasia in heterozygous familial hypercholesterolemia. Circulation. 1995;91(5):1375-80.

Markis JE, Joffe CD, Cohn PF, Feen DJ, Herman MV, Gorlin R. Clinical significance of coronary arterial ectasia. Am J Cardiol. 1976;37(2):217-22.

Sorrell VL, Davis MJ, Bove AA. Current knowledge and significance of coronary artery ectasia: a chronologic review of the literature, recommendations for treatment, possible etiologies, and future considerations. Clin Cardiol. 1998;21(3):157-60.

Baer AZ, Rubin LG, Shapiro CA. Prevalence of coronary artery lesions on the initial echocardiogram in Kawasaki syndrome. Arch Pediatr Adolesc Med. 2006;160(7):686-90.

Tatli E, Surucu H, Aktoz M, Buyuklu M. Coronary artery ectasia in a patient with Behcet's disease. Saudi Med J. 2007;28(8):1281-2.

Suzuki H, Daida H, Tanaka M. Giant aneurysm of the left main coronary artery in Takayasu aortitis. Heart. 1999;81(2):214-7.

Pick RA, Glover MU, Vieweg WV. Myocardial infarction in a young woman with isolated coronary arteritis. Chest. 1982;82(3):378-80.

Cascio A, Maggio MC, Cardella F. Coronary involvement in Mediterranean spotted fever. New Microbiol. 2011;34(4):421-4.

Di Mario C, Zanchetta M, Maiolino P. Coronary aneurysms in a case of Ehlers-Danlos syndrome. Jpn Heart J. 1988;29(4):491-6.

Hakim FA, Gruden JF, Panse PM, Alegria JR. Coronary artery ectasia in an adult Noonan syndrome detected on coronary CT angiography. Heart Lung Circ. 2013;22(12):1051-3.

Eleftheriadis D, Eleftheriadis N. Coronary artery disease and systemic vasculitis: case report and review. Coronary artery diseases. 2012:281-300.

Garg NJ. Inflammasomes in cardiovascular diseases. Am J Cardiovasc Dis. 2011;1(3):244-54.

Chen H, Wang J, Wang JA, Shi GP. Role of lysosomal cathepsins in post-myocardial infarction remodeling. N. J Med Sci. 2011;4(4):173-7.

Antoniadis AP, Chatzizisis YS, Giannoglou GD. Pathogenetic mechanisms of coronary ectasia. Int J Cardiol. 2008;130(3):335-43.

Chakrabarti S, Thomas E, Wright JG, Vettukattil JJ. Congenital coronary artery dilatation. Heart. 2003;89(6):595-6.

Yetkin E, Acikgoz N, Sivri N. Increased plasma levels of cystatin C and transforming growth factor-β1 in patients with coronary artery ectasia: can there be a potential interaction between cystatin C and transforming growth factor-β1. Coron Artery Dis. 2007;18(3):211-4.

Turhan H, Yetkin E. Coronary artery ectasia: is it a destructive inflammatory lesion of the vascular wall?. Int J Cardiol. 2007;118(2):241.

Gokkusu C, Tulubas F, Unlucerci Y, Ozkok E, Umman B, Aydin M. Homocysteine and pro-inflammatory cytokine concentrations in acute heart disease. Cytokine. 2010;50(1):15-8.

Yndestad A, Holm AM, Müller F. Enhanced expression of inf lammatory cytokines and activation markers in T-cells from patients with chronic heart failure. Cardiovasc Res. 2003;60(1):141-6.

Schroecksnadel K, Walter RB, Weiss G, Mark M, Reinhart WH, Fuchs D. Association between plasma thiols and immune activation marker neopterin in stable coronary heart disease. Clin Chem Lab Med. 2008;46(5):648-54.

Avanzas P, Arroyo-Espliguero R, Quiles J, Roy D, Kaski JC. Elevated serum neopterin predicts future adverse cardiac events in patients with chronic stable angina pectoris. Eur Heart J. 2005;26(5):457-63.

Dejana E, Breviario F, Caveda L. Leukocyte-endothelial cell adhesive receptors. Clin Exp Rheumatol. 1994;12(^sSuppl 10):S25-8.

Ayhan SS, Oztürk S, Erdem A. Nötrofil/lenfosit oraninin koroner ektazisi varligi ve yayginligi ile iliskisi. Turk Kardiyol Dern Ars. 2013;41(3):185-90.

Sarli B, Baktir AO, Saglam H. Neutrophil-to-lymphocyte ratio is associated with severity of coronary artery ectasia. Angiology. 2013;65(2):147-51.

Syal SK, Kapoor A, Bhatia E. Vitamin D deficiency, coronary artery disease, and endothelial dysfunction: observations from a coronary angiographic study in Indian patients. J Invasive Cardiol. 2012;24(8):385-9.

Demir M, Keceoglu S, Melek M. The relationship between plasma eosinophil count and coronary artery ectasia. Cardiol Rev. 2013;4(4-5):159-64.

Landay A, Desai S. Immune activation and inflammation: role in co-morbidities in HIV disease. .

Markovic BB, Bergovec M, Reiner Z, Sertic J, Vincelj J, Markovic M. Deletion polymorphism of the angiotensin I-converting enzyme gene in elderly patients with coronary heart disease. Coll Antropol. 2007;31(1):179-83.

Chen Q, Jin M, Yang F, Zhu J, Xiao Q, Zhang L. Matrix metalloproteinases: inflammatory regulators of cell behaviors in vascular formation and remodeling. Mediators Inflamm. 2013;2013(2013):1-14.

Wuyts B, Delanghe J, De Buyzere M. Angiotensin I-converting enzyme insertion/deletion polymorphism: clinical implications. Acta Clin Belg. 1997;52(6):338-49.

Ceyhan K, Koc F, Ozdemir K. Coronary ectasia is associated with impaired left ventricular myocardial performance in patients without significant coronary artery stenosis. Med Princ Pract. 2012;21(2):139-44.

Sociedade Brasileira de Angiologia e Cirurgia Vascular (SBACV)"> Sociedade Brasileira de Angiologia e Cirurgia Vascular (SBACV)">
5ddd80d40e882512371da3e9 jvb Articles
Links & Downloads
1677-7301 (Electronic)
J Vasc Bras ©2024 All rights reserved.

J Vasc Bras

Share this page
Page Sections