Coronary Artery Ectasia Patients Research Articles

Ectatic coronary arteries, a cause for myocardial infarction with non-obstructive coronary arteries

Ectatic coronary arteries are an abnormal dilation of the coronary arteries and can contribute to the development of myocardial infarction with non-obstructive coronary arteries (MINOCA). We present a case of a previously unscreened 27-year-old man who presented with ischaemic type chest pain and was found to have ectatic coronary arteries on coronary angiogram. Despite the absence of significant stenosis, the patient experienced an acute myocardial infarction. The patient was treated with dual antiplatelet therapy and statins, and subsequent assessments showed normal echocardiography findings. Coronary artery ectasia (CAE) is a relatively uncommon condition often associated with coronary artery disease (CAD) and atherosclerosis. While antiplatelet therapy is indicated in CAE patients, the use of anticoagulation remains uncertain. Further research and clinical guidelines are needed to establish standardised management approaches for patients with CAE and MINOCA.

Endothelin-converting Enzyme-1b Genetic Variants Increase the Risk of Coronary Artery Ectasia.

Coronary artery ectasia (CAE), defined as a 1.5-fold or greater enlargement of a coronary artery segment compared to the adjacent normal coronary artery, is frequently associated with atherosclerotic coronary artery disease (CAD). Membrane-bound endothelin converting enzyme-1 (ECE-1) is involved in the maturation process of the most potent vasoconstrictor ET-1. Polymorphisms in the endothelin (ET) gene family have been shown associated with the development of atherosclerosis. This study aims to investigate the effects of rs213045 and rs2038089 polymorphisms in the ECE-1 gene which have been previously shown to be associated with atherosclerosis and hypertension (HT), in CAE patients. Ninety-six CAE and 175 patients with normal coronary arteries were included in the study. ECE-1b gene variations rs213045 and rs2038089 were determined by real-time PCR. The frequencies of rs213045 C > A (C338A) CC genotype (60.4% vs. 35.4%, p < 0.001) and rs2038089 T > C T allele (64.58% vs. 35.42%, p = 0.017) were higher in the CAE group compared to the control group. The multivariate regression analysis showed that the ECE-1b rs213045 CC genotype (p = 0.001), rs2038089 T allele (p = 0.017), and hypercholesterolemia (HC) (p = 0.001) are risk factors for CAE. Moreover, in nondiabetic individuals of the CAE and control groups, it was observed that the rs213045 CC genotype (p < 0.001), and rs2038089 T allele (p = 0.003) were a risk factor for CAE, but this relationship was not found in the diabetic subgroups of the study groups (p > 0.05). These results show that ECE-1b polymorphisms may be associated with the risk of CAE and this relationship may change according to the presence of type II diabetes.

Receptor for advanced glycation end products polymorphisms in coronary artery ectasia

BackgroundAlthough the implication of receptor of advanced glycation endproducts (RAGE) has been reported in coronary artery disease, its roles in coronary artery ectasia (CAE) have remained undetermined. Furthermore, the effect of RAGE polymorfisms were not well-defined in scope of soluble RAGE (sRAGE) levels. Thus, we aimed to investigate the influence of the functional polymorphisms of RAGE -374T > A (rs1800624) and G82S (rs2070600) in CAE development. MethodsThis prospective observational study was conducted in 2 groups selected of 2452 patients who underwent elective coronary angiography (CAG) for evaluation after positive noninvasive heart tests. Group-I included 98 patients with non-obstructive coronary artery disease and CAE, and Group-II (control) included 100 patients with normal coronary arteries. SNPs were genotyped by real-time PCR using Taqman® genotyping assay. Serum sRAGE and soluble lectin-like oxidized receptor-1 (sOLR1) were assayed by ELISA and serum lipids were measured enzymatically. ResultsThe frequencies of the RAGE -374A allele and -374AA genotype were significantly higher in CAE patients compared to controls (p < 0.001). sRAGE levels were not different between study groups, while sOLR1 levels were elevated in CAE (p = 0.004). In controls without systemic disease, -374A allele was associated with low sRAGE levels (p < 0.05), but this association was not significant in controls with HT. Similarly, sRAGE levels of CAE patients with both HT and T2DM were higher than those no systemic disease (p = 0.02). The -374A allele was also associated with younger patient age and higher platelet count in the CAE group in both total and subgroup analyses. In the correlation analyses, the -374A allele was also negatively correlated with age and positively correlated with Plt in all of these CAE groups. In the total CAE group, sRAGE levels also showed a positive correlation with age and a negative correlation with HDL-cholesterol levels. On the other hand, a negative correlation was observed between sRAGE and Plt in the total, hypertensive and no systemic disease control subgroups. Multivariate logistic regression analysis confirmed that the -374A allele (p < 0.001), hyperlipidemia (p < 0.05), and high sOLR1 level (p < 0.05) are risk factors for CAE. ROC curve analysis shows that RAGE -374A allele has AUC of 0.713 (sensitivity: 83.7 %, specificity: 59.0 %), which is higher than HLD (sensitivity: 59.2 %, specificity: 69.0 %), HT (sensitivity: 62.4 %, specificity: 61.1 %) and high sOLR1 level (≥0.67 ng/ml)) (sensitivity: 59.8 %, specificity: 58.5 %). ConclusionBeside the demonstration of the relationship between -374A allele and increased risk of CAE for the first time, our results indicate that antihypertensive and antidiabetic treatment in CAE patients causes an increase in sRAGE levels. The lack of an association between the expected -374A allele and low sRAGE levels in total CAE group was attributed to the high proportion of hypertensive patients and hence to antihypertensive treatment. Moreover, the RAGE -374A allele is associated with younger age at CAE and higher Plt, suggesting that -374A may also be associated with platelet activation, which plays a role in the pathogenesis of CAE. However, our data need to be confirmed in a large study for definitive conclusions.

Differential Expression of Circulating Damage-Associated Molecular Patterns in Patients with Coronary Artery Ectasia.

Coronary artery ectasia (CAE) is defined as abnormal dilation of a coronary artery with a diameter exceeding that of adjacent normal arterial segment by >1.5 times. CAE is a pathological entity of the coronary arteries and characterized as a variant of coronary atherosclerosis. CAE frequently coexists with coronary artery disease (CAD). While inflammation appears to be involved, the pathophysiology of CAE remains unclear. Damage-associated molecular patterns (DAMPs), defined as endogenous molecules released from stressed or damaged tissue, are deemed as alarm signals by the innate immune system. Inflammatory agents can generate DAMPs and DAMPs can create a pro-inflammatory state. In a prospective cross-sectional study, we enrolled 29 patients with CAE and non-obstructive CAD, 19 patients with obstructive CAD without CAE, and 14 control subjects with normal (control) coronary arteries age- and sex-matched with the CAE patients, to investigate the differential expression of plasma DAMPs. Patients with CAE and non-obstructive CAD had increased plasma levels of the DAMPs S100B, S100A12, HMGB1, and HSP70, the DAMPs receptor TLR4, and miR328a-3p compared to CAD and controls. Plasma levels of the mir328a-3p target the protective soluble form of the DAMPs receptor for advanced glycation end products (sRAGE), and the antioxidant DJ-1 was decreased in both CAE and CAD compared to controls. In an in vitro human umbilical vein endothelial cells model, circulating levels of S100B, HMGB1, HSP70 as well as CAE patient plasma induced inflammatory responses. The differential expression of the DAMPs S100B, HSP70, HMGB1, and their receptors TLR4 and sRAGE in CAE versus CAD makes them attractive novel biomarkers as therapeutic targets and therapeutics.

Next-generation sequencing of prolidase gene identifies novel and common variants associated with low prolidase in coronary artery ectasia.

Decreased collagen biosynthesis and increased collagenolysis can cause ectasia progression in the arterial walls. Prolidase is a key enzyme in collagen synthesis; a decrease in prolidase activity or level may decrease collagen biosynthesis, which may contribute to ectasia formation. Considering that, the variations in PEPD gene encoding prolidase enzyme were evaluated by analyzing next-generation sequencing (NGS) for the first time together with known risk factors in coronary artery ectasia (CAE) patients. Molecular analysis of the PEPD gene was performed on genomic DNA by NGS in 76 CAE patients and 76 controls. The serum levels of prolidase were measured by the sandwich-ELISA technique. Serum prolidase levels were significantly lower in CAE group compared to control group, and it was significantly lower in males than females in both groups (p < 0.001). On the other hand, elevated prolidase levels were observed in CAE patients in the presence of diabetes (p < 0.001), hypertension (p < 0.05) and hyperlipidemia (p < 0.05). Logistic regression analysis demonstrated that the low prolidase level (p < 0.001), hypertension (p < 0.02) and hyperlipidemia (p < 0.012) were significantly associated with increased CAE risk. We identified four missense mutations in the PEPD gene, namely G296S, T266A, P365L and S134C (novel) that could be associated with CAE. The pathogenicity of these mutations was predicted to be "damaging" for G296S, S134C and P365L, but "benign" for T266A. We also identified a novel 5'UTR variation (Chr19:34012748 G>A) in one patient who had a low prolidase level. In addition, rs17570 and rs1061338 common variations of the PEPD gene were associated with low prolidase levels in CAE patients, while rs17569 variation was associated with high prolidase levels in both CAE and controls (p < 0.05). Our findings indicate that the low serum prolidase levels observed in CAE patients is significantly associated with PEPD gene variations. It was concluded that low serum prolidase level and associated PEPD mutations may be potential biomarkers for the diagnosis of CAE.

Five-years' prognostic analysis for coronary artery ectasia patients with coronary atherosclerosis: A retrospective cohort study.

BackgroundMost of coronary artery ectasia (CAE) patients have comorbid coronary atherosclerosis. It was lack of prognostic data for CAE patients with coronary heart disease (CHD) and for whom with acute myocardial infarction (AMI).ObjectiveTo determine the overall prognosis for CAE patients.Materials and methodsThis study was a retrospective cohort study. Fifty-one patients with CAE and comorbid AMI (CAE + AMI) and 108 patients with CAE and comorbid CHD (CAE + CHD) were enrolled and matched to non-CAE subjects at a ratio of 1:3 using a propensity score method, respectively. Controls for CAE + AMI group were 153 AMI patients, controls for CAE group were 324 CHD patients and 329 participants with relatively normal coronary arteries (CON). We followed them up to observe major cardiovascular events (MACE).ResultsThe Kaplan-Meier curves showed that the prognosis in CAE + AMI group was worse than in AMI group (5-year non-MACE rate: 62.70% vs. 79.70%, P = 0.010), the prognosis in CAE group was worse than in CHD and CON groups (5-year non-MACE rate: 74.10% vs. 85.80% and 96.70%, respectively, P = 0.000). The main MACEs in CAE + AMI and CAE groups were AMI reoccurrence (19.61% vs. 4.57%, P = 0.002) and re-hospitalization due to repeated angina pectoris (14.81% vs. 8.33% and 2.74%, P = 0.000), respectively. Additionally, the COX regression analysis revealed that the protective factors for preventing MACE in CAE + AMI group included antiplatelet agents (hazard ratio = 0.234, P = 0.016) and angiotensin-converting enzyme inhibitor/angiotensin receptor inhibitor (ACEI/ARB, hazard ratio = 0.317, P = 0.037). Whereas the main factor promoting MACE in CAE group was the degree of coronary stenosis (Gensini score, hazard ratio = 1.011, P = 0.022).ConclusionThe prognosis of patients with CAE + AMI was worse than that of those with AMI. The overall prognosis of patients with CAE was worse than that of those with CHD. CAE + AMI and CAE groups had different characteristics; the former was prone to AMI reoccurrence, and the latter was prone to repeated angina pectoris. To prevent MACE, medications, including antiplatelets and ACEI/ARBs, are indicated for patients with CAE + AMI, whereas prevention of the progression of atherosclerotic lesions is indicated for patients with CAE.

Clinical Predictors of Coronary Artery Ectasia.

Coronary artery ectasia (CAE) is defined as abnormal dilation of a coronary artery ≥1.5 times the normal segment. We aimed to determine the prevalence and clinical predictors of CAE. This was a prospective analysis performed on 6465 patients undergoing coronary angiography. Patients were divided based on the presence or absence of CAE and compared for angiographic characteristics and clinical risk factors. The prevalence of CAE was 7%, CAE associated with coronary artery stenosis was 5.4%, and isolated CAE was 1.6%. The mean age of presentation in CAE patients was 60years, with male predominance (83.8%) and stable angina was the most common presentation. The left anterior descending artery (LAD) (51.7%) was the most commonly involved vessel, with diffuse ectasia more commonly seen in right coronary artery and discrete ectasia in LAD. Type 4 CAE was the most common type (92.4%). Hypertension, diabetes, smoking, dyslipidemia, and obesity were found in 62.4%, 35.3%, 45.3%, 54.9%, and 23.3%, respectively in CAE patients, with significant association with smoking (Odds Ratio = 3.06). The prevalence of CAE was 7% and was frequently associated with atherosclerotic coronary disease. Smoking was a significant predisposing factor for CAE.

Metabolomic analysis of serum from pure coronary artery ectasia patients based on UPLC-QE/MS technique

BackgroundCoronary artery ectasia (CAE) is a cardiovascular disorder characterized by abnormal coronary artery dilation and disturbed coronary flow. The exact pathophysiology of CAE is still unclear. We aimed to investigate differences in metabolomic profiles between CAE patients and healthy controls. MethodsRadial artery blood samples were collected from 14 pure CAE patients, 12 mixed CAE patients with atherosclerosis, and 14 controls with normal angiography. Differential serum metabolites were analyzed by untargeted ultra-high performance liquid chromatography-mass spectrometry. Serum ICAM-1, VEGF, ROS, and glutathione levels were also measured. ResultsTen metabolites distinguished pure CAE patients from controls and mixed CAE, including 1-cyano-2-hydroxy-3-butene, 2,3-dihydro-6-methyl-5-(5-methyl-2-furanyl)-1H-pyrrolizine, 2-propionylpyrrole, 2-pyrrolidinone, 3-(2-furanylmethylene)pyrrolidine, D-alanine, furanofukinin, o-ethyltoluene, rotundine A, and SM(d18:1/18:1(9Z)). Related metabolic pathways include amino acid metabolism, sphingolipid dysfunction, energy metabolism, mitochondrial dysfunction, and oxidative stress. Serum concentrations of ICAM-1, VEGF and ROS were significantly elevated in CAE patients compared to controls, while glutathione decreased significantly in CAE patients. Moreover, ICAM-1 levels were negatively correlated with 2-propionylpyrrole, and VEGF levels were negatively correlated with SM(d18:1/18:1(9Z)), while GSH and ROS levels were correlated with the abundance of SM(d18:1/18:1(9Z)), further confirming systemic inflammation and oxidative stress in CAE. ConclusionsThis is the first report describing differential serum metabolomic profiles of pure CAE patients compared to mixed CAE and healthy controls, which revealed 10 potential biomarkers that can provide an early diagnosis of pure CAE. These discriminatory metabolites and related metabolic pathways can help to better understand the pathogenesis of pure CAE.

Evaluation of Drugs and Strategies for Treating Coronary Artery Ectasia: Update and Future Perspective

Context: Although the mechanisms involved in the pathogenesis of coronary artery ectasia (CAE) and its treatment methods are not known for certainty, increased inflammatory and coagulation responses can be responsible for the formation of ectasia due to vascular disorders. Evidence Acquisition: The content used in this paper was obtained from English language articles (2005 - 2020) retrieved from the PubMed database and Google scholar search engine using “coronary artery ectasia”, “treatment”, “drug”, and “aneurysm” keywords. Results: The proven effect of inflammation and coagulation in CAE has posed a significant challenge for disease management. Therefore, anti-inflammatory and anticoagulation drugs can be treatment options for these patients. Increased inflammatory responses and some coagulation factors in CAE patients is undeniable. The study of these two systems in CAE patients and the evaluation of drugs affecting these mechanisms to achieve a definitive conclusion requires further and more extensive studies. Conclusions: We evaluated the hypothesis that anti-inflammatory and anticoagulation drugs with improved vascular endothelial function may accelerate the healing process of CAE patients; thus, they may be treatment options. Finally, it can be said that identifying molecular pathways related to drugs can improve their effectiveness in treating patients and increasing their survival. In addition, identifying upstream and downstream pathways can help diagnose the disease pathogenesis in addition to treating patients.

Inflammatory Biomarkers in Coronary Artery Ectasia: A Systematic Review and Meta-Analysis.

Isolated coronary artery ectasia (CAE) is a relatively rare clinical entity, the pathogenesis of which is poorly understood. More and more evidence is accumulating to suggest a critical inflammatory component. We aimed to elucidate any association between neutrophil to lymphocyte ratio and coronary artery ectasia. A systematic MEDLINE database, ClinicalTrials.gov, medRxiv, Scopus and Cochrane Library search was conducted: 50 studies were deemed relevant, reporting on difference in NLR levels between CAE patients and controls (primary endpoint) and/or on high-sensitive CRP, IL-6, TNF-a and RDW levels (secondary endpoint), and were included in our final analysis. (PROSPERO registration number: CRD42021224195). All inflammatory biomarkers under investigation were found higher in coronary artery ectasia patients as compared to healthy controls (NLR; SMD = 0.73; 95% CI: 0.27–1.20, hs-CRP; SMD = 0.96; 95% CI: 0.64–1.28, IL-6; SMD = 2.68; 95% CI: 0.95–4.41, TNF-a; SMD = 0.50; 95% CI: 0.24–0.75, RDW; SMD = 0.56; 95% CI: 0.26–0.87). The main limitations inherent in this analysis are small case-control studies of moderate quality and high statistical heterogeneity. Our findings underscore that inflammatory dysregulation is implicated in coronary artery ectasia and merits further investigation.

Treatment and Outcome of Patients With Coronary Artery Ectasia: Current Evidence and Novel Opportunities for an Old Dilemma.

Coronary artery ectasia (CAE) is defined as a diffuse or focal dilation of an epicardial coronary artery, which diameter exceeds by at least 1. 5 times the normal adjacent segment. The term ectasia refers to a diffuse dilation, involving more than 50% of the length of the vessel, while the term aneurysm defines a focal vessel dilation. CAE is a relatively uncommon angiographic finding and its prevalence ranges between 0.3 and 5% of patients undergoing coronary angiography. Although its pathophysiology is still unclear, atherosclerosis seems to be the underlying mechanism in most cases. The prognostic role of CAE is also controversial, but previous studies reported a high risk of cardiovascular events and mortality in these patients after percutaneous coronary intervention. Despite the availability of different options for the interventional management of patients with CAE, including covered stent implantation and stent-assisted coil embolization, there is no one standard approach, as therapy is tailored to the individual patient. The abnormal coronary dilation, often associated with high thrombus burden in the setting of acute coronary syndromes, makes the interventional treatment of CAE patients challenging and often complicated by distal thrombus embolization and stent malapposition. Moreover, the optimal antithrombotic therapy is debated and includes dual antiplatelet therapy, anticoagulation, or a combination of them. In this review we aimed to provide an overview of the pathophysiology, classification, clinical presentation, natural history, and management of patients with CAE, with a focus on the challenges for both clinical and interventional cardiologists in daily clinical practice.

Acute Coronary Syndrome Revealing Coronary Artery Ectasia: Case Report

Coronary artery ectasia (CAE) is a dilation of the coronary artery lumen. The term "ectasia" differs from "coronary aneurysm". The first one refers to diffuse dilation of a coronary artery, while the second designate a focal coronary dilation. In most of cases, it is associated with atherosclerotic disease. CAE predispose to acute coronary events because it disturbs coronary flow and increases blood viscosity. Conventionally, CAE was treated by oral anticoagulants and it has been considered as a valid treatment option. The usual treatment of acute coronary syndrome (ACS) including dual antiplatelet therapy (DAPT) is widely employed in CAE patients presenting with ACS.We report the case of a 71year-old man who suffered from angina chest pain revealing a myocardial infraction with inferior ST-elevation. Coronary angiography demonstrated diffused coronary artery ectasia with thrombotic occlusion in the distal segment of right coronary artery. It was managed with medical treatment including DAPT and oral anticoagulation.

Development and Validation of a Nomogram for Predicting the Risk of Adverse Cardiovascular Events in Patients with Coronary Artery Ectasia

Coronary artery ectasia (CAE) is a rare finding and is associated with poor clinical outcomes. However, prognostic factors are not well studied and no prognostication tool is available. In a derivation set comprising 729 consecutive CAE patients between January 2009 and June 2014, a nomogram was developed using Cox regression. Total of 399 patients from July 2014 to December 2015 formed the validation set. The primary outcome was 5-year major adverse cardiovascular events (MACE), a component of cardiovascular death and nonfatal myocardial infarction. Besides the clinical factors, we used quantitative coronary angiography (QCA) and defined QCA classification of four types, according to max diameter (< or ≥5 mm) and max length ratio (ratio of lesion length to vessel length, < or ≥1/3) of the dilated lesion. A total of 27 cardiovascular deaths and 41 nonfatal myocardial infarctions occurred at 5-year follow-up. The nomogram effectively predicted 5-year MACE risk using predictors including age, prior PCI, high sensitivity C-reactive protein, N-terminal pro-brain natriuretic peptide, and QCA classification (area under curve [AUC] 0.75, 95% CI 0.68–0.82 in the derivation set; AUC 0.71, 95% CI 0.56–0.86 in the validation set). Patients were classified as high-risk if prognostic scores were ≥155 and the Kaplan–Meier curves were well separated (log-rank p < 0.001 in both sets). Calibration curve and Hosmer–Lemeshow test indicated similarity between predicted and actual 5-year MACE survival (p = 0.90 in the derivation and p = 0.47 in the validation set). This study developed and validated a simple-to-use method for assessing 5-year MACE risk in patients with CAE.

Is Coronary Artery Ectasia a Progressive Disease? A Self-Controlled Retrospective Cohort Study.

Objective: It is essential to understand whether coronary artery ectasia (CAE) progresses over time because the patients might be under the risk of coronary rupture, and stent implant should be avoided if ectatic changes progress.Methods: A consecutive series of 99 CAE patients who had undergone coronary angiography at least twice were enrolled and followed up for 1–16 years until they received a second angiogram. Subjects were divided into two groups (1–5 vs. 5–16 years of follow-up), then the basic clinical characteristics and coronary artery images were compared over time.Results: (1) All CAE patients exhibited atherosclerosis, and a majority presented with acute myocardial infarction. Most baseline clinical characteristics were relatively stable. (2) Atherosclerosis (indicated by the distribution of stenosis in coronary vessels) and the Gensini scores progressed significantly. Ectasia extent showed minimal changes as indicated by blood vessel involvement, Markis type, coronary blood flow, ectasia diameter, and ectasia length. (3) Multilinear regression analysis revealed that the underlying factors related to stenosis evolution indicated by fold of Gensini score were: longer time interval, lower baseline Gensini score, and higher hypersensitive C-reactive protein concentration. (4) There was a relationship between the ectatic diameter and the extent of stenosis.Conclusions: For CAE patients with atherosclerosis followed for 1–16 years, there was minimal CAE progression, while the atherosclerosis progressed and the ectasia extent was related to degree of stenosis. The results indicate that prevention and treatment of atherosclerotic changes might have more clinical significance than addressing ectatic changes.

Abstract 12511: Differential Regulation of Circulating Damage-Associated Molecular Patterns in Patients With Coronary Artery Ectasia

Introduction: Coronary artery ectasia (CAE) defined as localized or diffuse non-obstructive coronary lesions is a rare but well-recognized pathological entity of the coronary arteries and characterized as a variant of coronary atherosclerosis. CAE commonly coexists with coronary artery disease (CAD). Although inflammation appears to be involved, the pathophysiology behind CAE remains unclear. Danger-associated molecular patterns (DAMPs) are altered metabolism products of necrotic or stressed cells, which are deemed as alarm signals by the innate immune system. Inflammatory agents are DAMP generators and DAMPs create a pro-inflammatory state. Hypothesis: We aimed to investigate the different patterns of serum DAMPs in patients with CAE, obstructive CAD and normal coronary arteries and the prognostic role of these in the pathogenesis of CAE. Methods: In this prospective cross-sectional study, 28 patients with CAE and nonobstructive CAD were enrolled in the study, 19 patients with obstructive CAD but without CAE, and 18 control subjects with normal coronary arteries that have been matched with the CAE patients for age and sex were also enrolled in our study population. Venous blood samples of the participants were collected for serum DAMP evaluation. Results: Patients with CAE and non-obstructive CAD had increased (30-35%) serum levels of the DAMPs, the receptor for advanced glycation end products (RAGE) ligand S100B and the toll-like receptor 4 ligand heat shock protein (HSP)70 compared to control subjects and patients with CAD. Additionally, CAE and non-obstructive CAD patients had decreased (30-40%) serum levels of potential DAMPs, the antioxidant DJ-1 and soluble (s)RAGE, a decoy molecule that bind excess RAGE ligands, compared to control subjects and CAD patients. Positive correlations were observed between S100B and HSP70 (p=00564), and DJ-1 and sRAGE (p=0.00461). All evaluated serum DAMPs were not different in CAD patients compared to control subjects. Conclusion: The differential regulation of the DAMPs S100B, HSP70, DJ-1 and sRAGE in CAE versus CAD makes them attractive novel biomarkers as therapeutic targets and therapeutics.

Assessment of Longitudinal Left Ventricular Function in Patients with Coronary Artery Ectasia by 2D Speckle Tracking Echocardiography

Abstract Background Coronary artery ectasia (CAE) is one of the uncommon cardiovascular disorders. CAE is one of the known risk factors for acute coronary syndrome, its incidence ranges from 1.5%-5% of patients undergoing coronary angiography, with predominance in males. Coronary artery ectasia (CAE) is defined as dilatation of an arterial segment to a diameter at least 1.5 times that of an adjacent normal artery and involves at least one third of the affected artery (1)(1). The exact pathogenesis of CAE is not well established; however, Coronary atherosclerosis is detected in more than 50% of the patients. Objective To evaluate global left ventricle longitudinal strain by 2D speckle tracking echocardiography in patients with coronary artery ectasia and without significant (&amp;gt;50%) coronary artery stenosis. Patients and Methods This study carried on sixty patients referred to cath lab of Ain Shams university hospital for elective coronary angiography during period between January 2018 and Augest 2019. The patients were divided in to two groups (Group A) included thirty patients with ectasia in one or more of the coronary arteries without any significant coronary artery stenosis and (Group B) included thirty patients with normal coronary angiographic findings serving as control group. Results The present study showed a statistically significant decrease in EF comparing CAE group to control group .As regards other echocardiography parameters, there was a highly significant difference of LVEDD, LVEDD index, LVESD,, LVESD index, LV mass, LV mass index, LA volume and LA volume index between the two groups. Global peak longitudinal strain showed highly significant difference between two groups as its mean value was significantly lower in the CAE group. Conclusion In our study, we have concluded that global peak longitudinal strain was significantly impaired in patients with coronary artery ectasia without significant coronary artery lesion denoting subclinical LV systolic dysfunction .LV diastolic dysfunction was more prevalent in coronary artery ectasia patients compared to control subjects.

Prevalence and Long-term Outcomes of Patients with Coronary Artery Ectasia Presenting with Acute Myocardial Infarction

Coronary artery ectasia (CAE) is described in 5% of patients undergoing coronary angiography. Previous studies have shown controversial results regarding the prognostic impact of CAE. The prevalence and prognostic value of CAE in patients with acute myocardial infarction (AMI) remain unknown. In 4788 patients presenting with AMI referred for coronary angiography the presence of CAE (defined as dilation of a coronary segment with a diameter ≥1.5 times of the adjacent normal segment) was confirmed in 174 (3.6%) patients (age 62 ± 12 years; 81% male), and was present in the culprit vessel in 79.9%. Multivessel CAE was frequent (67%). CAE patients were more frequently male, had high thrombus burden and were treated more often with thrombectomy and less often was stent implantation. Markis I was the most frequent angiographic phenotype (43%). During a median follow-up of 4 years (1-7), 1243 patients (26%) experienced a major adverse cardiovascular event (MACE): 282 (6%) died from a cardiac cause, 358 (8%) had a myocardial infarction, 945 (20%) underwent coronary revascularization and 58 (1%) presented with a stroke. Patients with CAE showed higher rates of MACE as compared to those without CAE (36.8% versus 25.6%; p <0.001). On multivariable analysis, CAE was associated with MACE (HR 1.597; 95% CI 1.238-2.060; p <0.001) after adjusting for risk factors, type of AMI and number of narrowed coronary arteries. In conclusion, the prevalence of CAE in patients presenting with AMI is relatively low but was independently associated with an increased risk of MACE at follow-up.

Clinical outcome of patients with ST-elevation myocardial infarction and angiographic evidence of coronary artery ectasia.

ObjectivesThe aim of this study was to describe the prevalence of coronary artery ectasia (CAE) in patients with ST‐elevation myocardial infarction (STEMI) and to compare the long‐term outcome of subjects with and without CAE undergoing emergent coronary angiography.BackgroundThe prognostic impact of CAE in STEMI patients has been poorly investigated.MethodsThis retrospective, single‐center, study included consecutive patients with STEMI undergoing emergent coronary angiography from January 2012 to December 2017. The primary endpoint was the assessment of recurrent myocardial infarction (MI) in patients with versus those without CAE at the longest available follow‐up. The propensity score weighting technique was employed to account for potential selection bias between groups.ResultsFrom 1,674 patients with STEMI, 154 (9.2%) had an angiographic evidence of CAE; 380 patients were included in the no CAE group. CAE patients were more often males and smokers, and showed a lower prevalence of diabetes than no CAE patients. After percutaneous coronary intervention, the corrected thrombolysis in MI frame count (p < .001) and the myocardial blush grade (p < .001) were significantly lower in CAE than in no CAE patients.The mean follow‐up was 1,218.3 ± 574.8 days. The adjusted risk for the primary outcome resulted significantly higher in patients with CAE compared to those without (adjusted HR: 1.84; p = .017). No differences in terms of all‐cause and cardiac death were found between groups.ConclusionsIn this study, STEMI patients with CAE had a distinct clinical and angiographic profile, and showed a significantly higher risk of recurrent MI than those without CAE.

The Relationship of Inflammation Parameters with Obstruction in Coronary Artery Ectasia

Background: Coronary artery ectasia (CAE) is a coronary artery disease that can progress in a wide clinical spectrum, from asymptomatic cases to stable angina pectoris or acute coronary syndrome. CAE can present with an acute coronary syndrome without an obstructive lesion. Although many studies comparing isolated CAE with normal coronary arteries and coronary artery disease, CAE patients with obstructive type lesions (obstructive CAE) have never been evaluated. In this study, we aimed to compare obstructive CAE patients and isolated CAE patients in terms of various inflammatory parameters.Materials and Methods: A total of 190 patients were enrolled, including 95 obstructive CAE patients and 95 age and sex-matched isolated CAE patients. All participants were evaluated in the study consisted of patients admitted to the emergency department and diagnosed with NSTE-ACS. Systemic inflammatory parameters such as Platelet/lymphocyte ratio (PLR), Neutrophil/lymphocyte ratio (NLR), Monocyte/HDL ratio, CRP and sedimentation of the patients, were compared between two groups.Results: CRP value was found significantly higher in obstructive CAE, compared to isolated CAE [5.5 (3.0-9.0) mg/L, 4.0 (3.0-6.0) mg/L (P=0.003) respectively]. PLR value was found significantly higher in obstructive CAE compared to isolated CAE [143±76, 120±45 (p=0.015) respectively]. In multivariable logistic regression analysis, only CRP was an independent predictor of obstruction in CAE [OR:1.075 (1.011-1.142), p=0.021].Conclusions: To the best of our knowledge, this study is the first to evaluate the effects of obstructive lesions on inflammatory parameters in patients with CAE presenting with acute coronary syndrome. We have shown that systemic inflammation is increased in the presence of obstructive coronary artery disease in CAE patients.

A promising marker in patients with coronary artery ectasia: Uric acid / HDL ratio

Aim: Elevated levels of uric acid and low levels of high-density lipoprotein (HDL) cholesterol are associated with cardiovascular events and mortality. We investigated a novel marker, uric acid/HDLratio (UHR), in coronary artery ectasia patients (CAE). Materials and Methods: The present study included 104 patients (58 male, 46 female; mean age, 61±12 years) diagnosed as having isolated CAE and 110 controls (44 male, 66 female; mean age, 60±12 years) whose coronary artery findings were normal as revealed by coronary angiography. Medical records of all the patients were reviewed and the data were collected retrospectively. Baseline characteristics, hematologic and biochemistry parameters were recorded, and we calculated the value of UHRResults: The CAE group had significantly higher values of uric acid (6.48±1.62 vs. 5.37±1.12; p0.001) and UHR (0.15±0.05 vs. 0.11±0.05; p0.001). Spearman’s correlation test showed a significant association of uric acid and UHR with CAE (r=0.40, p0.001 and r=0.51, p0.001, respectively). On the other hand, HDL had a negative correlation with the presence of CAE (r=0.44, p0.120 UHR (%) values had a sensitivity of 72% and specificity of 68% for the determination of CEA.Conclusion: We observed in our study the finding in which the uric acid and UHR values were higher in individuals with CAE compared to non-CAE subjects. There was an association between UHR and CAE.