Endothelial dysfunction in patients with myocardial ischemia or infarction and nonobstructive coronary arteries.

PURPOSE: The syndromes of myocardial infarction/myocardial ischemia with No Obstructive Coronary Artery Disease (MINOCA/INOCA) are seen more and more often. Endothelial dysfunction (ED) leading to ischemic events has been reported in many of these patients. We aimed to compare patients with MINOCA and INOCA regarding brachial artery flow-mediated endothelium-dependent vasodilation (flow-mediated dilation [FMD]) and plasma concentration of cardiotrophin-1 (CT-1). METHODS: We included 42 patients with MINOCA and 38 patients with INOCA. Endothelial function was assessed by measuring FMD% and nitroglycerin-mediated dilatation (NMD%) in the brachial artery. The plasma level of CT-1 was determined by solid-phase enzyme-linked immunosorbent assay. RESULTS: FMD% was significantly lower in MINOCA than in INOCA patients (6.45 ± 2.65 vs 8.94 ± 3.32, P < .001), without significant difference in NMD% (10.69 ± 3.19 vs 12.16 ± 3.69, P = .06). Plasma CT-1 levels were not significantly different: 40.1 pg/mL (22.5-102.1) vs 37.2 pg/mL (23.5-67.2), P = .53. CONCLUSION: Our results suggest worse ED in MINOCA than in INOCA patients, but demonstrated no difference in CT-1 levels between patients with stable and unstable ischemic heart disease and normal coronary arteries.

Carotid Intima Media Thickness and Its Association With Total Bilirubin Levels in Patients With Coronary Artery Ectasia.

Atherosclerosis plays an important role in the etiopathogenesis of coronary artery ectasia (CAE). The relationship between total bilirubin (TBil) and carotid intima media thickness (cIMT) in patients with CAE has not been fully investigated. Hence, we evaluated the relationship between TBil levels and cIMT in 142 consecutive eligible patients with CAE, newly diagnosed coronary artery disease (CAD), and normal coronary arteries. There were no significant differences in TBil (P = .772) and cIMT (P = .791) between the CAE and CAD groups. Bilirubin levels were significantly lower in both CAE and CAD groups compared to the controls (P < .01). The cIMT was significantly higher in both CAE and CAD groups compared to control participants (P < .01). A negative correlation between cIMT and TBil was found in all the groups (P < .01, r = .354). We show for the first time that patients with CAE and CAD have lower TBil and greater cIMT compared to controls with normal coronary angiograms.

Association between serum adropin levels and isolated coronary artery ectasia in patients with stable angina pectoris.

OBJECTIVE: Dilation of one or more coronary artery segments to a diameter at least 1.5 times that of a normal adjacent segment is referred to as coronary artery ectasia (CAE). Adropin is a protein involved in endothelial function and is shown to have a protective effect on the regulation of cardiac functions. Atherosclerosis and endothelial dysfunction play an important role in the development of CAE. The aim of this study was to investigate the association between serum adropin levels and isolated CAE. METHODS: Patients with stable angina pectoris who underwent coronary angiography (CAG) between August 2017 and July 2018 were evaluated prospectively. A total of 92 subjects were included in the study-40 patients over 18 years old and diagnosed with isolated CAE based on CAG findings and a control group of 52 patients. RESULTS: Serum adropin level was found to be significantly lower in the isolated CAE group compared to the control group (1019.57 pg/mL and 1151.10 pg/mL, respectively, p=0.010). The isolated CAE group also exhibited a significantly higher mean platelet volume than that in the control group (10.75 fL and 10.17 fL, respectively, p=0.011). CONCLUSION: Our results show that there is an association between low serum adropin level and isolated CAE.

Soluble EMMPRIN levels discriminate aortic ectasia in Marfan syndrome patients.

Marfan syndrome (MFS) is a rare genetic disease characterized by a matrix metalloproteases (MMPs) dysregulation that leads to extracellular matrix degradation. Consequently, MFS patients are prone to develop progressive thoracic aortic enlargement and detrimental aneurysm. Since MMPs are activated by the extracellular MMP inducer (EMMPRIN) protein, we determined whether its plasmatic soluble form (sEMMPRIN) may be considered a marker of thoracic aortic ectasia (AE). Methods: We compared plasma sEMMPRIN levels of 42 adult Caucasian MFS patients not previously subjected to aortic surgery with those of matched healthy controls (HC) by ELISA. In the MFS cohort we prospectively evaluated the relationship between plasma sEMMPRIN levels and the main MFS-related manifestations. Results: MFS patients had lower plasma sEMMPRIN levels (mean±SD: 2071±637 pg/ml) than HC (2441±642 pg/ml, p=0.009). Amongst all considered MFS-related clinical features, we found that only aortic root dilatation associated with circulating sEMMPRIN levels. Specifically, plasma sEMMPRIN levels negatively correlated with aortic Z-score (r=-0.431, p=0.004), and were significantly lower in patients with AE (Z-score≥2, 1788±510 pg/ml) compared to those without AE (Z-score<2, 2355±634 pg/ml; p=0.003). ROC curve analysis revealed that plasma sEMMPRIN levels discriminated patients with AE (AUC [95%CI]: 0.763 [0.610-0.916], p=0.003) with 85.7% sensitivity, 76.2% specificity, and 81% accuracy. We defined plasma sEMMPRIN levels ≤2246 pg/ml as the best threshold discriminating the presence of AE in MFS patients with an odds ratio [95%CI] of 19.2 [3.947-93.389] (p<0.001). Conclusions: MFS patients are characterized by lower sEMMPRIN levels than HC. Notably, plasma sEMMPRIN levels are strongly associated with thoracic AE.

The Use of Endoscopic Ultrasound in the Evaluation of Unexplained Biliary Dilation.

Isolated biliary dilation, as an incidental diagnosis, is increasing owing to an increase in the use of noninvasive abdominal imaging and poses a diagnostic challenge to physicians especially when further noninvasive diagnostic testing fails to reveal an etiology. This article reviews available data describing the natural history of this clinical scenario and the impact of endoscopic ultrasound examination in the evaluation of unexplained dilation of the common bile duct.

Visfatin as marker of isolated coronary artery ectasia and its severity.

Several studies have demonstrated the relationship between visfatin and increased risk of diseases caused by inflammation, however, the relationship between visfatin and coronary artery ectasia (CAE) is still unknown. The aim of our study is to investigate the association between serum visfatin with presence of coronary ectasia and its severity. We enrolled 85 individuals including 35 CAE patients (mean age: 58.40 ±â€¯9.82 years) and 50 control persons (mean age: 53.24 ±â€¯8.81 years). These participants underwent some biochemical tests including visfatin, fasting blood glucose and lipid profiles. In univariate analysis, the serum level of visfatin was significantly associated with ectasia in all patients with CAE and CAD coexisting with CAE groups, but a trend toward significance in isolated CAE group. In multivariate analysis, visfatin showed independently significant association with presence of ectasia in all patients with ectasia and in CAD coexisting with ectasia groups, but not significant in isolated CAE group. Visfatin was also independently associated with severity of ectasia according to MARKIS classification. We conclude that visfatin independently can be the useful predictor for the presence and severity of coronary ectasia.

Comparing Serum Level of Vitamin D3 in Patients With Isolated Coronary Artery Ectasia and Normal Coronary Artery Individuals.

BACKGROUND: Coronary artery ectasia (CAE) is identified as dilation of one or more segments of coronary arteries that reaches 1.5 times or more, compared with near segments that are normal. Several etiologies like atherosclerosis, autoimmune diseases and congenital anomalies have been proposed for this condition. Vitamin D deficiency activates the renin-angiotensin-aldosterone system, which affects the cardiovascular system. For these reasons, we investigated the serum level of vitamin D in patients with CAE compared with individuals with normal coronary arteries. METHODS: The study group included 30 patients (20 males and 10 females, mean age: 57 ± 9 years) with isolated CAE without any stenotic lesions, and the control group consisted of 60 age/gender matched subjects who had normal coronary angiograms (CAG) (40 males and 20 females, mean age: 57 ± 8 years). All participants underwent CAG at Tehran Heart Center between December 2015 and March 2016. Along with routine lab tests, vitamin D, serum albumin, calcium, phosphorus and alkaline phosphatase levels were analyzed and the unadjusted and adjusted effects of vitamin D on CAE were evaluated using logistic regression model. RESULTS: The median vitamin D level of the patients with CAE was lower than that of the control group (6.5 [3.0, 18.8] ng/mL vs. 17.7 [8.9, 27.1] ng/mL; P = 0.002). The logistic regression model showed that vitamin D deficiency was a predictor for the presence of CEA (P = 0.013). After adjustment for confounding variables, this association remained significant (P = 0.025). CONCLUSION: An association between CAE and vitamin D deficiency was found in our study.

Low-Circulating Homoarginine is Associated with Dilatation and Decreased Function of the Left Ventricle in the General Population.

Low homoarginine is an independent marker of mortality in heart failure patients and incident cardiovascular events. Whether homoarginine is related with healthier cardiac structure and function is currently unclear. We used data of the population-based "Study of Health in Pomerania" (SHIP-Trend) to assess this relation. Homoarginine was measured in serum using liquid chromatography-tandem mass spectrometry. Linear regression models assessed the relation between homoarginine and several structural as well as functional parameters and N-terminal pro B-type natriuretic peptide (NTproBNP). All models were adjusted for age, sex, body mass index, and renal function. A total of 3113 subjects (median age 48 (25th percentile 37 to 75th percentile 60) years, 46% male) were included. A standard deviation decrease in homoarginine was associated with a larger left ventricular diastolic diameter (0.3; 95%-confidence interval (CI): 0.2 to 0.5 mm; p < 0.001), left ventricular systolic diameter (0.38; 95%-CI: -0.22 to 0.54 mm; p < 0.001) as well as a less relative wall thickness (⁻0.003 95%-CI: -0.006 to -0.0008; p = 0.01), left ventricular ejection fraction (⁻0.47; 95%-CI: ⁻0.79 to -0.15%; p < 0.01) and fractional shortening (-0.35; 95%-CI: -0.62 to 0.07%; p = 0.01). Low homoarginine was also related to higher NTproBNP (-0.02 95%-CI: -0.034 to -0.009 log pg/mL; p < 0.01). Lower serum homoarginine is associated with dilatation of the heart and decreased function. Prospective clinical studies should assess if homoarginine supplementation improves cardiac health in subjects with low serum concentrations.

Relationship Between Plasma Levels of Soluble CD40 Ligand and the Presence and Severity of Isolated Coronary Artery Ectasia.

OBJECTIVE: We aimed to investigate whether soluble CD40 ligand (CD40L) levels are higher in patients with isolated coronary artery ectasia (CAE) compared to patients with angiographically normal coronary arteries and those with stable coronary artery disease (CAD). MATERIALS AND METHODS: In all, 55 patients with isolated CAE without stenosis, 55 with stable CAD, and 55 control participants with angiographically normal coronary arteries were included. The CAE severity was determined according to the Markis classification. Plasma levels of soluble CD40 ligand were measured by enzyme-linked immunosorbent assay. RESULTS: The baseline characteristics of the 3 groups were similar. Plasma levels of soluble CD40 ligand were significantly higher in patients with CAE and CAD than in controls (2.6 ± 3.1 ng/mL and 2.0 ± 3.1 ng/mL vs 1.8 ± 2.1 ng/mL, P = .004). No difference was found between the CAE and CAD groups. Soluble CD40 ligand level was significantly higher in the type 1 Markis subgroup than that in the type 3 or type 4 subgroups ( P = .01). A receiver operating characteristic curve analysis revealed that soluble CD40 ligand level >1.2 ng/mL identified patients with isolated CAE. CONCLUSION: Significantly higher levels of soluble CD40 ligand were detected in patients with CAE than that in control participants with normal coronary arteries, suggesting that soluble CD40 ligand may be involved in the pathogenesis of CAE. The CD40-CD40 ligand system likely plays a role in the pathogenesis of CAE.

Serum apolipoprotein B is inversely associated with eccentric left ventricular hypertrophy in peritoneal dialysis patients.

OBJECTIVES: The study aimed to examine the relationship of serum apolipoprotein B level with left ventricular (LV) structural and functional characteristics, in particular, LV remodeling parameters in peritoneal dialysis (PD) patients. METHODS: A total of 182 patients with end-stage renal disease (ESRD) receiving PD were identified. Conventional echocardiography was performed for each patient, and echocardiographic characteristics were analyzed according to apo B quartile groups. Multivariate linear regression models were used to determine the associations between serum apo B and LV remodeling indices. RESULTS: A high serum apo B level was significantly related to the reduction in left atrium dimension (r = - 0.20, P = 0.011), LV dimensions (end-diastolic: r = - 0.27, P = 0.001; end-systolic: r = - 0.24, P = 0.003), peak velocities of early filling divided by peak velocities of atrial filling (r = - 0.38, P < 0.001), and LV volumetric dimension (end-diastolic: r = - 0.27, P < 0.001; end-systolic: r = - 0.28, P < 0.001). After adjustment for clinical confounding factors, the effect of serum apo B on LV eccentric remodeling modestly weakened but remained statistically significant (P = 0.038), while other associations were not significant. In multivariate linear regression analysis, conventional lipid profiles were not significantly associated with LV eccentric remodeling, whereas serum apo B was an independent determinant of LV dilatation (ß: - 42.10, 95% CI - 74.82 to - 9.38, P = 0.012). CONCLUSIONS: Serum apo B was significantly and inversely associated with LV dilatation, independently of conventional lipids and other CV risk factors in our ESRD patients undergoing PD. It suggested that low serum apo B level could be a powerful risk marker for eccentric left ventricular geometry remodeling and could be potentially used to risk-stratify PD patients.

Increased plasma asymmetric dimethylarginine level is associated with ascending aorta dilatation: a case-control study.

BACKGROUND: Asymmetric dimethylarginine (ADMA) is an endogenous inhibitor of nitric oxide synthase. AIM: We aimed to determine plasma ADMA levels in patients with ascending aorta dilatation in comparison to those without aorta dilatation, and to evaluate the diagnostic, predictive, and prognostic value of serum ADMA level for aorta dilatation. METHODS: This was a cross-sectional case-control study. A total of 104 consecutive patients (female/male, 35/69; mean age, 62.75 ± 13.11 years) diagnosed with ascending aorta dilatation (≥ 4.5 cm) on echocardiography (case group), and 52 age-and gender-matched patients (female/male, 17/35; mean age, 63.44 ± 7.56 years) with normal aorta dimensions (≤ 3.8 cm) (control group) were included. Routine biochemical and haematological analysis in addition to measurement of serum ADMA level were performed. RESULTS: The mean diameter of ascending aorta measured on echocardiography was 4.95 ± 0.57 cm and 3.34 ± 0.36 cm in patients with aorta dilatation and those without aorta dilatation, respectively (p < 0.001). Serum ADMA level was significantly higher in patients with aorta dilatation than in the control group (1.70 ± 1.12 µmol/L vs. 0.79 ± 0.76 µmol/L, respectively, p < 0.001). There was significant positive correlation between ADMA level and aortic diameter in Spearman correlation analysis (r = 0.317, p < 0.001). In linear regression analysis, ADMA was found to be a significant independent predictor of aorta diameter (Beta = 0.26, p < 0.001). Receiver-operator characteristic curve analysis also revealed that serum ADMA cut-off level over 0.29 µmol/L predicts aorta dilatation (≥ 4.5 cm) with 94% sensitivity and 92% specificity and with high ac-curacy (area under curve: 0.786; 95% confidence interval: 0.709-0.863, p < 0.001). CONCLUSIONS: Serum ADMA level is diagnostic for ascending aorta dilatation with high sensitivity and specificity, and should be considered for use in clinical diagnosis of aorta dilatation.

Association of serglycin levels with isolated coronary artery ectasia.

BACKGROUND: Serglycin plays an important role in the inflammatory status, but the relationship between coronary artery ectasia (CAE) and serglycin is still unknown. AIM: In this study, we aimed to investigate the association of serglycin level with isolated CAE. METHODS: Fifty-two patients with isolated CAE and 35 individuals with normal coronary angiography were included into the study. The Markis classification and number of ectatic coronary arteries were recorded. Plasma serglycin levels were measured. RESULTS: Multivariate logistic regression analysis revealed that serglycin and high-sensitivity C-reactive protein were indepen-dently associated with the presence of CAE. In receiver operating characteristics curve analysis the cut of serglycin level for the prediction of isolated CAE was 13.5, with a sensitivity of 88.5% and a specificity of 84.8%. However, there was no association between serglycin levels and Markis classification. CONCLUSIONS: Serglycin levels are significantly and independently higher in patients with CAE.

Big endothelin-1 level is a useful marker for predicting the presence of isolated coronary artery ectasia.

CONTEXT: Endothelin-1(ET-1) has been implicated in coronary artery disease (CAD) and may be associated with coronary artery ectasia (CAE). OBJECTIVE: To clarify the relationship between big ET-1 and isolated CAE. METHODS: We measured big ET-1 with ELISA in 216 patients (CAE, n = 72; CAD, n = 72; normal, n = 72) and evaluated the link with isolated CAE. RESULTS: The level of plasma big ET-1 was significantly higher in patients with isolated CAE (p < 0.001). Big ET-1 was strongly and independently associated with CAE by multivariate analysis (OR 95%CI: 1.026 (1.018-1.034), p = 0.000). CONCLUSIONS: Big ET-1 may be a useful predictor for the presence of isolated CAE.

Plasma thiols and thiol-disulfide homeostasis in patients with isolated coronary artery ectasia.

BACKGROUND AND AIMS: Thiol/disulfide homeostasis has an important role in the antioxidant defense system. Oxidative stress may contribute to the pathogenesis of coronary artery ectasia. The aim of this study was to evaluate plasma thiol levels and thiol/disulfide homeostasis in patients with isolated coronary artery ectasia. METHODS: Forty-one patients with isolated coronary artery ectasia and 72 patients with normal coronary arteries were included in the study. Markis classification and number of ectatic coronary arteries were recorded. Plasma total thiol levels, native thiol levels and disulfide levels were measured. Thiol/disulfide homeostasis was appraised by calculating thiol/disulfide ratio. RESULTS: Plasma native thiol levels were significantly lower (336.9 (252.9-374.1) vs. 353.1 (327.0-380.0), p = 0.041) and disulfide levels were significantly higher (18.9 ± 6.3 vs. 16.6 ± 3.4, p = 0.014) in patients with coronary artery ectasia than control patients. Both native thiol/disulfide and total thiol/disulfide ratio was significantly lower in the coronary artery ectasia group (p < 0.001). Multivariate logistic regression analysis revealed that native thiol levels, disulfide levels and native thiol/disulfide ratio were independently associated with the presence of coronary artery ectasia. Thiol/disulfide ratio was not different according to number of ectatic coronary arteries and there was no association between thiol/disulfide ratio and Markis classification. CONCLUSIONS: Plasma thiol/disulfide homeostasis is altered in patients with coronary artery ectasia.

Transcriptional expression profiles of the main proteinases and their regulators in coronary artery ectasia patients' mononuclear cells.

OBJECTIVE: Proteolytic enzymes might contribute to coronary artery ectasia (CAE) through the destruction of extracellular matrix (ECM) vessel components. This study aimed to find out if peripheral blood mononuclear cells (PBMCs) served as a source of those proteinases and their regulators. METHOD: In this study, transcriptional expression profiles of the main proteinases and their regulators were detected in the PBMCs of CAE patients as follows: (1) matrix metalloproteinases (MMP) 1, 2, 3, 8, 9, 10, 12 and 13; (2) the serine proteinases elastase: cathepsin G and proteinases 3; (3) the cysteine proteinases: cathepsin L and cathepsin S; (4) the main endogenous inhibitors for the above proteinases: tissue inhibitors of metalloproteinase (TIMP) 1 and 2, α1-antitrypsin (α1-PI) and α2-macroglobulin (A2M); (5) twelve cytokines that could regulate the above proteinases. RESULT: The characteristic changes in CAE were: (1) MMP1 and MMP9 increased while the serine and cysteine families did not change; (2) the four proteinase inhibitors did not change in the CAE group; (3) among the 12 cytokines, interleukin-1 alpha (IL1A), platelet-derived growth factor (PDGF), interferon gamma (IFNγ) and growth differentiation factor 15 (GDF15) were elevated. Partial correlation analysis showed that MMP1 significantly correlated with IL1A and with IFNγ, and MMP9 correlated with IFNγ and with GDF 15. CONCLUSION: PBMCs might participate in the pathological process of CAE by the increased expression of MMP1, MMP9, IL1A, IFNγ and GDF15.

Disequilibrium of Blood Coagulation and Fibrinolytic System in Patients With Coronary Artery Ectasia.

Thrombus formation and myocardial infarction are not uncommon in patients with coronary artery ectasia (CAE). In light of this, the present study aims to systemically evaluate the blood coagulation and fibrinolytic systems in CAE patients. In this study, we enrolled 30 patients with CAE, 30 patients with coronary atherosclerosis disease (CAD), and 29 subjects with normal coronary arteries (control). The coagulation system was evaluated using a routine coagulation function test performed in the hospital laboratory before coronary angiography, and measurements included prothrombin time, international normalized ratio, activated partial thromboplastin time, fibrinogen time, and thrombin time. The evaluation of the fibrinolytic system included measurements of D-dimer, euglobulin lysis time, plasminogen activator inhibitor 1, plasminogen, plasminogen activity assay, α1-antitrypsin (α1-AT), α2 plasmin inhibitor (α2-PI), and α2-macroglobulin (α2-MG). Alpha1-AT, α2-PI, and α2-MG also inhibit activities of 3 neutrophil serine proteases, namely human neutrophil elastase (HNE), cathepsin G (CG), and proteinase 3 (PR3); therefore, the plasma levels of these 3 proteinases were also evaluated.In CAE patients, the circulating coagulation system was normal. For the fibrinolytic system, a decrease of plasminogen activity was observed (P = 0.029) when compared with CAD patients, and the concentrations of α1-AT (both P < 0.001), α2-PI (P = 0.002 and P = 0.025), and α2-MG (P = 0.034 and P < 0.001) were significantly elevated when compared with CAD patients and normal controls. Moreover, the plasma levels of HNE (both P < 0.001) and CG (P = 0.027 and 0.016) in CAE patients were also significantly higher than those of the CAD and control groups. There was no difference in plasma PR3 concentration among these 3 groups.Disequilibrium of the coagulation/fibrinolytic system may contribute to thrombus formation and clinical coronary events in patients with CAE. The increased plasma concentrations of α1-AT, α2-PI, and α2-MG might provide beneficial effects by inhibiting the proteinases and restraining the ectatic process; on other hand, they led to unfavorable results by inhibiting plasmin and decreasing thrombus degradation in CAE patients.

Plasma Endocan Levels in Patients With Isolated Coronary Artery Ectasia.

Endocan is a soluble proteoglycan, secreted by human vascular endothelial cells. Endocan is a marker for vascular pathologies and an important mediator of angiogenesis, strongly associated with inflammation, vascular endothelial dysfunction, and atherosclerosis. The relationship between coronary artery ectasia (CAE) and endocan has not been evaluated. We aimed to investigate this association. Fifty-four patients with isolated CAE without coronary stenosis and 30 controls with normal coronary angiogram were included in this study. Endocan plasma concentrations were measured using an enzyme-linked immunosorbent assay. Patients with isolated CAE had significantly higher levels of endocan compared to the controls (18.9 ± 7.3 vs 15.6 ± 3.6 ng/mL; P = .007). There was a significant correlation between endocan levels and severity of isolated CAE according to the Markis classification ( r = -.593, P < .001). Plasma endocan levels may reflect the presence and severity of isolated CAE, suggesting that endocan may be involved in pathogenesis of isolated CAE.

The Association Between α1-Antitrypsin and Coronary Artery Ectasia.

Coronary artery ectasia (CAE) is associated with coronary artery disease (CAD). The underlying pathophysiology of CAE is not fully understood. α1-antitrypsin (A1AT) plays a role in the tissue protease system, and AAT-1 deficiency (A1ATD) has been shown to be related to CAD. We compared A1AT serum levels in patients with and without CAE to determine the association between A1AT levels and the extent of ectasia using the Markis score. We included 50 patients (38 males) with isolated CAE and 46 patients (28 males) with normal coronary arteries after coronary angiography. The levels of A1AT were measured by nephelometry. The median A1AT levels were lower in patients with isolated CAE than in the control group (1.27 ng/mL [range: 1.07-1.37 ng/mL] vs 1.43 ng/mL [range: 1.27-1.59 ng/mL]; P < .001). According to the Markis classification, the extent of CAE was not correlated with A1AT levels ( P = .41). Our results demonstrate an inverse relationship between serum A1AT levels and CAE. α1-antitrypsin is fundamental for the stability and integrity of the arterial wall. Lack of elastase inhibition in cases of A1ATD may contribute to ectasia formation by facilitating proteolysis and weakening the arterial wall.

SERUM LEVELS OF ENDOTHELIAL MONOCYTE ACTIVATING PEPTIDE II IN TYPE 1 DIABETES.

Was investigated serum level of endothelial monocyte activating peptide II (EMAP-II) and endothelium-dependent dilatation in type 1 diabetes and possible relation between those. We found an increase serum level of EMAP-II and decrease of endothelium-dependent dilatation in type 1 diabetes. It was significant correlation between EMAP-II and HbAc1, blood glucose, total cholesterol, LDL, triglycerides and inverse correlation between EMAP-II and HDL, endotheliumdependent dilatation. The revealed change of EMAP-II serum level reflects an endothelial dysfunction in type 1 diabetes, alteration of carbohydrate and lipid metabolism could influence of this pathway.