scholarly journals Circulating Exosomal miRNAs as Novel Biomarkers for Stable Coronary Artery Disease

2020 ◽  
Vol 2020 ◽  
pp. 1-11
Author(s):  
Ping Zhang ◽  
Tao Liang ◽  
Yao Chen ◽  
Xuan Wang ◽  
Tianlong Wu ◽  
...  
Keyword(s):  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Cardiovascular Diseases ◽  
Protein Concentration ◽  
Stable Coronary Artery Disease ◽  
Control Group ◽  
Diagnostic Biomarkers ◽  
Exosomal Mirnas ◽  
Artery Disease ◽  
Serum Exosomes

Exosomal miRNAs are currently being explored as a novel class of biomarkers in cardiovascular diseases. However, few reports have focused on the value of circulating exosomal miRNAs as biomarkers for stable coronary artery disease (SCAD). Here, we aimed to investigate whether miRNAs involved in cardiovascular diseases in circulating exosomes could serve as novel diagnostic biomarkers for SCAD. Firstly, the serum exosomes were isolated and purified by the ExoQuick reagent and identified by transmission electron microscopy, western blot, and nanoparticle tracking analysis. Then, the purified exosomes were quantified by measuring the exosome protein concentration and calculating the total protein amount. Next, eight miRNAs involved in cardiovascular diseases, miR-192-5p, miR-148b-3p, miR-125a-3p, miR-942-5p, miR-149-5p, miR-32-5p, miR-144-3p, and miR-142-5p, were quantified in circulating exosomes from the control group ( n = 20 ) and the SCAD group ( n = 20 ) by quantitative real-time polymerase chain reaction (qPCR). Finally, the gene targets of the differentially expressed miRNAs were predicted, and the functions and signaling pathways of these targets were analyzed using an online database. The isolated exosomes had a bilayer membrane with a diameter of about 100 nm and expressed exosomal markers including CD63, Tsg101, and Flotillin but negatively expressed Calnexin. Both the exosome protein concentration and total protein amount exhibited no significant differences between the two groups. The qPCR assay demonstrated that among the eight miRNAs, the expression levels of miR-942-5p, miR-149-5p, and miR-32-5p in the serum exosomes from the SCAD group were significantly higher than that from the control group. And the three miRNAs for SCAD diagnosis exhibited AUC values of 0.693, 0.702, and 0.691, respectively. GO categories and signaling pathways analysis showed that some of the predictive targets of these miRNAs were involved in the pathophysiology processes of SCAD. In conclusion, our findings suggest that serum exosomal miR-942-5p, miR-149-5p, and miR-32-5p may serve as potential diagnostic biomarkers for SCAD.

scholarly journals Paraoxonase-1 and Simvastatin Treatment in Patients with Stable Coronary Artery Disease

2016 ◽  
Vol 2016 ◽  
pp. 1-10
Author(s):  
Rafał Januszek
Keyword(s):  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Stable Coronary Artery Disease ◽  
Paraoxonase 1 ◽  
High Density Lipoproteins ◽  
Pon1 Activity ◽  
Control Group ◽  
Simvastatin Treatment ◽  
Simvastatin Therapy ◽  
Artery Disease

Background.Paraoxonase-1 (PON1) is the crucial antioxidant marker of high-density lipoproteins. The present study is aimed at assessing the effect of simvastatin treatment on PON1 activity and its relationship to Q192R and M55L polymorphisms in subjects with stable coronary artery disease (CAD).Methods.The patient group was composed of 53 individuals with stable CAD, and the control group included 53 sex-matched police officers without CAD. CAD patients were treated with simvastatin 40mg/day for 12 months. Respectively, flow mediated dilatation (FMD), serum hs-CRP and TNF-αlevels, urinary 8-iso-PGF2αconcentrations, and PON1 activity were evaluated in definitive intervals.Results.There was no effect of simvastatin treatment on urinary 8-iso-PGF2α. Simvastatin treatment significantly increased FMD value, decreased CRP and TNF-αconcentration. After adjusting for PON1 genotypes, significantly higher PON1 activity was noted in the 192R allele carriers, in both groups. Regardless of genotype, PON1 activity remained stable after simvastatin treatment.Conclusions.The present study confirms a positive effect of simvastatin therapy on endothelial function and inflammatory markers in secondary prevention. Simvastatin treatment shows no effects on PON1 activity and 8-isoprostanes level. The effect of simvastatin therapy on PON1 activity is not modulated by Q192R and M55L polymorphisms.

Preoperative Rosuvastatin Protects Patients with Coronary Artery Disease Undergoing Noncardiac Surgery

Cardiology ◽  
2015 ◽  
Vol 131 (1) ◽  
pp. 30-37 ◽  
Author(s):  
Jinggang Xia ◽  
Yang Qu ◽  
Chunlin Yin ◽  
Dong Xu
Keyword(s):  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Emergency Surgery ◽  
Stable Coronary Artery Disease ◽  
Myocardial Necrosis ◽  
Noncardiac Surgery ◽  
Control Group ◽  
Artery Disease ◽  
Experimental Group

Objectives: We explored whether preoperative rosuvastatin could protect the cardiac health of patients with coronary artery disease undergoing emergency, noncardiac surgery. Methods: We randomized 550 noncardiac emergency surgery patients with stable coronary artery disease on long-term statin therapy to treatment with and without preoperative rosuvastatin. All patients received rosuvastatin after surgery. We evaluated the incidence of myocardial necrosis and major adverse cardiovascular and cerebrovascular events (MACCE) 30 days and 6 months after surgery. Results: Creatinine kinase-myocardial band (CK-MB) isoform elevations occurred less frequently 12 and 24 h after noncardiac emergency surgery in the experimental group than in the control group (p = 0.029). After surgery, the incidence of MACCE was also lower in the experimental group than in the control group (p = 0.019). The difference was mainly due to the incidence of perioperative myocardial infarction (p = 0.029). Multivariable analysis found that rosuvastatin reload reduced the incidence of MACCE 52% 6 months after surgery (p = 0.03). Conclusions: Preoperative rosuvastatin reload therapy decreases the incidence of myocardial necrosis and MACCE after noncardiac emergency surgery in patients with stable coronary artery disease on long-term statin therapy.

scholarly journals Concentration of lipoprotein - associated phospholipase A2 in chronic dental diseases and stable coronary artery disease

2013 ◽  
Vol 26 (3) ◽  
pp. 273-275
Keyword(s):  
Coronary Artery Disease ◽  
Risk Factor ◽  
Coronary Artery ◽  
Phospholipase A2 ◽  
Human Life ◽  
Stable Coronary Artery Disease ◽  
Serum Lipoprotein ◽  
Control Group ◽  
Dental Diseases ◽  
Artery Disease

Lipoprotein-associated phospholipase A2 (Lp-PLA2) is an enzyme that has been shown to be a risk factor of cardiovascular disease (CVD) and that is involved in the degradation of the phospholipid mediator platelet-activating factor (PAF), a potent mediator of inflammation. The aim of the present study was to investigate concentration of Lp-PLA2 in control group and patients with chronic dental diseases and stable coronary artery disease (CAD). We studied 10 patients with chronic dental diseases, 10 patients with stable coronary artery disease and 10 healthy individuals as controls. Our patients with stable coronary artery disease were using anti-hypertension medicaments, acetylsalicylic acid and statins although patients with chronic dental diseases were not. A plasma Lp-PLA2 assay kit (ELISA, Human, Life Inc., Wuhan, China) was used. Our results showed that both groups of patients with chronic dental diseases and stable coronary artery disease had significantly increased Lp-PLA2 mass as compared to controls. However, Lp-PLA2 mass in patients with chronic dental diseases and stable coronary artery disease was non-significant statistically. We concluded that patients with chronic dental diseases have increased the serum lipoprotein-associated phospholipase A2, which is believed to be an independent cardiovascular risk factor, although future studies are required.

scholarly journals Garlic Extract (Allicin) Improves the Proliferation of Endothelial Progenitor Cell (EPC) from Patients with Stable Coronary Artery Disease

2020 ◽  
Vol 8 (A) ◽  
pp. 65-69
Author(s):  
Yudi Her Oktaviono ◽  
Budi Susetyo Pikir ◽  
Fatimah Alzahra ◽  
Makhyan Jibril Al-Farabi ◽  
Alisia Yuana Putri
Keyword(s):  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Endothelial Progenitor Cell ◽  
Peripheral Blood ◽  
Progenitor Cell ◽  
Stable Coronary Artery Disease ◽  
Immunohistochemical Method ◽  
Control Group ◽  
Artery Disease ◽  
And Function

BACKGROUND: The reduced number and function of endothelial progenitor cell (EPC) in stable coronary artery disease (SCAD) patients aggravate endothelial dysfunction and inhibit neovascularization, thus lead to atherosclerosis. Garlic is currently believed to increase the number and function of EPC. AIM: Therefore, this in vitro study was conducted to analyze the effect of garlic extract (allicin) on the proliferation of EPC in patients with SCAD. METHODS: Mononuclear cells were isolated from peripheral blood of eight SCAD patients and cultured on colony-forming unit (CFU)-Hill medium for 3 days. Samples were divided into two groups: Group treated with allicin and control group. The treatment group was then divided into three subgroups which received 10, 50, and 100 mg/ml of doses and incubated for 48 h. EPC proliferation was assessed using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) cell proliferation assay. Immunohistochemical method of CD34+ was performed for EPC identification. Data were analyzed using independent t-test and ANOVA. RESULTS: MTT assay showed a significant increase in EPC proliferation in the allicin group compared to the control group (0.2811 ± 0.008 vs. 0.194 ± 0.151, p < 0.05) and significant improvements were observed in each dose increment. CFU-Hill quantification shows the addition of EPC colony in high-dose allicin. Immunohistochemical method shows positive CD34+ expression. CONCLUSION: Allicin increases EPC proliferation dose-dependently from peripheral blood of SCAD patients.

Abstract 222: HDL-ApoA-I Exchange Rate is Inversely Correlated With Coronary Artery Disease Stability

2014 ◽  
Vol 34 (suppl_1) ◽  
Author(s):  
Mark S Borja ◽  
Yumin He ◽  
Jacques Genest ◽  
Michael N Oda
Keyword(s):  
Coronary Artery Disease ◽  
Acute Coronary Syndrome ◽  
Coronary Artery ◽  
Electron Paramagnetic Resonance Spectroscopy ◽  
Stable Coronary Artery Disease ◽  
Control Group ◽  
Resonance Spectroscopy ◽  
Coronary Syndrome ◽  
Artery Disease ◽  
Stable Cad

Objective: The exchange of apolipoprotein A-I between lipid-associated and lipid-free states is a key step in reverse cholesterol transport and is representative of HDL’s functional status. Reduced HDL-apoA-I exchange (HAE) is associated with the presence of cardiovascular disease. To build on this observation, we investigated the hypothesis that HAE in a coronary artery disease-identified patient decreases with increased coronary artery disease instability. Method: HAE was measured by electron paramagnetic resonance spectroscopy (EPR), wherein nitroxide-labeled lipid-free apoA-I is introduced into apolipoprotein B-depleted plasma, incubated at 37°C and measured. When added to plasma, the nitroxide-labeled apoA-I specifically interacts with HDL and displaces resident apoA-I. The EPR spectrum reports the population of lipid-bound, spin labeled apoA-I, which is directly proportional to the amount of resident apoA-I displaced. The relative level of apoA-I displaced is representative of the plasticity of HDL and its ability to make lipid-poor apoA-I available for ABCA1-mediated cholesterol efflux. We measured HAE in the plasma of three groups: stable coronary artery disease (n=22), 3 months following acute coronary syndrome (n=19), and a control group with no history of coronary artery disease (n=15). Results: HAE was significantly lower in both the stable coronary artery disease and acute coronary syndrome groups, compared to the control group (P<0.001 and, P<0.0001, respectively). Remarkably, the ACS subjects also had significantly lower HAE compared to those with stable CAD (P<0.01). By comparing HAE to apoA-I and HDL-C levels, we observed that stable CAD and ACS subjects have lower HAE per milligram/deciliter of apoA-I, consistent with a qualitative deficiency in their apoA-I. Conclusions: HAE activity is a by-product of apoA-I qualitative status, which is inversely correlated with coronary artery disease stability.

scholarly journals EFFECT OF PLATELET RICH PLASMA ON PROLIFERATION OF ENDOTHELIAL PROGENITOR CELL (EPC) OF STABLE CORONARY ARTERY DISEASE PATIENT

2019 ◽  
Vol 40 (2) ◽  
Author(s):  
Ronald Rendy Hehanusa ◽  
Andrianto Andrianto ◽  
Budi S Pikir
Keyword(s):  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Endothelial Progenitor Cell ◽  
Peripheral Blood ◽  
Progenitor Cell ◽  
Platelet Rich Plasma ◽  
Stable Coronary Artery Disease ◽  
Control Group ◽  
Endothelial Progenitor ◽  
Artery Disease

ABSTRACT Effect of Platelet Rich Plasma (PRP) on Proliferation of Endothelial Progenitor Cell (EPC) of Stable Coronary Artery Disease Patient Ronald R Hehanusa, Andrianto, Budi S Pikir   Background : Endothelial Progenitor Cell (EPC) is the progenitor of endothelial cell which has important role in  regulation of vascular wall integrity and homeostasis, to protect vessels from inflamation and thrombosis, that leads into pathogenesis of coronary artery disease. Growth factors proven has important role to stimulate transduction signal in the process of proliferation of EPC. Platelet Rich Plasma (PRP) contains variety of growth factors, wellknown role in homeostasis and wound healing process. Therefore, this study was conducted to analyze the effect of PRP on proliferation of EPC of Stable Coronary Artery Disease (SCAD) patient. Objective : To analyze the effect of Platelet Rich Plasma (PRP) on the proliferation of Endothelial Progenitor Cell (EPC) from peripheral blood of patient with SCAD    Methods : This is an in vitro, true experimental, post-test only control group design. The mononuclear cells were isolated from peripheral blood of SCAD patient and cultured in M-199 medium. EPC divided into 3 groups, which received Platelet Rich Plasma (PRP), Platelet Poor Plasma (PPP), and control. After 14 days of incubation, immunocytochemical examination was performed, EPC which marked with CD34, FITC labeled,was counted using immunofluoroscence microscope. Data analysis using ANOVA test. Result : Cell counting showed significant increase of EPC proliferation in PRP group compared to PPP group (1.052 ± 0.16 vs 0.762 ± 0.19, p = 0.003), and control group as well (1.052 ± 0.16 vs 0.068 ± 0.05, p = 0.000). EPC proliferation in PPP group also increase significantly compared to control group (0.762 ± 0.19 vs 0.068 ± 0.05, p = 0.000). Conclusion : Platelet Rich Plasma (PRP) increase EPC proliferation significantly from peripheral blood of SCAD patient.   Keywords : EPC proliferation, PRP, SCAD

scholarly journals The Effect of a WeChat-Based Tertiary A-Level Hospital Intervention on Medication Adherence and Risk Factor Control in Patients With Stable Coronary Artery Disease: Multicenter Prospective Study (Preprint)

2021 ◽  
Author(s):  
Boqun Shi ◽  
Xi Liu ◽  
Qiuting Dong ◽  
Yuxiu Yang ◽  
Zhongxing Cai ◽  
...  
Keyword(s):  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Medication Adherence ◽  
Stable Coronary Artery Disease ◽  
Intervention Group ◽  
Control Group ◽  
Artery Disease ◽  
Multicenter Prospective Study ◽  
Level Hospital

BACKGROUND In China, ischemic heart disease is the main cause of mortality. Having cardiac rehabilitation and a secondary prevention program in place is a class IA recommendation for individuals with coronary artery disease. WeChat-based interventions seem to be feasible and efficient for the follow-up and management of chronic diseases. OBJECTIVE This study aims to evaluate the effectiveness of a tertiary A-level hospital, WeChat-based telemedicine intervention in comparison with conventional community hospital follow-up on medication adherence and risk factor control in individuals with stable coronary artery disease. METHODS In this multicenter prospective study, 1424 patients with stable coronary artery disease in Beijing, China, were consecutively enrolled between September 2018 and September 2019 from the Fuwai Hospital and 4 community hospitals. At 1-, 3-, 6-, and 12-month follow-up, participants received healthy lifestyle recommendations and medication advice. Subsequently, the control group attended an offline outpatient clinic at 4 separate community hospitals. The intervention group had follow-up visits through WeChat-based telemedicine management. The main end point was medication adherence, which was defined as participant compliance in taking all 4 cardioprotective medications that would improve the patient’s outcome (therapies included antiplatelet therapy, β-blockers, statins, and angiotensin-converting-enzyme inhibitors or angiotensin-receptor blockers). Multivariable generalized estimating equations were used to compare the primary and secondary outcomes between the 2 groups and to calculate the relative risk (RR) at 12 months. Propensity score matching and inverse probability of treatment weighting were performed as sensitivity analyses, and propensity scores were calculated using a multivariable logistic regression model. RESULTS At 1 year, 88% (565/642) of patients in the intervention group and 91.8% (518/564) of patients in the control group had successful follow-up data. We matched 257 pairs of patients between the intervention and control groups. There was no obvious advantage in medication adherence with the 4 cardioprotective drugs in the intervention group (172/565, 30.4%, vs 142/518, 27.4%; RR 0.99, 95% CI 0.97-1.02; <i>P</i>=.65). The intervention measures improved smoking cessation (44/565, 7.8%, vs 118/518, 22.8%; RR 0.48, 95% CI 0.44-0.53; <i>P</i>&lt;.001) and alcohol restriction (33/565, 5.8%, vs 91/518, 17.6%; RR 0.47, 95% CI 0.42-0.54; <i>P</i>&lt;.001). CONCLUSIONS The tertiary A-level hospital, WeChat-based intervention did not improve adherence to the 4 cardioprotective medications compared with the traditional method. Tertiary A-level hospital, WeChat-based interventions have a positive effect on improving lifestyle, such as quitting drinking and smoking, in patients with stable coronary artery disease and can be tried as a supplement to community hospital follow-up. CLINICALTRIAL ClinicalTrials.gov NCT04795505; https://clinicaltrials.gov/ct2/show/NCT04795505

scholarly journals Association between cardiac autonomic nervous dysfunction and the severity of coronary lesions in patients with stable coronary artery disease

2018 ◽  
Vol 46 (9) ◽  
pp. 3729-3740 ◽  
Author(s):  
Yafei Chen ◽  
Yijun Yu ◽  
Wusong Zou ◽  
Mingjing Zhang ◽  
Yuting Wang ◽  
...  
Keyword(s):  
Coronary Artery Disease ◽  
Heart Rate ◽  
Coronary Artery ◽  
Heart Rate Recovery ◽  
Stable Coronary Artery Disease ◽  
Multivariate Logistic Regression Analysis ◽  
Control Group ◽  
Autonomic Nervous ◽  
Coronary Lesions ◽  
Artery Disease

Objective Autonomic dysfunction is recognized in patients with coronary artery disease (CAD) and is related to worse cardiovascular outcome. This study aimed to evaluate cardiac autonomic nervous function by heart rate recovery (HRR) and heart rate variability (HRV), and demonstrate their relationship with the severity of coronary lesions in patients with stable CAD (SCAD). Methods Consecutive patients without CAD (controls, n = 65) and those with SCAD (n = 63) were included in this study. Patients with SCAD were further divided into single- or two-/three-vessel disease, as well as <70% or ≥70% stenosis subgroups. The association between HRR/HRV and coronary lesions was analysed. Results HRR and HRV values were significantly lower in the SCAD group compared with the control group. Multivariate logistic regression analysis showed that abnormal HRR and HRV were risk factors of SCAD. Moreover, delayed HRR was a risk factor of the severity of coronary lesions. Conclusions Our results show that autonomic function is impaired in patients with SCAD and delayed HRR is closely related to the severity of coronary lesions.

Free IGF-1, Intact IGFBP-4, and PicoPAPP-A are Altered in Acute Myocardial Infarction Compared to Stable Coronary Artery Disease and Healthy Controls

2018 ◽  
Vol 51 (02) ◽  
pp. 112-119 ◽  
Author(s):  
Athanasios Anastasilakis ◽  
Dimitrios Koulaxis ◽  
Jagriti Upadhyay ◽  
Eirini Pagkalidou ◽  
Nikoleta Kefala ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Binding Protein ◽  
Stable Coronary Artery Disease ◽  
Control Group ◽  
Healthy Controls ◽  
Lower Accuracy ◽  
Artery Disease ◽  
Stable Cad

AbstractInsulin-like growth factor-1 (IGF-1) and its binding proteins have been implicated in the pathophysiology of coronary artery disease (CAD) and myocardial infarction (MI). We investigated components of the IGF-1 system in circulation at the time of acute MI and following reperfusion in relation to levels of stable CAD patients and controls. Patients with MI (MI Group, n=31) treated with percutaneous coronary intervention (PCI) were compared to patients with stable CAD subjected to scheduled PCI (CAD Group, n=40) and controls with symptoms mimicking CAD without stenosis in angiography (Control Group, n=43). The number and extent of stenosis were recorded. Total and free IGF-1, total and intact IGF binding protein (IGFBP)-3 and -4, pico-Pregnancy Associated Plasma Protein-A (PAPP-A), and the known markers ALT, AST, CK and CK-MB were measured at baseline and 6 or 24 h after the intervention. Patients with MI had higher free IGF-1 (p=0.003) and PAPP-A (p=0.011), but lower intact IGFBP-4 (p=0.006) compared with patients with stable CAD or healthy controls. None of the investigated molecules changed following reperfusion or correlated with the extent of stenosis. AST (p<0.001), CK (p<0.001) and CK-MB (p<0.001), were also higher. Free IGF-1, intact IGFBP-4 and PAPP-A could predict MI, but with lower accuracy than CK-MB. In conclusion, free IGF-1 levels are higher in MI compared to CAD patients and controls and this could result from increased cleavage of its binding protein IGFBP-4 by the higher PAPP-A levels. Free IGF-1, intact IGFBP-4, and/or PAPP-A are inferior to CK-MB as predictors or markers of myocardial damage.

scholarly journals EFFECT OF STATINS ON ENDOTHELIAL PROGENITOR CELL (EPC) MIGRATION FROM PERIPHERAL BLOOD OF STABLE CORONARY ARTERY DISEASE PATIENT

2019 ◽  
Vol 40 (1) ◽  
Author(s):  
Tyagita Rani Savitri ◽  
Yudi Her Oktaviono ◽  
Djoko Soemantri
Keyword(s):  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Endothelial Progenitor Cell ◽  
Peripheral Blood ◽  
Progenitor Cell ◽  
Stable Coronary Artery Disease ◽  
Control Group ◽  
Endothelial Progenitor ◽  
Artery Disease ◽  
Transwell System

Penelitian Klinis ABSTRAK   Efek Pemberian Statin Terhadap Migrasi Endothelial Progenitor Cell (EPC) Pada Darah Tepi Penderita Penyakit Jantung Koroner Stabil Tyagita Verdena Rani Savitri, Yudi Her Oktaviono, Djoko Soemantri   Latar Belakang: Endothlelial progenitor cell (EPC) berpartisipasi dalam perbaikan endotel dan pertumbuhan pembuluh darah baru. Farmakoterapi kardiovaskular telah dibuktikan dapat memperbaiki jumlah dan fungsi EPC pada penderita dengan risiko kardiovaskular. Banyak studi melaporkan bahwa statin memiliki efek yang menguntungkan terhadap EPC dengan meningkatkan jumlah dan fungsi EPC, termasuk didalamnya adalah fungsi migrasi. Oleh karena itu, kami melakukan penelitian untuk menganalisis efek tiga statin yang berbeda terhadap migasi EPC. Tujuan: Untuk menganalisis efek pemberian statin terhadap migrasi EPC pada darah tepi penderita penyakit jantung koroner stabil. Metode: Penelitian ini kami lakukan secara in vitro true experimental post-test only control group design. Sel mononuklear diisolasi dari darah tepi penderita penyakit jantung koroner stabil dan dilakukan kultur dalam medium Stemline II Hematopoietic Stemcell Expansion Medium selama 3 hari. Kemudian sampel dibagi menjadi empat kelompok yaitu kelompok simvastatin 0.5 µmol/L,, atorvastatin 0.5 µmol/L, rosuvastatin 0.5 µmol/L dan kelompok kontrol kemudian diinkubasi selama 48 jam. Metode imunositokimia dilakukan untuk identifikasi EPC dengan mengevaluasi ekspresi CD34+. Pada hari ke-5 kultur, sel di pindahkan ke bagian atas transwell system sebanyak 5x105 sel per sumur perlakuan , kemudian di inkubasi selama 1 hari. Sel yang berpindah pada sumur transwell system bagian bawah dihitung dengan automatic cell counter dengan pewarnaan typhan blue. Data dianalisis dengan independent t test dan ANOVA. Hasil: Hasil independent t test terhadap hasil migrasi pada transwell system menunjukkan peningkatan bermakna terhadap migrasi EPC pada kelompok simvastatin, atorvastatin, dan rosuvastatin dibandingkan dengn kelompok kontrol (234000 ± 1290. 994, 265000 ± 1290. 994, 203000 ± 1290. 994 vs 174071.43 ± 1426. 785, p<0.05). Migrasi EPC juga berbeda antar kelompok statin, dimana efek tertinggi didapatkan pada kelompok atorvastatin. Migrasi EPC pada kelompok atorvastatin lebih tinggi daripada kelompok simvastatin (265000 ± 1290. 994 vs 234000 ± 1290. 994, p<0.05), dan simvastatin lebih tinggi daripada kelompok rosuvastatin (234000 ± 1290. 994 vs 203000 ± 1290. 994, p<0.05). Pemeriksaan imunositokimia menunjukkan ekspresi positif terhadap CD34+. Kesimpulan: Statin meningkatkan migrasi EPC pada darah tepi penderita penyakit jantung koroner stabil. Efek tertinggi tampak pada kelompok atorvastatin, diikuti kelompok simvastatin, dan rosuvastatin.   Kata kunci: Migrasi EPC, simvastatin, atorvastatin, rosuvastatin     Clinical Research   ABSTRACT   Effect of Statins on Endothelial Progenitor Cell (EPC) Migration from Peripheral Blood of Stable Coronary Artery Disease Patient   Tyagita Verdena Rani Savitri Yudi Her Oktaviono Djoko Soemantri     Background: Endothelial progenitor cell (EPC) participates in endothelial repair and new blood vessel growth. Cardiovascular pharmacotherapy has been shown to improve the amount and function of EPC in patients with cardiovascular risk. Many studies report that statins have a beneficial effect on EPC by increasing the number and function of EPC, including the migration function. Therefore, we conducted a study to analyze the effects of three different statins on EPC migration. Objective: To analyze the effect of statins on EPC migration from peripheral blood of stable coronary artery disease (SCAD) patient. Methods: This was an in vitro true experimental post-test only control group design. The MNCs were isolated from peripheral blood of SCAD patient and were cultured in Stemline II Hematopoietic Stemcell Expansion Medium in 3 days. Then samples were put into four groups, simvastatin 0.5 µmol/L, atorvastatin 0.5 µmol/L, rosuvastatin 0.5 µmol/L and control, then incubated for 48 hours. Immunocytochemical examination was performed to evaluate expression of CD34+. On the 5th day of culture, 5x105 cells per group were transferred to the upper chamber of the transwell system, then incubated for 1 day. Cells that migrated to the lower chamber of transwell system were calculated by automatic cell counter with typhan blue coloring. Data were analyzed by independent T-test and ANOVA. Results: The results of independent T-tests showed a significant increase in EPC migration in the simvastatin, atorvastatin, and rosuvastatin groups compared with the control group (234000 ± 1290.994, 265000 ± 1290.994, 203000 ± 1290. 994 vs 174071.43 ± 1426 785, p <0.05). EPC migration also differed between statin groups, where the highest effect was found in the atorvastatin group. EPC migration in the atorvastatin group was higher than the simvastatin group (265,000 ± 1290,994 vs 234,000 ± 1290,994, p <0.05), and simvastatin was higher than the rosuvastatin (234,000 ± 1290,994 vs 203000 ± 1290. 994, p < 0.05). Immunocytochemical examination showed a positive expression on CD34+. Conclusion: Statins increase EPC migration from peripheral blood of SCAD patient. Atorvastatin showed the highest EPC migration, followed by simvastatin, and rosuvastatin. Keywords: EPC migration, simvastatin, atorvastatin, rosuvastatin    

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