Background: Inflammation has been evidenced as a critical contributable mechanism for the atrial fibrillation (AF) onset and development. As the consistent inflammatory and oxidative marker, the effects of white blood cell (WBC) and its differential on lone atrial fibrillation (LAF) were investigated in the study.Methods: A total of 126 patients with paroxysmal LAF who scheduled for rhythm control drug therapy and 120 age-and gender-matched subjects in sinus rhythm were included sequentially. Peripheral blood sample and clinic data were collected during the first evaluation. Recurrence of AF was evaluated by outpatient clinics and telephone visits for the following 12 months.Results: Peripheral eosinophil count, neutrophil count, and left atrial diameter (LAD) were significantly higher in LAF than control. Within a follow-up of 12 months, 56 patients (44.4%) had developed AF recurrence. Patients with AF recurrence had higher eosinophil count and LAD. Univariable analyses showed a statistically significant relationship between eosinophil count (P = 0.042), LAD (P = 0.030), and AF recurrence. Multivariate logistic regression analysis showed that LAD (OR: 1.090 per 1mmincrease; 95% CI: 1.007-1.180; P = 0.032) and eosinophil (OR: 1.643 per 1 x 108/L increase; 95% CI: 1.047-2.578; P = 0.031) were independent predictors of AF recurrence during antiarrhythmic drug therapy.Conclusion: Our results support the association of the WBC response and its components with the LAF. Especially, the peripheral eosinophil and LAD may play important roles in mediating inflammation and atrial remodeling in AF.

Objectives: Beta-blockers have improved the prognosis of patients with dilated cardiomyopathy as they improve left ventricular (LV) systolic function and structure, which are crucial for myocardial recovery. However, to date, no accurate methods can predict the effectiveness of beta-blocker therapy. Our goal was to evaluate whether peripheral endothelial function could be a useful predictor for beta-blocker responses and related LV reverse remodeling (LVRR) in patients with idiopathic dilated cardiomyopathy (IDC).Methods: Fifty-two IDC patients were recruited and underwent brachial artery flow-mediated dilation (FMD). Beta-blockers were titrated to doses tolerable for each patient. LV function and structure were measured by echocardiography. A positive response to beta-blockers was defined as an increase of >= 10% in LV ejection fraction (LVEF). LVRR was defined as an increase of >= 10% in LVEF and a decrease of >= 15% in LV end-systolic volume (LVESV).Results: Baseline FMD was 8.4 +/- 3.0% in IDC patients and significantly lower than healthy controls. At three-month follow-up, 54% of patients had a positive beta-blocker response and 40% achieved LVRR. Patients with a positive response to beta-blockers or with LVRR had significantly higher baseline FMD values than those without. FMD was the most significant predictor of changes in LVEF and LVESV. The sensitivity and specificity of baseline FMD to predict beta-blocker responses was 64.3% and 83.3%, respectively, and to predict LVRR was 61.9% and 80.6%, respectively. Beta-blockers themselves did not influence FMD values.Conclusions: FMD could serve as an independent predictor for monitoring beta-blocker therapy effectiveness in IDC patients. (C) 2016 Published by Elsevier Ireland Ltd.

BACKGROUND:Patients with metabolic syndrome are at increased risk for cardiovascular disease. Combination lipid-lowering therapy is often needed in patients with metabolic syndrome and mixed dyslipidemia. The aim of this study was to compare the effect of statin combined with a new hypolipidemic agent, coenzyme A (CoA) with moderate-dose statin monotherapy in subjects with metabolic syndrome and mixed dyslipidemia by evaluating data from a subgroup of patients with metabolic syndrome and mixed dyslipidemia from a previously conducted randomized study.METHODS:In the present post hoc analysis, 212 patients were included, receiving statin monotherapy (n = 94) or statin combined with CoA 400 U/day (n = 118) for 8 weeks. The lipoprotein profile was determined at baseline and week 8 visits. Attainment of low-density lipoprotein-cholesterol (LDL-C) < 100 mg/dL, non-high-density lipoprotein-cholesterol (HDL-C) < 130 mg/dL, and the combined goal of these two parameters was also evaluated.RESULTS:The mean percent change was more prominent with CoA plus statin compared with placebo plus statin in triglyceride (TG) (-32.5% vs. -8.7%, respectively; P = 0.0002), total cholesterol (-9.6% vs. -3.6%, P = 0.013), LDL-C (-7.5% vs. 2.1%, P = 0.033), and non-HDL-C (-14.3% vs. -6.4%, P = 0.011). Treatment with CoA plus statin resulted in larger percentages of participants attaining lipid goals for LDL-C (70.3% vs. 56.4%, P = 0.044), non-HDL-C (60.2% vs. 45.7%, P = 0.039), and the combined goal of LDL-C and non-HDL-C (57.6% vs. 42.6%, P = 0.038) than statin monotherapy.CONCLUSION:These results demonstrate that CoA plus statin therapy was more effective in improving lipoprotein parameters than statin alone in patients with metabolic syndrome and mixed hyperlipidemia.

AbstractThe aim of the study was to evaluate the efficacy and safety of 1-h infusion of recombinant human atrial natriuretic peptide (rhANP) in combination with standard therapy in patients with acute decompensated heart failure (ADHF).This was a phase III, randomized, double-blind, placebo-controlled, multicenter trial. Eligible patients with ADHF were randomized to receive a 1-h infusion of either rhANP or placebo at a ratio of 3:1 in combination with standard therapy. The primary endpoint was dyspnea improvement (a decrease of at least 2 grades of dyspnea severity at 12 h from baseline). Reduction in pulmonary capillary wedge pressure (PCWP) 1 h after infusion was the co-primary endpoint for catheterized patients. Overall, 477 patients were randomized: 358 (93 catheterized) patients received rhANP and 118 (28 catheterized) received placebo. The percentage of patients with dyspnea improvement at 12 h was higher, although not statistically significant, in the rhANP group than in the placebo group (32.0% vs 25.4%, odds ratio=1.382, 95% confidence interval [CI]: 0.863–2.212, P = 0.17). Reduction in PCWP at 1 h was significantly greater in patients treated with rhANP than in patients treated with placebo (−7.74 ± 5.95 vs −1.82 ± 4.47 mm Hg, P < 0.001). The frequencies of adverse events and renal impairment within 3 days of treatment were similar between the 2 groups. Mortality at 1 month was 3.1% in the rhANP group vs 2.5% in the placebo group (hazard ratio = 1.21, 95% CI: 0.34–4.26; P > 0.99).1-h rhANP infusion appears to result in prompt, transient hemodynamic improvement with a small, nonsignificant, effect on dyspnea in ADHF patients receiving standard therapy. The safety of 1-h infusion of rhANP seems to be acceptable. (WHO International Clinical Trials Registry Platform [ICTRP] number, ChiCTR-IPR-14005719.)

目的:对比分析失代偿性心力衰竭患者中单剂与重复左西孟坦静脉注射治疗的疗效差异.方法:入选我院连续收治的失代偿性心力衰竭(NYHA心功能分级Ⅲ～Ⅳ级,左室射血分数低于40％)患者共89例,随机分入单剂组(44例)和重复组(45例).所有患者均在常规抗心衰治疗(个体化合理应用肾素-血管紧张素-醛固酮系统抑制剂、β受体阻滞剂、利尿剂、洋地黄等)的基础上给予左西孟坦针剂标准治疗(初始负荷剂量12 μg·kg-1静脉推注10 min、继以0.2μg· kg-1·min-1的剂量微泵持续静脉注射24 h).重复组患者1个月后再次给予上述剂量左西孟坦治疗.比较两组首次治疗后3个月的心功能分级、超声心动图、血N末端脑钠肽前体(NT-proB-NP)水平的差异.结果:与单剂组患者相比,重复组患者的NYHA心功能分级改善更明显[(-1.02±0.79)∶(-1.51±0.66),P＜0.01];左室射血分数改善[(2.9±7.1)％∶(6.7±8.1)％,P＜0.05]及心肌做功指数改善[(-0.05±0.14)∶(-0.22±0.13),P＜0.01]程度均达到统计学差异;血NT-proBNP水平降幅显著[(-822.6±454.2) pg/ml∶(-1 188.0±422.6)pg/ml,P＜0.01].结论:对于失代偿性心力衰竭患者在单剂左西孟坦治疗1个月后再次重复给药,可进一步改善患者的心功能水平.

The association between the estrogen receptor α gene (ESR1) PvuII polymorphism (c.454-397T>C) and coronary artery disease (CAD) is controversial. Thus, we conducted a meta-analysis to evaluate the relationship. Data were collected from 21 studies encompassing 9926 CAD patients and 16710 controls. Odds ratios (ORs) with 95% confidence intervals (CIs) were used to assess the relationship between PvuII polymorphism and CAD. The polymorphism in control populations in all studies followed Hardy-Weinberg equilibrium. We found a significant association between ESR1 PvuII polymorphism and CAD risk in all subjects. When the data were stratified by region, a significant association between ESR1 PvuII polymorphism and CAD risk was observed in Asian populations but not in Western populations. The current study suggests that ESR1 PvuII polymorphism has an important role in CAD susceptibility.

Background Patients with mixed hyperlipidemia usually are in need of combination therapy to achieve low-density lipoprotein cholesterol (LDL-C) and triglyceride (TG) target values for reduction of cardiovascular risk. This study investigated the efficacy and safety of adding a new hypolipidemic agent, coenzyme A (CoA) to stable statin therapy in patients with mixed hyperlipidemia. Methods In this multi-center, 8-week, double-blind study, adults who had received ≥8 weeks of stable statin therapy and had hypertriglyceridemia (TG level at 2.3-6.5 mmol/L) were randomized to receive CoA 400 U/d or placebo plus stable dosage of statin. Efficacy was assessed by the changes in the levels and patterns of lipoproteins. Tolerability was assessed by the incidence and severity of adverse events (AEs). Results A total of 304 patients with mixed hyperlipidemia were randomized to receive CoA 400 U/d plus statin or placebo plus statin (n = 152, each group). After treatment for 8 weeks, the mean percent change in TG was significantly greater with CoA plus statin compared with placebo plus statin (-25.9% vs -4.9%, respectively; p = 0.0003). CoA plus statin was associated with significant reductions in TC (-9.1% vs -3.1%; p = 0.0033), LDL-C (-9.9% vs 0.1%; p = 0.003), and non- high-density lipoprotein cholesterol (-13.5% vs -5.7%; p = 0.0039). There was no significant difference in the frequency of AEs between groups. No serious AEs were considered treatment related. Conclusions In these adult patients with persistent hypertriglyceridemia, CoA plus statin therapy improved TG and other lipoprotein parameters to a greater extent than statin alone and has no obviously adverse effect. Trial registration Current Controlled Trials ClinicalTrials.gov ID NCT01928342 .

Background: Chronic atrial fibrillation (AF) is characterized by a remodeling process with prominent atrial fibrosis. Fibrocytes, a bone marrow-derived population of fibroblast-like cells, have been placed at the center of a number of fibrosing conditions. The purpose of this study was to evaluate the contribution of fibrocytes to atrial fibrosis in patients with chronic AF and the possible mechanisms.Methods and Results: We enrolled 22 consecutive valvular heart disease patients with chronic AF (>6 months: CAF group) and 15 valvular heart disease patients in sinus rhythm served as controls (SR group). Left atrial tissue samples were obtained during cardiac surgery. The infiltration of fibrocytes into the atrial interstitium was observed by confocal microscopy. The number of atrial fibrocytes was approximately three-fold higher in the CAF group compared with the SR controls, and positively correlated with both the atrial collagen volume fraction (r=0.713; P=0.0002) and the left atrial volume index (r=0.631; P=0.002). In the peripheral blood samples collected before the operation, approximately 2.5-fold higher percentage of circulating fibrocytes was identified in the CAF group. These fibrocytes showed a stronger proliferative capacity (approximate to 2.5-fold) and higher level expression of collagen I and alpha-SMA (approximate to 2-fold and 4-fold, respectively) compared with the SR controls.Conclusions: The results suggested that fibrocytes may be involved in atrial fibrosis in chronic AF through enhanced profibrotic characteristics.

Retraction notice for The Effect of Coenzyme A Capsule on Serum Triglyceride Concentration in Patients with Hypertriglyceridemia: Results of a Multicenter Clinical Trial by Tianming Xuan, Bifeng Wu, Yunpeng Shang, Jiangtao Lai, Xiaosheng Hu, Zhong Liu, and Junzhu Chen The article has been retracted due to its earlier publication in substantially similar form as follows: Effect and Safety of coenzyme A on Hyperlipidemia by Zhao Shu-ping, Chen Ya-qin, Chen Jun-zhu, Lai Jiang-tao, published in the Chinese Journal of New Drugs and Clinical Remedies; 2012:242-245. The Effects of Coenzyme A on Serum Lipids in Patients With Hyperlipidemia: Results of a Multicenter Clinical Trial by Ya-qin Chen, Shui-ping Zhao, Jun-zhu Chen and Jiangtao Lai, published in the Journal of Clinical Endocrinology & Metabolism on January 4, 2013 jc.2012-2702. DOI:10.1210/jc.2012-2702.

AIM To compare the effects of coenzyme A(CoA) and pantethine on plasma lipid levels in Chinese patients with moderate hyperlipidemia.METHODS In the prospective,randomized,double-blind, multi-centre,phaseⅢclinical trial,223 patients with hyperlipidemia(triglyceride(TG) 2.3 - 6.5 mmol·L~(-1)) were randomly received CoA 400 U·d~(-1)(po,n = 118) and pantethine 600 mg·d~(-1)(po,n =118) for 8 weeks. After 4 weeks and 8 weeks,blood routine,urine routine,hepatic function,renal function,blood glucose, blood lipid and creatine kinase were measured.The primary end point was the percentage change in TG from baseline to 4 weeks and 8 weeks,and the secondary efficacy parameters were variation rates of plasma total cholesterol(TC),low - density lipoprotein cholesterol(LDL - C) and high - density lipoprotein cholesterol (HDL-C).Adverse events were compared in two groups after the treatment.RESULTS After the treatment for 4 weeks,TG levels of the CoA group and the pantethine group were reduced 26.0%and 17.4%respectively, with 33.3%and 16.5%after 8 weeks treatment.The difference between two groups was significant(P0.01). Compared with the pantethine group,the reduction rate of TC in the CoA group was higher(P0.05).After the treatment,there was no significant difference of LDL-C and HDL-C between two groups(P0.05).There was also no significant difference of drug - related adverse event rates between two groups(P0.05). CONCLUSIONS CoA 400 U·d~(-1) and pantethine 600 mg·d~(-1) had the effect on lowing TG with good safety and tolerance in the moderate hyperlipidemia patients,and CoA was better than pantethine.

Retraction notice for “The Effect of Coenzyme A Capsule on Serum Triglyceride Concentration in Patients with Hypertriglyceridemia: Results of a Multicenter Clinical Trial” by Tianming Xuan, Bifeng Wu, Yunpeng Shang, Jiangtao Lai, Xiaosheng Hu, Zhong Liu, and Junzhu Chen The article has been retracted due to its earlier publication in substantially similar form as follows: Effect and Safety of coenzyme A on Hyperlipidemia by Zhao Shu-ping, Chen Ya-qin, Chen Jun-zhu, Lai Jiang-tao, published in the Chinese Journal of New Drugs and Clinical Remedies; 2012:242-245. The Effects of Coenzyme A on Serum Lipids in Patients With Hyperlipidemia: Results of a Multicenter Clinical Trial by Ya-qin Chen, Shui-ping Zhao, Jun-zhu Chen and Jiangtao Lai, published in the Journal of Clinical Endocrinology & Metabolism on January 4, 2013 jc.2012-2702. DOI:10.1210/jc.2012-2702.

Objective To evaluate the clinical application of implantable cardioverter defibrillator (ICD) / cardiac resynchronization therapy-defibrillator (CRT-D) for primary prevention in sudden cardiac death (SCD) high-risk Chinese patients. Methods Eighty patients treated with ICD / CRT-D implantation for primary prevention of SCD in our unit between 2009 and 2011 were enrolled in the study. Single-chamber or dual-chamber ICDs were implanted in 33 cases and CRT-D in 47 cases. Of the 80 cases, 44 (55.0%) had non-ischemic cardiomyopathy and 22 (27.5%) had ischemic cardiomyopathy. All the patients were followed up at one and three months after implantation, and every six months thereafter or when prompted by an ICD event. Results During an average follow-up of 23 ± 7 months, 11 (13.7%) patients had unplanned readmis sions and 4 (5.0% ) died. Thirty-eight ICD therapy events were recorded, including 26 appropriate ICD therapies and 12 inappropriate therapies, of the later were due to atrial fibrillation. Conclusions ICD / CRT-D for primary prevention of SCD may recognize malignant rapidarrhythmia in a short time so that the patients can be treated timely. Therefore, it can reduce the sudden cardiac death rate in high-risk patients.

The T gene, which was cloned from the mitochondria of tumorous stem mustard (Brassica juncea var. tumida), is a cytoplasmic male sterility (CMS)-related gene that can produce two transcripts, T1170 and T1243. The latter is transcribed with the uncleaved intron TinII. In our previous study, transgenic Arabidopsis thaliana plants over-expressing the T1243 transcript (OE-T1243) showed a severe male-sterile phenotype, whereas OE-T1170 plants did not. However, the functional mechanism of the T gene in B. Juncea remained unknown. In this study, microscopic analyses of paraffin sections of anthers confirmed that OE-T1243 plants did not produce normal pollen, whereas OE-T1170 plants did. We analyzed the transcription of 15 anther development-related genes and found that transcript levels of nozzle/sporocyteless and barely any meristem 1 and 2 were markedly lower in OE-T1243 plants than those in wild type, while the transcript levels of these genes in OE-T1170 plants were unchanged. To investigate the potential roles of TinII, we inserted the TinII sequence upstream of a minimal region (−60) of the cauliflower mosaic virus 35S promoter fused to the 5′ end of the β-glucuronidase (GUS) reporter gene. Analysis of the transgenic plants suggested that TinII acted as an enhancer to significantly increase GUS expression. The potential action mechanism is that the TinII intron acts as an enhancer to affect the function of the CMS-related gene T.

目的 检测特发性肺动脉高压(IPAH)患者外周血内皮祖细胞(EPCs)数量,分析EPCs和肺动脉压力的关系.方法 收集28例住院的IPAH患者为IPAH组,选择同期20例健康志愿者为对照组,采用体外培养外周血EPCs,激光共聚焦显微镜鉴定正在分化的EPCs,在倒置相差显微镜下计数EPCs数目.同时对28例IPAH患者经右心漂浮导管检测肺动脉压力.结果 对照组外周血EPCs为(34.7±7.6)个,IPAH组外周血EPCs为(61.6±10.4)个,两组外周血EPCs数量比较,差异有统计学意义(P＜0.05).经右心漂浮导管检测,肺动脉平均压力与外周血EPC水平呈负相关(r=-0.625,P＜0.001).结论 IPAH患者外周血EPCs数量低于正常对照组,并和肺动脉压力呈负相关,提示EPCs的减少可能加重IPAH患者内皮功能的紊乱,EPCs可能参与IPAH形成的病理生理过程.

OBJECTIVES The aim of the study was to evaluate the lipid-lowering effects and clinical safety of a natural hypolipidemic compound, coenzyme A (CoA) capsule, in Chinese patients with moderate dyslipidemia. METHODS A total of 244 subjects (170 males and 74 females; aged 18-75 y) having moderate dyslipidemia (triglyceride [TG], 2.3-6.5 mmol · L(-1)) were randomly divided into 3 groups, to which placebo (group A, n = 81), CoA 200 U/d (group B, n = 79), and CoA 400 U/d (group C, n = 84) were administered, respectively. Blood lipoproteins, liver and renal functions, blood glucose, and complete blood count were measured at the baseline and after 4 or 8 weeks of treatment. RESULTS After treatment for 4 weeks, TG was reduced by 5.1, 15.7, and 14.4% in groups A, B, and C, respectively. After treatment for 8 weeks, TG decreased .9, 21.7, and 36.1%, respectively. Compared with group A, the primary efficacy outcome TG in groups B and C significantly decreased (P < .01), and the difference between groups B and C was also significant (P < .01). Plasma total cholesterol, low-density lipoprotein cholesterol, and high-density lipoprotein cholesterol were not significantly different. Furthermore, there was no difference in blood glucose, hepatic and renal function test parameters, incidence of myopathy, or gastrointestinal tract symptoms among the 3 groups. CONCLUSION CoA can effectively reduce plasma TG levels in subjects with moderate dyslipidemia and has no obvious adverse effect.

<正>动脉粥样硬化从青年开始并一直持续好几十年,最终导致非致命或致命的心血管事件,包括心肌梗死、脑卒中和猝死。零级预防和一级预防的开展,可以预防大部分心血管病。通过减少烟草的消耗、限制食盐的摄入、鼓励身体锻炼与提高饮食质量等公共政策和

Objective To investigate the effectiong of idiopathic pulmonary arterial hypertension ( IPAH ) on bone morphogenetic protein-2 ( BMP-2 ) and counts of endothelial progenitor cells ( EPC ) , and the co relationg between and BMP-2 and pulmary arterial pressure(PAP) and the counts of EPC. Methods The patients with IPAH ( n =28 ) diagnosed by the examination of right heart floating catheters for pulmonary arterial pressure were selected as experimental group, and healthy volunteers were selected as control group. The concentration of plasma BMP-2 was detected by using enzyme-linked immunosorbent assay ( ELISA ) and EPC in peripheral blood were counted under the microscope. Results The difference in plasma BMP-2 had statistical significance between IPAN group and contrlo group [ ( 0.1294 ± 0.0292 )μ g/mL vs.( 0.0898 ± 0.0295 )μ g/mL, P <0.01], and the difference in EPC counts also had statistical significance [ ( 26.75 ± 5.87 ) piece vs.( 42.65 ± 8.37 ) piece, P <0.01]. The relation of BMP-2 and PAP was positive, while negative between BMP-2 and EPC. Conclusion IPAH caused the increase of BMP-2 while desease of EPC, the relation between BMP-2 and PAP or BMP-2 and EPC was existed in IPAH patients.

Background/Aims: Circulating fibrocytes (CFs) have been placed at the center of a number of fibrosing conditions. Recently, attention has been drawn to the non-anticoagulant activities of low molecular weight heparin (LH), especially its anti-fibrotic effects. The purpose of this study was to investigate the effects of LH on CFs differentiation and possible underlying mechanisms. Methods/Results: CFs were cultured from human peripheral blood mononuclear cells and identified by dual-immunofluorescence staining. Incubation with LH inhibited CFs trans-differentiation by upregulating CD34 and downregulating pro-Collagen I and a-SMA in a concentration- and time-dependent manner, all of which were detected by flow cytometry. Similar effects were observed after incubation with L-NAME, an inhibitor of NOS. NO production was measured by Griess methods and markedly decreased in CFs treated with LH. Three NOS isoforms were assessed by western blot and nNOS was the predominant isoform involved in this process. Additionally, LH and L-NAME had similar down-regulating effects on the expression of TGF-β1 and pSmad2/3, which indicated that TGF-β/Smad pathway might be a downstream signaling of nNOS/NO during LH treatment. Conclusion: These results suggested that LH could exhibit anti-fibrotic effects by inhibiting CFs transdifferentiation, in which the involvement of nNOS/NO and TGF-β/Smad pathway were identified.

AIM To evaluate the dose-dependent efficacy and safety of coenzyme A(CoA)capsule in Chinese patients with hyperlipidemia.METHODS In the randomized,placebo-controlled,double-blind,multi-centre,phase Ⅱclinical trial,244 hyperlipidemia patients(triglyceride(TG)2.3-6.5 mmol·L-1)were randomly received placebo(po,n = 81),CoA 200 U·d-1(po,n = 84)or CoA 400 U·d-1 group(po,n = 79)for 8 weeks.Blood routine,urine routine,hepatic function,renal function,blood glucose and blood lipid were measured at 4 weeks and 8 weeks.The primary end point was the percentage change in TG from baseline to week 4 and week 8.Variation rates of plasma total cholesterol(TC),low-density lipoprotein cholesterol(LDL-C)and high-density lipoprotein cholesterol(HDL-C)were the secondary end points.Adverse events were compared after the treatment.RESULTS After the treatment for 4 weeks,TG levels of the placebo group,the CoA 200 U·d-1group and the CoA 400 U·d-1group were reduced 5.1%,15.7% and 14.4% respectively,and 0.9%,21.7% and 36.1% after 8 weeks treatment.Compared with the placebo group and the baseline level,TG levels in the CoA 200 U·d-1 group and the CoA 400 U·d-1 group significantly decreased(P < 0.01),and there was significant difference between the CoA 200 U·d-1 group and 400 U·d-1 group(P < 0.01).There were no significant differences of TC,LDL-C and HDL-C(P > 0.05)and drug-related adverse event rates(P = 0.11)among the three groups after the treatment.CONCLUSION It was shown that CoA reduced serum TG level effectively and with good safety and tolerance in the hyperlipidemia patients.