The coronary artery ectasia and ABO blood groups distribution

The Investigation of Relationship between Coronary Artery Ectasia, Benign Prostatic Enlargement, and Lower Urinary Tract Symptoms

Objective: The specific causative mechanisms of abnormal luminar dilatation in Coronary Artery Ectasia (CAE) are essentially unknown. Destruction of extracellular matrix may be responsible for the ectasia formation. Thus, we investigated the role of Matrix Metalloproteinases (MMP9), and inflammatory marker (high-sensitive C-reactive protein) in CAE patients. Methods: This study consisted of 30 consecutive CAE patients, 30 obstructive Coronary Artery Disease (CAD) patients, and 20 controls with normal coronary arteries undergoing cardiac catheterization. Plasma levels of MMP-9, and hs-CRP were measured. Results: Hs-CRP level was significantly higher in the CAE group than both in CAD and control groups (2.3±0.5, 1.19±0.54, 0.8±0.3 mg/l, respectively, both p<0.001), while, MMP-9 level was significantly higher in both CAE group and CAD than control groups (27.71±4.7, 25.2±4.1, 18.6±3.3 ng/ml, respectively, both p<0.001). In subgroup analyses, MMP-9 level was significantly higher in CAE patients with multivessel involvement compared with those with single-vessel ectasia (29.4±3.1 vs. 25.2±5.5 ng/ml, P=0.01), while hs CRP level was comparable in both groups (2.3±0.52 vs. 2.4±0.45 ng/ml, P=0.82). Conclusions: Our results suggest that the increased levels of MMP-9, hs-CRP may be responsible for ectasia formation in patients with CAE and plasma level of MMP-9 is correlated with the severity of CAE.

Receptor for advanced glycation end products polymorphisms in coronary artery ectasia

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.

In the past, the relationship between coronary artery disease (CAD) and been studied extensively. The ABO blood group has a significant effect on homeostasis and is therefore associated with adverse cardiovascular events. This study aimed to determine the distribution of ABO blood group and rhesus (Rh) status (ABO/Rh) in patients with different severity of CAD in Iranian community. A total of 1,236 CAD patients undergoing angiography were evaluated and their ABO/Rh blood type was determined in a study center between February 2005 and December 2010. Of the 1,236 records, only 1,046 medical documents recorded the number of involved vessels. The patients were classified according to the number of significantly affected stenotic vessels into single vessel (1VD), two vessels (2VD), and three vessels (3VD) disease subgroups. A substantially different ABO/Rh blood groups distribution was seen in the examined samples (O: 29.7%, A: 39.7%, B: 22.2%, AB: 8.3%, Rh positivity: 89.2%). The ABO/Rh blood group phenotype distribution in CAD patients with 1VD, 2VD, and 3VD was as follows: 37.5%, 41.3%, and 41.5%, respectively, for group A; 24.1%, 20.5%, and 20.6%, respectively, for group B; 31.2%, 26.8%, and 30.2%, respectively, for group O; 7.1%, 11.4% and 7.7%, respectively, for group AB (p = 0.26), and 88.7%, 90.5%, and 87.6%, respectively, for Rh positivity, (p = 0.47). In addition, no significant correlation was not found among the ABO/Rh blood group distribution and the number of vessels involved, however, according to the different distribution of ABO/Rh blood group in CAD patients and healthy population, ABO/Rh might have an unknown role in CAD patients. Keywords: Coronary artery disease, Blood group, Stenosis, Vessel, Rhesus.

Context: Distribution of blood groups varies among ethnic groups throughout the world. Blood groups of tribals should be determined as they are ethnically different from the main population of Bangladesh. Materials and Methods: To observe the distribution pattern of ABO and Rh blood groups and to compare the groups among Manipuris (1434) and Khasias (204), this descriptive crosssectional study was conducted in the Department of Physiology, Dhaka Medical College, Dhaka, from July 2006 to June 2007. Manipuris were divided in Bishnupriya (658), Meitei (460) and Meitei-Pangan (316) according to their ethnic origin. Data were collected from Manipuri (12) and Khasia (2) localities selected by systematic random sampling. ABO and Rh blood groups of participants were determined by the antigen antibody agglutination test of slide method. Data from groups were compared by chi-square test with 95% confidence limit. Results: There are significant variations in the distribution of ABO (p&lt;0.001) and Rh (p&lt;0.001) blood groups among all study groups. Blood group A was more frequent among Meiteis (40%) and Meitei-Pangans (42.41%) whereas blood group O was more frequent in Bishnupriyas (47.72%) and Khasias (35.29%). In all tribal communities, AB blood group was least frequent. Rh positive participants (97.43%) were more than Rh negative (2.57%). In Khasias, no Rh negative group was found. Rh negativity was more in Bishnupriyas (4.9%) which was significantly higher than Meiteis (0.87%) and Meitei-Pangans. (1.94%) (X2=16.7; p&lt;0.001). Conclusion: Distribution of ABO blood groups varies among the Manipuris and Khasias. Significant variation is also found in three groups of Manipuris and the distribution corresponds with the pattern of their ancestors. Key words: ABO blood group; Rh blood group; tribal population; Sylhet. DOI: http://dx.doi.org/10.3329/jdmc.v20i1.8581 J Dhaka Med Coll. 2011; 20(1) :44-50

The specific causative mechanisms of abnormal luminar dilatation in coronary artery ectasia (CAE) are essentially unknown. Destruction of extracellular matrix may be responsible for the ectasia formation. Thus, we investigated the role of matrix metalloproteinases (MMP9), and inflammatory marker (high-sensitive C-reactive protein) in CAE patients. This study consisted of 30 consecutive CAE patients, 30 obstructive coronary artery disease (CAD) patients, and 20 controls with normal coronary arteries undergoing cardiac catheterization. Plasma levels of MMP-9, and hs-CRP were measured. Hs-CRP level was significantly higher in the CAE group than both in CAD and control groups (2.3 ± 0.5, 1.19 ± 0.54, 0.8 ± 0.3 mg/l, respectively , both p < 0.001 ), while , MMP-9 level was significantly higher in both CAE group and CAD than control groups (27.71 ± 4.7, 25.2 ± 4.1 , 18.6 ± 3.3 ng/ml, respectively , both p < 0.001 ). In subgroup analyses, MMP-9 level was significantly higher in CAE patients with multivessel involvement compared with those with single-vessel ectasia (29.4 ± 3.1 vs. 25.2 ± 5.5 ng/ml, P = 0.01), while hs CRP level was comparable in both groups (2.3 ± 0.52 vs. 2.4 ± 0.45 ng/ml, P = 0.82). Our results suggest that the increased levels of MMP-9, hs-CRP may be responsible for ectasia formation in patients with CAE and plasma level of MMP-9 is correlated with the severity of CAE.

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.

The relation between coronary artery ectasia (CAE) and erectile dysfunction (ED) has not been studied so far. Hence, we decided to investigate the erectile function score in patients with CAE. We investigated the international index of erectile function (IIEF)-5 score in 34 men with CAE, 38 men with coronary artery disease (CAD), and 30 male controls with normal coronary arteries whose mean ages were 53.2 ± 5.6, 51.4 ± 7.8, and 49.6 ± 8.6 years, respectively. Erectile function was evaluated by the five-item version of the IIEF-5. Each question is scored from 0 to 5. CAE was defined as being without any stenotic lesions with a visual assessment of the coronary arteries showing a luminal dilatation 1.5-fold or more of the adjacent normal coronary segments. IIEF-5 scores in CAE group were found statistically significantly lower than the control group (P<0.001). There were no statistically significant differences in IIEF-5 scores between CAE and CAD groups (P=0.13). We have shown for the first time that patients with CAE have lower IIEF-5 scores compared with controls with normal coronary angiograms. Many studies reported that endothelial dysfunction in patients with CAE was more dominant than those with CAD. This study suggests that ED and CAE may be different manifestations of a common underlying vascular pathology and vasculogenic ED is frequently seen in CAE at least as much as in CAD.

AimThe present study was designed to investigate mean platelet volume (MPV) values in coronary artery ectasia (CAE) patients in comparison with individuals with coronary artery disease and normal coronary angiograms.Material and methodsPatients with stable angina pectoris and scheduled for angiography were included in the study. Those with isolated coronary ectasia were evaluated in the coronary angiography. Mean platelet volume was measured in 126 patients (mean age: 57.2 ±11.3 years) with isolated CAE, 126 patients (mean age: 56.3 ±10.4 years) with coronary artery disease (CAD) and 122 control subjects (mean age: 58.1 ±11.1 years). Coronary artery ectasia was defined as lack of stenotic lesion, on visual assessment, of the coronary arteries with a luminal dilatation 1.5-fold or more of the adjacent normal coronary segments. Mean platelet volume values were recorded in all patients. Ectasia severity was evaluated and categorized in accordance with the Markis categorization.ResultsA significant difference with respect to age, sex, hypertension, diabetes mellitus, and cigarette use between the study groups was not found (p > 0.05). Mean platelet volume was significantly higher in patients with CAE and CAD than in the control group (9.8 ±3.8 fl and 9.7 ±3.9 fl vs. 8.8 ±3.3 fl, p < 0.001). There were no statistically significant differences between CAE and CAD groups. When type I and type IV subgroups were compared in patients with coronary artery ectasia, MPV was detected as statistically high in the type I subgroup (p = 0.026).ConclusionsIt was shown that patients with CAE and CAD have higher MPVs than subjects with normal coronary angiograms. Moreover, it was detected that in coronary artery ectasias, the increase in MPV is related to both the atherosclerotic process and severity of the disease.

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.

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.

Dysregulation of the metabolism of the extracellular matrix (ECM) may contribute to coronary artery ectasia (CAE). This study evaluated the turnover of main ECM components and related proteolytic enzymes activities. In this study, thirty patients with CAE, 30 patients with coronary artery disease (CAD) and 30 subjects with normal coronary arteries (Control) were selected. The following circulating ECM metabolism markers were measured: soluble elastin (sElastin), collagen type I cross-linked telopeptides (ICTP), procollagen type I carboxy terminal peptide (PICP), protocollagen III N-terminal propeptide (PIIINP), and procollagen a1(III) C-terminal propeptide (PIIICP). Serum total elastase activity and total matrix metalloproteinase (MMP) activity were also determined. The level of sElastin was higher in the CAE group than in the CAD and Control groups (P1 = 0.009, P2 = 0.000). There was no difference in ICTP (P = 0.168) or PIIICP (P = 0.079) among the three groups. PICP was significantly elevated in CAE (P1 = 0.001, P2 = 0.002). PIIINP was also significantly increased in CAE (P1 = 0.002, P2 = 0.007). Total elastase activity was higher in the CAE group than in the other two groups (P1 = 0.006, P2 = 0.022). Total MMP activity was significantly higher in the CAE group than the Control group (P2 = 0.013) but not higher than the CAD group (P1 = 0.477). In conclusion, within CAE patients the main changes in ECM metabolism were increased degradation of elastin fibres and the transition of collagen from type III to type I. Elastase and MMPs appear to be associated with this kind of ECM turnover.

To investigate the clinical and angiographic characteristics of coronary artery ectasia (CAE) and its relation with the inflammatory marker, HsCRP. An observational study. Rawalpindi Institute of Cardiology, Rawalpindi, from April 2015 till November 2016. Eighty-one patients with CAE and 57 age matched patients with stenotic coronary artery disease (CAD), but without CAE, were included in the study. Clinical, angiographic, and laboratory data were documented. Chi-square test was used to compare coronary risk factors between two groups. T test was used to compare means between the groups. Analysis of variance was used to analyse HsCRP levels among various types of ectasia. Correlation analysis was used to study association of ectasia with different risk factors. Males were predominant in both with & without CAE. Hypertension, smoking and obesity were significantly more common among CAE patients than those without (60.5% vs. 52.6%, 56.8% vs. 43.9% and 80.2% vs. 14%, respectively). Diabetes was much less in CAE group (32.1% vs. 42.1%). HsCRP was higher in patients with CAE than those without and was significantly higher in patients with more extensive ectasia. Majority (65.4%) of CAE patients had significant CAD; whereas, only 7.4% had isolated CAE. Most common artery involved was RCA (70.4% of total) and most common pattern was single ectatic vessel. Obesity and smoking predispose to CAE, along with male sex and hypertension. While diabetes is negatively associated with CAE. HsCRP levels tend to be higher in ectasia patients, especially those with severe forms. Finally, CAE has a predilection for RCA.

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.