Relation between Serum Apelin Level and CAE

Relation amongst Serum Apelin Level and CAE rock-bottom Apelin Levels in Isolated coronary thrombosis Artery ectasisM.Zihni Bilik, M.Ata Akal, Halit Acet, Abdulkadir Yaldaz, Murat Yksel, Nihat Polat, Mesut Aydan, Mustafa Oylumlu, Sait Alan ,Faruk Erta incision of Cardiology, Medicine Faculty, Dicle University, Diyarbakr, TurkeyAbstractIntroduction Etiopathogenesis of coronary arteria ectasia (CAE) is completely unknown. Most of CAE develop with coronary arteria disease. Association of atherosclerotic coronary arteria disease and apelin has been examined in previous studies. In isolate coronary artery ectasia the subprogram of germ plasm apelin has not been studied yet. analyze In this charter, we investigated the relation between plasma apelin directs and coronary artery ectasia.Material and methods reckon population included totally 54 patients. 26 patients with isolated CAE (53.68.1 long time ) 28 patients as agree assort with normal coronary arteries (51.6 8.8 yea rs) and with standardised risk portions and demographic properties . Apelin takes were measured development an enzyme immunoassay (ELISA) .Results Apelin levels in CAE group were earthshakingly depress apelin= 0.116ng/ml (0.086-0.319) than those in control group 0.689ng/ml (0.077-1.067) (P =0.033).Glucose, creatinine,total cholesterol, triglyceride, beta-lipoprotein-C, HDL-C levels were not significantly variant between groups (P 0.05).Conclusions In this study we showed that patients with isolated CAE necessitate lessen plasma apelin levels. Therefore in that location may be an association between decreased plasma apelin level and isolated CAE. get wind words apelin, coronary artery ectasia, atherosclerosisIntroductionApelin is an adipocytokine and endogenous ligand for the angiotensin-like 1 receptor (APJ). The function of apelin is not clear in the cardiovascular system. Apelin may play an opposite role to the renin-angiotensin-aldosterone system as a compensatory me chanism. It is decrease in patients with fancy failure.1Increased apelin expression has been found in coronary vessels, cardiomyocytes, large conduit vessels 2 vascular glitter musculus cells, and endothelial cells.3Some functions of apelin have been described, much(prenominal) as positive inotropism 4 ,endothelium-dependent vasodilation 5,cardiac contractility,6 and the reduction of vascular wall inflammation.CAE has been specify as abnormal dilatation of a segment of coronary artery that 1.5 times larger than the diameter of neighboring(a) normal segments of artery.7The incidence of CAE has been describe to account for 0.3% to 4.9% in patients underwent coronary angiography. 8Although the exact mechanisms leading to CAE atomic number 18 not clear up to now, atherothrombosis, endothelial dysfunction and vasculit have been intimateed as executable responsible factors. CAE has also been account in association with various conditions such as congenital coronary anomalies, connective tissue diseases, and vasculitis and failed placid muscle cells. 9,10Apelin has a role in endothelium-dependent vasodilation. CAE may dependent to endothelium-dependent vasodilation mechanism. 5 So at that place may be relation between apelin and CAE.In our knowledge there is not any study in the literature about apelin and CAE.AimIn this study we aimed to examine the relation between serum apelin level and CAE.Material and methods shoot population included totally 54 patients that were admitted to Cardiology plane section of Dicle University.Twenty six patients with isolated CAE ( 53.68.1 years ) as CAE group and 28 patients as control group with normal coronary arteries that proven angiographically (51.6 8.8 years) with alike(p) risk factors and demographic properties to CAE group were included .Cases who had malignancy, sum total failure ,acute coronary syndrome, renal disease, collagen tissue diseases, vasculitis,coronary artery disease were excluded from the study .The study was approved by the Local Ethics Committee and informed consent was obtained from each patient.Study designAll patients underwent detailed physical examination. dust mass list (BMI) was calculated as weight divided by squ be of height. clinical laboratory analyses were performed in Dicle University Biochemistry Laboratories (Diyarbakar, Turkey). Biochemical streamlets were performed by Abbott C16000 (USA) biochemical autoanalyzer with original kits and haematological counts were measured by an automated hematology analyzer (Abbott Cell-Dyn 3700 Abboott Laboratory, Abbott Park, IL) in circumferential venous p atomic number 18ntage samples . Standart methods were used to measure total and high parsimony lipoprotein cholesterol (HDL),triglycerides and fasting glucose.Serum obtained by centrifuge was stored at 80C until analysis for apelin measurement. These were studied at the Biochemistry Laboratory of Dicle University .Apelin levels were measured using an enzyme imm unoassay (ELISA) (Phoenix Pharmaceuticals, Inc., California,USA) according to the manufacturers instructions, and expressed as ng/ml.Evaluation of coronary artery ectasia by coronary angiographycoronary angiography was routinely performed using the Allura Xper FD10 (Philips, Amsterdam, The Netherlands) through femoral artery by Judkins proficiency without use of nitroglycerine. The contrast agent was Iopamiro 370 (Bracco, Milan, Italy) that used in all patients. each(prenominal) angiogram was evaluated concurrently by two interventional cardiologists who were blinded to the study and to each other. Angiographically CAE was veritable when diameter of dilated segment of coronary artery was 1.5 times larger than bordering normal segments.Statistical analysisData were analyzed with SPSS software pas seul 18.0 for Windows (SPSS Inc, Chicago, Illinois). The Kolmogorov-Smirnov test was used to verify that continuous variables were normally distributed. Continuous variables are listed a s mean standard deviation, categorical variables are listed as percentages. The nonsymbiotic sample t-test or Mann-Whitney U test was used for continuous variables and the chi-square test for categorical variables. Statistical significance was defined as p ResultsThe study was included a total of 54 patients. CAE group included 26 patients with coronary ectasia (mean age 53.68.1 years) and %73.1 (n=19) of patients were male. Control group included 28 control patients with normal coronary arteries (mean age 51.6 8.8 years) and 64.3% (n =18) of patients were male.There was no departure between two groups regarding basal demographical data (P0.05).Demographic characteristics of the groups are presented in Table 1.We found apelin levels in CAE group significantly lower apelin= 0.116ng/ml (0.086-0.319) than those in control group 0.689ng/ml (0.077-1.067) (P =0.033).Glucose, creatinine,total cholesterol, triglyceride, LDL-C, HDL-C levels were not significantly different between group s (P 0.05).Table 1 Baseline characteristics of the study populationEctasia Grup (n=26)Control Grup (n=28)P taxAge (years)53.68.151.6 8.80.38Male n(% )19 (%73.1)18(%64.3)0.49hypertension n(%)15 (%58)12(%43)0.18Diabetes Mellitus n(%)4 (%15)6 (%21)0.57BMI (kg/m)28.1 426.7 4.20.24Smoking n(%)13 (%50)12 (%46)0.79Glucose mg/dl10620124530.1Creatinine mg/dl0.860.20.820.10.38Total cholesterol mg/dl19647195370.98LDL mg/dl12842113330.14HDL mg/dl411040100.92Triglyseride mg/dl cxlv771841150.15Apelin ng/ml0.116 (0.086-0.319)*0.689 (0.077-1.067)*0.033*Median and interquartile range used.BMIBody mass index LDL Low-density lipoprotein cholesterol HDL uplifted density lipoprotein cholesterolFigure-1 Comparison of the plasma apelin level between CAE and control group. P=0.033Discussion CAE has been defined as abnormal dilatation of a segment of coronary artery that 1.5 times larger than the diameter of adjacent normal segments of artery. 7The etiology of CAE is not fully understood. Various mechani sms are theory to be the reason of CAE. Approximately a half of CAE is due to atherosclerosis of coronary artery. Atheromatous ulcerations in coronary artery or significant stenosis has been described in patients with ectasia.11,12Cardiovascular system is the main rank of apelin and its receptor APJ . In regulation of cardiovascular homeostasis, apelin may have an master(prenominal) role.13 Positive inotropism, vasodilation, decreased blood pressure and diuresis are some set up of apelin on cardiovascular system . Therefore apelin may have an antagonistic effect to the renin-angiotensin-aldosteron system .It is reduced in patients with heart failure.1Relation between apelin and coronary artery disease especially atherosclerosis is known. Kadoglou et al. showed that apelin concentrations are lower in CAD patients and it is banly correlated with severity of CAD. 14. Additionally, decreased apelin levels are observed in subjects with stable angina. Plasma apelin may have a role i n the progression and destabilization of atherosclerotic plaques.15.Attenuation of the vessel wall has been shown by Rath et al. in nonatherosclerotic forms of CAE .In their study vessel media degeneration and smooth muscle cell replacement by hyalinized collagen with intact vessel intima has been demo.16 In the pathogenesis of CAE, loss of the musculoelastic components of the vessel media have an important effect. 12,17Several factors other than atherosclerosis have a role in development of CAE such as endothelial dysfunction, vasculitis, congenital coronary anomalies, connective tissue diseases 9,10, aerophilic stres, vascular smooth muscle proliferation, abnormal collagen synthesis and increased inflammatory response. 18 Li L. et al. showed that apelin have a regulatory effect on proliferation of vascular smooth muscle cell and nitrous oxide production.19Nitric oxide is a potent vasodilator and plays important roles in protecting the cardiac vascular system against myocardial damage. It inhibits leukocyte adhesion ,platelet aggregation and vascular smooth muscle cell proliferation. 18In some studies there was a relation between apelin and nitric oxide. It is demonstrated that in the rat model, myocardial damage significantly reduces by oxidative dishonor reduction and enhancement of nitric oxide production when rats treated with apelin in postinfarct period.20Tatemoto K., et al. reported that apelin may be present in the endothelium and reduce blood pressure via nitric oxide dependent mechanism.21 Additionally polymorphism in the endothelial nitric oxide synthase gene has been explored in several studies in patients with CAE. 22 According to this ,impaired nitric oxide dependent vasodilation mechanism may consist to be the reason of ectasia.Malyszko et al. reported that in patients with transplanted kidneys apelin level is correlated with intracellular adhesion molecule, adiponectin and the presence of coronary arery disease in patients with transplante d kidneys. 23 Apelin is a member of adipocytokin like adiponectin. Dagli N. et al. examined a negative correlation between coronary artery ectasia diameter and plasma adiponectin level .24 Also in our study we obtained similar results that plasma apelin level in isolated CAE patients is significantly lower than in controls. According to upstart data adiponectin and apelin have cardioprotective effects . Despite exact mechanism is not clear it seems that, both of them protect vessel from atherosclerosis and ectasia.However, further studies are required to show the role of apelin in development of CAE.Conclusion In this study we showed that patients with isolated coronary artery ectasia have decreased plasma apelin level compared with normal coronary arteries. According to these data we suggest that apelin may have a role in developing CAE.Limitations of the studyBecause isolated CAE is rare entity ,the number of cases were limited. our study have a scummy population. Additionally, it is an important limitation on the part of the study that intravascular ultrasound (IVUS) was not conducted in the diagnosis of patients, as IVUS and autopsy can demonstrate atherosclerotic plaques in a wide area of the vessel lumen in patients whose coro-nary angiography is normalConflict of InterestThe authors declare no conflict of interest.References1.Chandrasekaran B, Dar O, McDonagh T. The role of apelin in cardiovascular function and heart failure. European ledger of heart failure 200810725-7322.Kleinz MJ, Davenport AP. Emerging roles of apelin in biology and medicine. Pharmacology therapeutics 2005107198-2113.Ronkainen VP, Ronkainen JJ, Hanninen SL, et al. Hypoxia inducible factor regulates the cardiac expression and secretion of apelin. FASEB daybook official publication of the conspiracy of American Societies for Experimental Biology 2007211821-18304.Hashimoto T, Kihara M, Ishida J, et al. Apelin stimulates myosin light chain phosphorylation in vascular smooth musc le cells. Arteriosclerosis, thrombosis, and vascular biology 2006261267-12725.Malyszko J, Malyszko JS, Pawlak K, Mysliwiec M. Visfatin and apelin, freshly adipocytokines, and their relation to endothelial function in patients with chronic renal failure. Advances in health check sciences 20085332-366.Farkasfalvi K, Stagg MA, Coppen SR, et al. Direct effects of apelin on cardiomyocyte contractility and electrophysiology. Biochemical and biophysical look into communications 2007357889-8957.Hartnell GG, Parnell BM, Pridie RB. Coronary artery ectasia. Its prevalence and clinical significance in 4993 patients. British heart diary 198554392-3958.Yamanaka O, Hobbs RE. Coronary artery anomalies in 126,595 patients undergoing coronary arteriography. Catheterization and cardiovascular diagnosis 19902128-409.Seabra-Gomes R, Somerville J, Ross DN, et al. Congenital coronary artery aneurysms. 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Heart and vessels 20092484-89Table 1 Baseline characteristics of the study populationGrup 1 (n=26)Grup 2 (n=28)P valueAge (years)53.68.151.6 8.8P0,05 0,38Male %19 (%73,1)18(%64,3)P0,05Hypertension %15 (%58)12(%43)P0,05Diabetes Mellitus %4 (%15)6 (%21)p0,05BMI (kg/m)28.1 426.7 4.2P0,05Smoking %13 (%50)12 (%46)P 0,05Glucose mg/dl10620124530.1Creatinine mg/dl0,860,20,820,10.38Total cholesterol mg/dl19647195370.98LDL mg/dl12842113330.14HDL mg/dl411040100. 92Triglyseride mg/dl145771841150.15