Inflammatory mediators of coronary artery ectasia

Shi-Min Yuan

doi:10.1590/jvb.2014.027

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.

Highlights

Coronary artery ectasia (CAE) has been defined as localized or diffuse dilation of the coronary arteries seen on coronary angiography and exceeding by 1.5 times the diameter of an adjacent and normal segment.[1,2] Prevalence of CAE among patients who underwent angiographic studies was 0.3-5.3%.3 Coronary artery ectasia may be the result of etiologies that are atherosclerotic (50%), congenital (20‐30%), related to inflammatory or connective tissue diseases (10-20%), or iatrogenic following coronary interventions (3-4%).[4]
matrix metalloproteinases (MMPs)-9 levels were higher in CAE than in coronary artery disease (CAD) and normal coronary artery (NCA) groups, and were much higher in CAD than in the NCA group (Figure 3)
tissue inhibitors of metalloproteinases (TIMPs)-2 was significantly reduced in CAE patients compared with NCA subjects (Figure 4)

Summary

Introduction

Coronary artery ectasia (CAE) has been defined as localized or diffuse dilation of the coronary arteries seen on coronary angiography and exceeding by 1.5 times the diameter of an adjacent and normal segment.[1,2] Prevalence of CAE among patients who underwent angiographic studies was 0.3-5.3%.3 Coronary artery ectasia may be the result of etiologies that are atherosclerotic (50%), congenital (20‐30%), related to inflammatory or connective tissue diseases (10-20%), or iatrogenic following coronary interventions (3-4%).[4]. Coronary artery ectasia (CAE) has been defined as localized or diffuse dilation of the coronary arteries seen on coronary angiography and exceeding by 1.5 times the diameter of an adjacent and normal segment.[1,2] Prevalence of CAE among patients who underwent angiographic studies was 0.3-5.3%.3. Ozbay et al.[8] reported an ectasia distribution of 60% in RCA, 57% in Cx and 50% in LAD, with 1-, 2- and 3-vessel ectasia accounting for 42.5%, 45% and 12.5%, respectively. Turhan et al.[7] reported CAE distribution of 81% in RCA, 78% in LAD and 75% in Cx, with 1-, 2- and 3-vessel ectasia proportions of 19%, 28% and 53%, while rates of 1- to 6-segmental ectasia were 3%, 9%, 41%, 16%, 22% and 9%, respectively, with a mean of 3.4±1.2 ectatic segments per case. Ectasia often presents in 3-vessel and 3-segment forms and is most commonly found in the RCA

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