阿托伐他汀联合非诺贝特治疗急性冠脉综合征的疗效观察

目的探究阿托伐他汀联合非诺贝特治疗急性冠脉综合征的临床效果。方法选取笔者所在医院2009年6月～2011年6月间收治的急性冠脉综合征患者43例,将其随机分为两组,对照组患者21例给予阿托伐他汀治疗,观察组患者22例给予阿托伐他汀联合非诺贝特治疗,分析两组患者的临床用药情况。结果两组患者低密度脂蛋白、胆固醇、三酰甘油、高密度脂蛋白等指标与治疗前相比均有明显改善,而观察组患者用药效果明显优于对照组,差异有统计学意义(P<0.05)。结论阿托伐他汀与非诺贝特联合应用治疗急性冠脉综合征疗效显著,值得临床推广应用。     

非诺贝特对高TG的2型糖尿病患者PCI术后的影响

目的通过前瞻性随机对比研究,观察非诺贝特联合阿托伐他汀对高TG的2型糖尿病患者药物洗脱支架置入术后的临床疗效。方法入选符合本研究标准的522例药物洗脱支架置入术后高TG的2型糖尿病患者,随机分为两组,联合治疗组249例,非诺贝特200mg晨日一次口服,阿托伐他汀20mg晚日一次口服;阿托伐他汀组273例,20mg晚日一次口服。疗程12个月。比较两组主要不良心血管事件发生情况、降脂疗效及安全性。结果非诺贝特联合阿托伐他汀组主要不良心血管事件发生率及血清TG明显低于阿托伐他汀组(P<0.05),而HDL-C明显高于阿托伐他汀组(P<0.05)。不良反应发生率相似。结论非诺贝特联合阿托伐他汀明显改善高TG的2型糖尿病患者药物洗脱支架置入术后的预后,两药联合安全有效。     

阿托伐他汀联合非诺贝特治疗混合型高脂血症52例

目的探讨阿托伐他汀联合非诺贝特治疗混合型高脂血症的临床疗效及其安全性。方法将104例混合型高脂血症患者随机分为观察组和对照组各52例,观察组采用阿托伐他汀联合非诺贝特治疗,对照组采用阿托伐他汀治疗,比较两组的临床效果及不良反应。结果观察组总有效率86.54%(45/52),对照组总有效率69.23%(36/52),两组比较有显著性差异(P<0.05);两组患者的TC、TG、LDL-C及HDL-C的水平与治疗前比较均有显著性差异(P<0.05),组间比较均有显著性差异(P<0.05)。结论阿托伐他汀联合非诺贝特治疗混合型高脂血症具有协同作用,能有效提高调脂效果,且安全性高,值得临床推广。     

非诺贝特与阿托伐他汀治疗高脂血症及高尿酸血症的效果比较

目的观察微粒化非诺贝特与阿托伐他汀对高脂血症合并高尿酸血症的治疗效果。方法55例高血脂症合并高尿酸血症患者随机分为两组。治疗组30例给予微粒化非诺贝特200mg／d;对照组25例给予阿托伐他汀10mg／d。两组患者均给治疗8周。比较两组临床疗效、血脂和血尿酸水平及不良反应。结果两组治疗后与治疗前比较,甘油三酯（TG）、总胆固醇（TC）差异均有统计学意义。治疗后治疗组与对照组TG差异有统计学意义。治疗组降低血尿酸效果好于对照组。两组均无严重不良反应。结论非诺贝特与阿托伐他汀均可用于高血酸症及高脂血症治疗,短时间内使血脂达标,减少脑血管病的危险因素。     

阿托伐他汀对老年Ⅱ型糖尿病高脂血症的疗效观察

目的:比较他汀类药物阿托伐他汀与贝特类药物非诺贝特治疗老年Ⅱ型糖尿病血脂紊乱的疗效.方法:122例老年Ⅱ型糖尿病高脂血症患者随机分为两组,治疗组(阿托伐他汀组)62例,男44例,女18例,对照组(非诺贝特组)60例,男43例,女17例.治疗组口服阿托伐他汀10 mg, 每晚一次(qn);对照组口服非诺贝特100 mg,每日3次,疗程8周,观察降脂疗效及不良反应.结果:阿托伐他汀降三酰甘油(TG)、总胆固醇 (TC)和低密度脂蛋白(LDL-C)优于非诺贝特(P<0.05);升高高密度脂蛋白(HDL-C)效果相似(P>0.05).结论:阿托伐他汀对老年Ⅱ型糖尿病血脂紊乱的疗效优于非诺贝特.     

阿托伐他汀联合非诺贝特治疗缺血性脑卒中的疗效及对患者血脂、高敏C反应蛋白水平的影响

目的:探讨阿托伐他汀联合非诺贝特防治缺血性脑卒中的临床效果及对患者治疗前后血脂、高敏C反应蛋白(hs-CRP)的影响。方法:64例缺血性脑卒中患者随机分为观察组与对照组各32例。两组患者均给予常规对症治疗,同时对照组给予阿托伐他汀片20 mg,po qn;观察组在对照组基础上再加用非诺贝特胶囊0.2 g,po qd。两组疗程均为3个月。比较两组患者治疗前后神经功能缺损评分、血脂和血清hs-CRP水平变化,及两组药品不良反应。随访1年,观察两组患者脑卒中复发情况。结果:治疗后两组CNDF评分均较治疗前显著降低(P<0.05),且观察组显著低于对照组(P<0.05)。治疗后观察组血脂、血清hs-CRP水平较治疗前明显改善(P<0.05),且均明显优于对照组(P<0.05);而对照组治疗前后血脂、血清hs-CRP水平差异无统计学意义(P>0.05)。两组不良反应发生率差异无统计学意义(P<0.05)。对照组复发率明显高于观察组(P<0.05)。结论:阿托伐他汀联合非诺贝特治疗缺血性脑卒中效果显著,可有效调节血脂、降低血清hs-CRP水平和不良脑血管事件的复发,值得临床推广使用。     

微粒化非诺贝特与阿托伐他汀对不同类型高脂血症患者血脂水平的影响

目的观察微粒化非诺贝特与阿托伐他汀对不同类型高脂血症的降脂疗效及耐受性。方法109例高血脂症的患者,随机分为两组。治疗组55例,给予微粒化非诺贝特200mg.d-1,po;对照组54例,给予阿托伐他汀10mg.d-1,po;两组患者均治疗8周。统计分析两组临床疗效、血脂水平和肝、肾功能,血尿酸及不良反应。结果治疗组降低三酰甘油(TG)明显优于对照组;治疗组降低总胆固醇(TC)、低密度脂蛋白胆固醇(LDL-C)稍优于对照组;微粒化非诺贝特治疗高血脂伴高尿酸血症效果明显,优于阿托伐他汀(P<0.01)。结论微粒化非诺贝特与阿托伐他汀均是高效、安全的降脂药物,可分别用于不同类型的高脂血症治疗,短时间内使血脂达标,减少脑血管病的危险因素。     

应用不同剂量阿托伐他汀治疗急性冠脉综合征临床疗效比较

目的：探讨不同剂量阿托伐他汀治疗急性冠脉综合征的临床疗效。方法：选择本院急性冠脉综合征患者82例,将上述患者随机分为观察组和对照组。两组患者均给予急性冠脉综合征常规治疗外,对照组患者给予阿托伐他汀每天10mg口服,观察组患者给予阿托伐他汀每天40mg口服。两组患者均连续服用6个月。对两组患者治疗前后血脂进行检测;观察两组患者出院后主要心脑血管事件。结果：观察组患者治疗后TG、TC、LDL-C水平与对照组治疗后比较,差异有统计意义（P〈0.05）;观察组复发性心绞痛、心力衰竭、心律失常发生率显著低于对照组,差异有统计学意义（P〈0.05）。结论：较大剂量阿托伐他汀（每天40mg）能够显著改善急性冠脉综合征患者血脂及减少心脑血管事件,临床效果显著。     

阿托伐他汀与非诺贝特治疗高脂血症的比较

目的:比较阿托伐他汀与非诺贝特治疗高脂血症的疗效及安全性.方法:高脂血症86例,随机分为阿托伐他汀组43例,给阿托伐他汀10 mg,qd,共8周;非诺贝特组43例,给非诺贝特200 mg,qd,共8周.结果:两组治疗4周,胆固醇(TC)、三酰甘油(TG)、低密度脂蛋白胆固醇(LDL-ch)均开始显著下降(P<0.01), 治疗8周高密度脂蛋白胆固醇(HDL-ch) 开始显著上升(P<0.05); 阿托伐他汀组治疗8周TC下降较非诺贝特组明显(P<0.05);不良反应发生率阿托伐他汀组9.3%,非诺贝特组4.7%,差异有极显著性(P<0.01).结论:两药均有明显的调脂作用,阿托伐他汀治疗8周TC下降明显优于非诺贝特,非诺贝特的不良反应发生率较低.     

对混合性高脂血症实施阿托伐他汀与非诺贝特治疗的临床效果

目的：观察混合性高脂血症实施阿托伐他汀与非诺贝特治疗的临床效果。方法：选取2012年3月～2015年2月东莞市黄江医院收治的混合性高脂血症患者106例作为研究对象,按照计算机数字法分为对照组（n=53）和治疗组（n=53）,对照组采用阿托伐他汀治疗,治疗组采用阿托伐他汀联合非诺贝特治疗,比较两组治疗效果。结果：经过1个疗程的治疗,两组TG、TC、LDL-C、HDL-C等血脂指标与治疗前相比,差异明显（P＜0.05）,治疗组TG、LDL-C改善情况优于对照组（P＜0.05）,治疗总有效率96.2%明显高于对照组79.3%,组间差异具有统计学意义（P＜0.05）。结论：混合性高脂血症实施阿托伐他汀与非诺贝特治疗效果确切,协同作用良好,可显著改善临床症状,提高调脂效果,具有临床推广价值。     

早期应用阿托伐他汀钙治疗急性冠状动脉综合征的临床研究

目的　观察早期应用阿托伐他汀钙治疗急性冠状动脉综合征 ( ACS)的疗效。方法　 71例 ACS患者随机分为两组 ,对照组和治疗组 ,随访 6个月 ,观察心脑血管事件发生情况以及服药前后纤维蛋白原 ( FIB)、C反应蛋白 ( CRP)的变化。结果　应用阿托伐他汀钙治疗组复发心绞痛、心力衰竭、紧急经皮冠状动脉成形术( PTCA) /冠状动脉搭桥术 ( CABG)因缺血再住院发生率下降 ,FIB、CRP减少。结论　早期应用阿托伐他汀钙治疗 ACS,效果肯定     

替格瑞洛联合阿托伐他汀治疗急性冠状动脉综合征临床研究

目的探讨替格瑞洛联合阿托伐他汀治疗急性冠状动脉综合征的临床疗效,以及对患者血清脑钠肽(BNP)和血清肌钙蛋白Ⅰ(cTnⅠ)水平的影响。方法选取医院2015年8月至2017年8月收治的急性冠状动脉综合征患者120例,按随机数字表法分为观察组和对照组,各60例。两组患者均予阿司匹林肠溶片及注射用依诺肝素钠基础治疗,并予阿托伐他汀钙片,观察组患者加用替格瑞洛片。结果观察组总有效率为91.67%,显著高于对照组的76.67%(P<0.05)。与治疗前比较,两组患者治疗后的左室射血分数(LVEF)和BNP水平均显著升高,左室收缩末期内径(LVESd)、左室舒张末期内径(LVEDd)和cTnⅠ水平均显著降低,且观察组患者上述指标改善程度均显著优于对照组(P<0.05)。观察组与对照组不良反应发生率相当(13.33%比8.33%,χ~2=0.776,P=0.378>0.05)。观察组心血管不良事件发生率为5.00%,显著低于对照组的16.67%(P<0.05)。结论替格瑞洛联合阿托伐他汀治疗急性冠状动脉综合征疗效较好,能改善心功能指标,降低血清BNP和cTnⅠ水平。     

阿托伐他汀的药理作用分析与控制血脂水平的临床疗效研究

目的总结阿托伐他汀的药理作用,探讨阿托伐他汀治疗冠心病高脂血症的疗效及机制。方法 120例患者随机分成观察组和对照组,两组均进行基础治疗,观察组同期加用阿托伐他汀,20mg/d,1次/d。对照组同期加用辛伐他汀,20mg/d,1次/d,疗程均为4周。治疗前后测定两组患者血脂水平与BNP浓度。结果治疗后与治疗前比较,两组TC、TG和LDL-C水平明显降低,HDL-C明显升高,尤其观察组明显（P〈0.05）;治疗后,观察组TC、TG、LDL-C和HDL-C水平与对照组比较,差异有统计学意义（P〈0.05）。两组治疗后BNP浓度明显降低,与治疗前比较差异有统计学意义（P均〈0.05）,且观察组较对照组降低更明显（P〈0.05）。观察组不良反应发生率为2/60（3.33%）,对照组为3/60（5%）,两组不良反应发生率差异无统计学意义（P〉0.05）。结论阿托伐他汀能够降低血脂水平,是治疗冠心病合并高脂血症安全有效的药物。     

瑞舒伐他汀与阿托伐他汀治疗对急性冠脉综合征患者脂蛋白与炎性因子影响对比分析

目的 探讨瑞舒伐他汀同阿托伐他汀治疗急性冠脉综合征的临床疗效及应用价值.方法 将本院治疗的急性冠脉综合征患者随机数字表法分为两组,对照组给予阿托伐他汀治疗,观察组采用瑞舒伐他汀治疗,记录两组效果.结果 观察组治疗后总胆固醇为(4.02±0.37) mmol/L,甘油三酯为(1.85±0.13)mmol/L,低密度脂蛋白为(2.46±0.28) mmol/L,显著优于对照组(P＜ 0.05).观察组治疗后高敏C反应蛋白为(3.11±0.52) mg/L,IL-6为(13.44±2.35) μg/ml,与对照组比较差异有统计学意义(P＜0.05).结论 瑞舒伐他汀治疗急性冠脉综合征可以有效降低患者血脂浓度,减轻患者体内血管炎症因子作用程度.     

盐酸替罗非班治疗非ST段抬高急性冠状动脉综合征40例临床疗效观察

目的探讨盐酸替罗非班治疗非ST段抬高急性冠状动脉综合征40例临床疗效。方法选择我院非ST段抬高型急性冠状动脉综合征80例,随机分为观察组和对照组。对照组采用常规治疗,观察组在常规治疗基础上给予替罗非班治疗。观察两组患者治疗后36h和治疗后30d内主要不良心血管事件发生情况,记录治疗期间出血发生情况。结果观察组患者治疗后36h主要不良心血管事件发生率显著低于对照组,差异有统计学意义(P<0.05);观察组患者治疗后30d主要不良心血管事件发生率显著低于对照组,差异有统计学意义(P<0.05)。观察组出血发生率与对照组比较,差异无统计学意义(P>0.05)。结论替罗非班能够降低非ST段抬高急性冠状动脉综合征患者主要不良心血管事件发生率,疗效显著,值得借鉴。     

Fenofibrate: a review of its use in dyslipidaemia

Fenofibrate is a fibric acid derivative indicated for the treatment of severe hypertriglyceridaemia and mixed dyslipidaemia in patients who have not responded to nonpharmacological therapies. The lipid-modifying effects of fenofibrate are mediated by the activation of peroxisome proliferator-activated receptor-α. Fenofibrate also has nonlipid, pleiotropic effects (e.g. reducing levels of fibrinogen, C-reactive protein and various pro-inflammatory markers, and improving flow-mediated dilatation) that may contribute to its clinical efficacy, particularly in terms of improving microvascular outcomes. Fenofibrate improves the lipid profile (particularly triglyceride [TG] and high-density lipoprotein-cholesterol [HDL-C] levels) in patients with dyslipidaemia. Compared with statin monotherapy, fenofibrate monotherapy tends to improve TG and HDL-C levels to a significantly greater extent, whereas statins improve low-density lipoprotein-cholesterol (LDL-C) and total cholesterol levels to a significantly greater extent. Fenofibrate is also associated with promoting a shift from small, dense, atherogenic LDL particles to larger, less dense LDL particles. Combination therapy with a statin plus fenofibrate generally improves the lipid profile to a greater extent than monotherapy with either agent in patients with dyslipidaemia and/or type 2 diabetes mellitus or the metabolic syndrome. In the pivotal FIELD and ACCORD trials in patients with type 2 diabetes, fenofibrate did not significantly reduce the risk of coronary heart disease events to a greater extent than placebo, and simvastatin plus fenofibrate did not significantly reduce the risk of major cardiovascular (CV) events to a greater extent than simvastatin plus placebo. However, the risk of some nonfatal macrovascular events and the incidence of certain microvascular outcomes were reduced significantly more with fenofibrate than with placebo in the FIELD trial, and in the ACCORD trial, patients receiving simvastatin plus fenofibrate were less likely to experience progression of diabetic retinopathy than those receiving simvastatin plus placebo. Subgroup analyses in the FIELD and ACCORD Lipid trials indicate that fenofibrate is of the greatest benefit in decreasing CV events in patients with atherogenic dyslipidaemia. Fenofibrate is generally well tolerated when administered alone or in combination with a statin. Thus, in patients with dyslipidaemia, particularly atherogenic dyslipidaemia, fenofibrate is a useful treatment option either alone or in combination with a statin.     

Efficacy of combination of atorvastatin and micronised fenofibrate in the treatment of severe mixed hyperlipidemia

OBJECTIVES: In patients with mixed lipid disorders, monotherapy may not effectively control all lipid abnormalities. We undertook this study to assess the efficacy of fenofibrate in combination with atorvastatin in patients with severe mixed dyslipidemia. METHODS: This was an 18-week, open-label study conducted in our lipid clinic. After a 6-week dietary baseline phase, patients received 200 mg/day micronised fenofibrate for 6 weeks. At the end of this period the subjects discontinued this treatment and received 40 mg/day atorvastatin for 6 weeks. Finally 200 mg/day of micronised fenofibrate was added to the statin therapy. RESULTS: Administration of micronised fenofibrate reduced serum triglycerides (P < 0.01) and total cholesterol and low-density lipoprotein (LDL) cholesterol (P < 0.05 for both parameters), while it evoked a significant increase in serum high-density lipoprotein (HDL) cholesterol levels (P < 0.05). Atorvastatin monotherapy induced a more pronounced decrease of total and LDL cholesterol. However, plasma triglycerides, although significantly lower than baseline values (P < 0.05), were higher than the values observed during treatment with fenofibrate. Moreover, serum HDL cholesterol concentrations were higher during fibrate therapy than during the statin one. During the combination therapy, the decrease in triglycerides was greater than that observed with fenofibrate alone, while the decrease in LDL cholesterol was more pronounced than that observed with atorvastatin alone. CONCLUSION: The combination of atorvastatin with micronised fenofibrate in patients with severe mixed dyslipidemia may have a favourable effect on some major coronary artery disease risk factors.     

Fenofibrate: a review of its use in primary dyslipidaemia, the metabolic syndrome and type 2 diabetes mellitus

Fenofibrate is a fibric acid derivative indicated for use in the treatment of primary hypercholesterolaemia, mixed dyslipidaemia and hypertriglyceridaemia in adults who have not responded to nonpharmacological measures. Its lipid-modifying effects are mediated by activation of peroxisome proliferator-activated receptor-alpha. Fenofibrate also has nonlipid (i.e. pleiotropic) effects (e.g. it reduces fibrinogen, C-reactive protein and uric acid levels and improves flow-mediated dilatation). Fenofibrate improves lipid levels (in particular triglyceride [TG] and high-density lipoprotein-cholesterol [HDL-C] levels) in patients with primary dyslipidaemia. Its lipid-lowering profile means that fenofibrate is particularly well suited for use in atherogenic dyslipidaemia (characterised by high TG levels, low HDL-C levels and small, dense low-density lipoprotein [LDL] particles), which is commonly seen in patients with the metabolic syndrome and type 2 diabetes mellitus. Indeed, fenofibrate improves the components of atherogenic dyslipidaemia in patients with these conditions, including a shift from small, dense LDL particles to larger, more buoyant LDL particles. Greater improvements in lipid levels are seen when fenofibrate is administered in combination with an HMG-CoA reductase inhibitor (statin) or in combination with ezetimibe, compared with monotherapy with these agents. In the DAIS study, fenofibrate significantly slowed the angiographic progression of focal coronary atherosclerosis in patients with type 2 diabetes. In terms of clinical outcomes, although no significant reduction in the risk of coronary events was seen with fenofibrate in the FIELD trial in patients with type 2 diabetes, treatment was associated with a significantly reduced risk of total cardiovascular disease (CVD) events, primarily through the prevention of non-fatal myocardial infarction and coronary revascularisation. Subgroup analyses revealed significant reductions in total CVD events and coronary heart disease events in patients with no previous CVD, suggesting a potential role for primary prevention with fenofibrate in patients with early type 2 diabetes. Improvements were also seen in microvascular outcomes with fenofibrate in the FIELD trial. Fenofibrate is generally well tolerated, both as monotherapy and when administered in combination with a statin. Combination therapy with fenofibrate plus a statin appears to be associated with a low risk of rhabdomyolysis; no cases of rhabdomyolysis were reported in patients receiving such therapy in the FIELD trial. Thus, fenofibrate is a valuable lipid-lowering agent, particularly in patients with atherogenic dyslipidaemia.     

阿托伐他汀治疗稳定型冠心病的临床效果观察

目的对阿托伐他汀治疗稳定型冠心病的临床效果进行分析。方法120例稳定型冠心病患者,随机分为对照组和观察组,每组60例。对照组患者采用常规治疗,观察组患者在对照组基础上联合阿托伐他汀治疗。比较两组患者治疗前后血脂指标水平、缺血事件发生情况。结果治疗前,两组患者总胆固醇(TC)、甘油三酯(TG)、低密度脂蛋白胆固醇(LDL-C)、高密度脂蛋白胆固醇(HDL-C)水平比较差异无统计学意义(P>0.05);治疗后,观察组患者TC(4.27±0.42)mmol/L、TG(2.14±0.59)mmol/L、LDL-C(0.93±0.52)mmol/L均低于对照组的(5.43±0.94)、(2.44±0.71)、(3.27±0.34)mmol/L,HDL-C(1.44±0.54)mmol/L高于对照组的(1.24±0.44)mmol/L,差异具有统计学意义(P<0.05)。观察组患者缺血事件发生率为5.0%,低于对照组的16.7%,差异具有统计学意义(P<0.05)。结论采用阿托伐他汀治疗稳定型冠心病有助于改善患者血脂指标,降低缺血事件发生率,为稳定型冠心病的临床治疗提供了参考依据。     

阿托伐他汀的药理及临床应用效果分析

目的 比较阿托伐他汀治疗急性冠脉综合征(ACS)的临床疗效,探讨其药理作用.方法 选择某医院急性冠脉综合征的患者86例,随机分为两组每组43例.治疗组采用早期给予阿托伐他汀联合ACS常规治疗,对照组仅给予常规治疗,治疗8周后,对比两组患者治疗前后血清中炎症因子的差异情况和血脂水平的变化情况.结果 治疗后两组患者的临床症状均得到改善,治疗组患者的血清炎症因子水平和血脂水平的下降幅度优于对照组,差异有统计学意义(P<0.05).结论 阿托伐他汀因其有较好的抗炎、改善血脂作用,对治疗ACS疗效确切.