阿托伐他汀联合依折麦布治疗混合型高脂血症的临床观察

目的观察阿托伐他汀联合依折麦布治疗混合型高脂血症的疗效和安全性。方法选取100例混合型高脂血症病人单用阿托伐他汀(20mg/d)治疗1个月后血脂不达标的30例病人为研究对象,观察接受阿托伐他汀(20mg/d)联合依折麦布(5mg/d)治疗后的血脂情况和不良反应发生情况。结果与治疗前相比,阿托伐他汀单用组和阿托伐他汀联合依折麦布治疗组总胆固醇(TC)、三酰甘油(TG)、低密度脂蛋白胆固醇(LDL-C)均降低,而HDL-C差异无统计学意义。两组谷丙转氨酶(ALT)、肌酸激酶(CK)比较差异无统计学意义。阿托伐他汀单用组调脂幅度:TC下降25%,LDL-C下降30%,TG下降30%;阿托伐他汀联合依折麦布治疗组在阿托伐他汀降脂基础上,TC下降35.9%,LDL-C下降39%,TG下降51.4%。两组不良反应均很轻微和少见。结论阿托伐他汀联合依折麦布治疗混合型高脂血症可以明显降低TC、LDL-C和TG,且不良反应轻微,耐受性好。     

联合调脂治疗对老年混合型高脂血症病人的疗效观察

目的观察小剂量阿托伐他汀联合非诺贝特/依折麦布治疗老年混合型高脂血症病人的临床疗效和安全性。方法选择2016年1月—2016年12月于我院就诊的老年混合型高脂血症病人120例,随机分为3组,各40例。对照组给予阿托伐他汀(20mg/d)治疗,观察一组给予阿托伐他汀(10mg/d)和非诺贝特(0.2g/d),观察两组给予阿托伐他汀(10mg/d)和依折麦布(10mg/d)联合治疗,疗程2个月。检测3组病人治疗前后总胆固醇(TC)、三酰甘油(TG)、低密度脂蛋白胆固醇(LDL-C)、高密度脂蛋白胆固醇(HDL-C)水平及高敏C反应蛋白(hs-CRP)水平等,并比较治疗效果和安全性。结果与治疗前比较,3组病人治疗后的TC、TG、LDL-C水平均明显降低,差异有统计学意义(P0.01),而HDL-C水平轻度升高,差异亦有统计学意义(P0.05);(2)治疗2个月后TC、LDL-C、非HDL-C的达标率均≥65%,总有效率均≥90%,3组比较无统计学意义(P0.05);(3)与对照组比较,治疗后观察组两组TG水平较低,但3组比较统计学意义(P0.05);3组比较,治疗后TC、LDL-C、hs-CRP水平在观察两组较低,有统计学意义(P0.05)。副作用发生率在观察二组亦较低,但未见统计学意义(P0.05)。结论与中等剂量的阿托伐他汀相比,小剂量阿托伐他汀与依折麦布联合不仅能更有效地降低混合型高脂血症病人的血脂水平,且能更好地降低hs-CRP的水平。     

阿托伐他汀联合烟酸缓释片治疗老年混合高脂血症的临床研究

临床试验证实阿托伐他汀降脂作用强于其他他汀类药物，其降脂作用与药物剂量有相关性，但他汀类药物剂量加倍后其降脂疗效提高非常有限，且不良反应随剂量增加呈线性增高，降TG及升高HDL-C作用相对贝特、烟酸类药物弱，故对混合型高脂血症的老年人，为提高血脂达标率，经常考虑联合用药，但他汀类药物与贝特类药物联用可引起横纹肌溶解。烟酸缓释片（本悦）具有全面的降脂作用，为升高HDL-C水平最为理想的调脂药物，胡大一及Van等报道缓释烟酸与阿托伐他汀联合治疗，可以克服目前降脂治疗达标率低的弱点。本研究进一步探讨联合应用小剂量阿托伐他汀联合本悦治疗老年混合性高脂血症临床疗效。     

阿托伐他汀联用烟酸缓释片治疗冠心病合并高脂血症的疗效观察

目的:研究阿托伐他汀联用烟酸缓释片治疗冠心病合并高脂血症的临床疗效及安全性。方法:入选60例冠心病合并高脂血症患者,随机分为2组即阿托伐他汀组和联合用药组,前者服用阿托伐他汀片,后者服用阿托伐他汀片联合烟酸缓释片,疗程均8周。服药前、服药4周及8周分别测定TC、TG、HDL-C、LDL-C值。结果:联合用药组降低LDL-C的能力优于阿托伐他汀组(P<0.05),升高HDL-C的能力明显优于阿托伐他汀组(P<0.01),降低TC的能力治疗8周后优于阿托伐他汀组(P<0.05)。其总有效率达96.7%,高于阿托伐他汀组86.7%(P<0.05)。无明显不良反应发生。结论:阿托伐他汀联合烟酸缓释片治疗冠心病合并高脂血症血脂达标率高,具有良好的临床疗效,安全性好。     

不同剂量阿托伐他汀联合依折麦布治疗高脂血症的效果

目的探讨不同剂量阿托伐他汀联合依折麦布治疗高脂血症的疗效。方法 400例高脂血症患者采用数字随机分组方法分为4组,每组100例,其中对照组给予阿托伐他汀20 mg/d治疗,治疗Ⅰ组给予阿托伐他汀5 mg/d联合依折麦布10 mg/d治疗,治疗Ⅱ组给予阿托伐他汀10 mg/d联合依折麦布10 mg/d治疗,治疗Ⅲ组给予阿托伐他汀20 mg/d联合依折麦布10 mg/d治疗,于降脂治疗后3、6、12个月测定血脂4项总胆固醇(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)的变化水平。结果(1)4个组治疗后3、6、12个月后LDL-C、TG、TC水平均较治疗前降低(P<0.05)。治疗后同一时间点:治疗Ⅲ组较对照、治疗Ⅰ组、治疗Ⅱ组3组LDL-C、TG、TC水平下调(P<0.05);4组间HDL-C上调水平无统计学差异(P>0.05);对照组、治疗Ⅰ组间LDL-C、TG、TC、HDL-C水平未见明显差异(P>0.05)。治疗后12个月,治疗Ⅱ组较对照、治疗Ⅰ组两组LDL-C、TG、TC水平下调具有统计学意义(P<0.05);治疗Ⅱ组、治疗Ⅲ组HDL-C上调具有统计学意义(P<0.05)。4组不良反应发生率。结论 20 mg阿托伐他汀联合10 mg依折麦布组患者的降脂效果明显优于单用20 mg阿托伐他汀组及小剂量阿托伐他汀联合依折麦布低剂量组,且不良反应的发生率无明显增加,安全性较好。     

阿托伐他汀联合非诺贝特治疗老年2型糖尿病并混合型高脂血症患者的疗效和安全性分析

目的探讨阿托伐他汀联合非诺贝特治疗老年2型糖尿病并混合型高脂血症患者的临床疗效与安全性。方法选择2014年1月—2016年8月该院门诊收治的52例老年2型糖尿病并混合型高脂血症患者作为此次研究对象,随机将患者分成对照组及治疗组,两组各有患者26例,对照组患者单用阿托伐他汀治疗,治疗组患者应用阿托伐他汀联合非诺贝特治疗,比较两组患者的临床疗效与安全性。结果治疗组患者的TC、TG、LDL-C以及HDL-C水平要显著优于对照组(P0.05);治疗组患者临床总有效率是92.31%,对照组患者临床总有效率是69.23%,治疗组临床疗效要显著优于对照组(P0.05);治疗组不良反应发生率是15.38%,对照组不良反应发生率是11.54%,组间比较差异无统计学意义(P0.05)。结论阿托伐他汀联合非诺贝特治疗老年2型糖尿病并混合型高脂血症患者能够获得显著临床疗效,安全性较高,值得临床大力推广。     

依折麦布联合瑞舒伐他汀钙治疗老年冠心病合并高脂血症的疗效观察

目的探讨依折麦布联合瑞舒伐他汀钙治疗老年冠心病合并高脂血症的临床疗效。方法选取64例老年冠心病合并高脂血症患者,随机分为治疗组和对照组。对照组仅给予瑞舒伐他汀钙,治疗组采用依折麦布联合瑞舒伐他汀钙治疗,比较两组的临床疗效、血脂水平及主要心脏不良事件。结果对照组总有效率为75.0%,治疗组总有效率为87.5%,治疗组疗效明显优于对照组（P〈0.05）。治疗组在胆固醇（TC）、三酰甘油（TG）、低密度脂蛋白胆固醇（LDL-C）及主要心脏不良事件发生率明显下降,高密度脂蛋白胆固醇（HDL-C）明显升高,与对照组相比差异有统计学意义（P〈0.05）。结论采用依折麦布联合瑞舒伐他汀钙治疗老年冠心病合并高脂血症可降低主要心脏不良事件发生率,提高疗效。     

辛伐他汀和非诺贝特对高脂血症患者血脂水平的影响

目的观察辛伐他汀和非诺贝特治疗高脂血症的临床疗效,对比分析二者对血清血脂水平的影响。方法将150例混合型高脂血症患者随机分为他汀组、贝特组、联合组三组,每组各50例,他汀组予以辛伐他汀10 mg/d治疗,贝特组予以非诺贝特200 mg/d治疗,联合组予以辛伐他汀10 mg/d和非诺贝特200 mg/d联合治疗,监测治疗前、治疗后12周的总胆固醇(TC)、低密度脂蛋白(LDL-C)、三酰甘油(TG)及高密度脂蛋白(HDL-C)的变化,同时监测谷丙转氨酶(ALT)、血尿素氮(BUN)、血肌酐(Cr)及肌酸激酶(CK)的变化。结果治疗12周后,三组TC、LDL-C、TG及HDL-C的变化均有所改善,差异具有统计学意义(P0.05)。他汀组(TC:4.21±0.62 mmol/L,LDL-C:3.21±0.61mmol/L)与贝特组(TC:4.91±0.53 mmol/L,LDL-C:3.52±0.52 mmol/L)比较,差异有统计学意义(P0.05),他汀组与联合组(TC:4.31±0.63 mmol/L,LDL-C:3.22±0.61 mmol/L)比较,差异无统计学意义(P0.05)。贝特组与联合组比较,差异有统计学意义(P0.05)。他汀组(HDL-C:1.21±0.22 mmol/L,TG:2.91±0.62 mmol/L)与贝特组(HDL-C:1.32±0.11mmol/L,TG:1.52±0.51 mmol/L)比较,差异无统计学意义(P0.05),他汀组与联合组(HDL-C:1.41±0.21 mmol/L,TG:1.21±0.62mmol/L)比较,差异有统计学意义(P0.05)贝特组与联合组比较,差异有统计学意义(P0.05)。三组不良反应比较,差异无显著性(P0.05)。结论联合应用辛伐他汀与非诺贝特对混合型高脂血症患者的总有效率要优于单独使用辛伐他汀或非诺贝特,且不良反应没有增高,具有良好的安全性。     

非诺贝特微粒化胶囊联合辛伐他汀对混合型高脂血症的治疗

目的:观察非诺贝特微粒化胶囊联合辛伐他汀治疗混合型高脂血症的疗效和安全性。方法:冠心病及有高危因素的混合型高脂血症患者72例,分为两组:辛伐他汀组36例,口服辛伐他汀20mg,每日1次;非诺贝特微粒化胶囊加辛伐他汀组(联合治疗组)36例,在辛伐他汀基础上加服非诺贝特微粒化胶囊200mg,每日1次;两组疗程均为8周。观察治疗前后血脂变化和相关不良反应。结果:①两组治疗后血清总胆固醇(TC)、低密度脂蛋白胆固醇(LDL-C)、甘油三酯(TG)、高密度脂蛋白胆固醇(HDL-C)均有改善(P0.05～0.01),但联合治疗组治疗后LDL-C和TG改善情况优于辛伐他汀组(P0.05)。②联合治疗组TC、LDL-C、TG的达标率分别为58.3%、44.4%、50.0%,三项达标率为36.1%,明显高于辛伐他汀组的13.9%(P0.01)。③两组均没有出现严重不良反应。结论:非诺贝特微粒化胶囊联合辛伐他汀对混合型高脂血症的冠心病及有高危因素患者有较好调脂作用,值得在临床推广应用。     

辛伐他汀联合非诺贝特治疗混合型高脂血症的疗效和安全性探讨

目的 评价辛伐他汀联合非诺贝特治疗混合型高脂血症的疗效和安全性.方法 选择冠心病合并混合型高脂血症患者46例,治疗前2周停服调脂药,随机分为辛伐他汀+非诺贝特联合组(A组n=23)和辛伐他汀单药组(B组n=23)两组.A组患者中男16例,女7例,年龄(60.01±8.25)岁,给予辛伐他汀20 mg,每晚睡前口服,非诺贝特0.1 g,每日2次,连续24周.B组患者中男15例,女8例,年龄(60.00±7.8)岁,给予辛伐他汀20 mg,每晚睡前口服,连续24周,服药前和服药24周后各测定TC、TG、LDL-C、HDL-C、GPT、CK一次.结果 治疗24周后,A组血清总胆固醇降低27.8%,TG下降56%,LDL-C下降41.4%,HDL-C升高22%.B组TC下降15.4%,TG下降11.6%,LDL-C下降24.7%,HDL-C上升11.5%(P<0.05),24周内A组有3例发生不稳定性心绞痛,B组有6例发生不稳定性心绞痛(P<0.05).两组没有患者因为严重不良反应事件而退出.结论 联合应用辛伐他汀和非诺贝特治疗混合型高脂血症与单药相比能更有效地降低高血脂水平,显著降低冠心病发病率,改善预后.     

Is combined lipid-regulating therapy safe and feasible for the very old patients with mixed dyslipidemia?

Objectives To detect the efficacy and safety of combined lipid-regulating therapies in the very old patients with mixed dyslipidemia and determine an appropriate therapy for them. Methods Four hundred and fifty patients aged over 75 with mixed dyslipidemia were divided into five groups according to different combination therapies. Lipid levels and drug related adverse events were tested during the study. Results Total cholesterol (TC) and low-density lipoprotein cholesterol (LDL-C) levels were reduced in every group compared to baseline: statin + ezetimibe: -30.0% and -55.5%; statin + policosanol: -31.1% and -51.2%; statin + fibrates: -23.7% and -44.6%; statin + niacin: -25.2% and -43.0%; and niacin + fibrates: -11.3% and -23.5%. The target achievement rates of LDL-C all exceeded 50%, except in niacin + fibrates (42.0%); statin + ezetimibe: 57.0%; statin + policosanol: 56.0%; statin + niacin: 52.0%; and statin + fibrates: 50.0%. However, overall, the niacin + fibrates group was the most effective in decreasing triglyceride (TG) and increasing high-density lipoprotein cholesterol (HDL-C) as follows: niacin + fibrates: -39.3% and 28.6%; statin + fibrates: -29.3% and 18.4%; statin + niacin: -18.5% and 16.7%; statin + ezetimibe: -17.1% and 7.1%; and statin + policosanol: -15.6% and 9.5%. The achievement rates of TG and HDL-C levels in niacin + fibrates (58.0% and 39.0%) were better than the other four groups: statin + niacin (34.0% and 34.0%), statin + fibrates (43.0% and 28.0%), statin + policosanol (30.0% and 24.0%) and statin + ezetimibe (28.0% and 25.0%). Patients in all five groups experiencing drug adverse events were only 2% and no severe adverse events occurred. Conclusions Statin + ezetimibe was the most effective group in lowering TC and LDL-C levels, while niacin + fibrates was the most effective in decreasing TG and increasing HDL-C levels. The commonly used combined lipid-regulating therapies with common dosages in this study were all quite safe and feasible for the very old patients with mixed hyperlipidemia.     

Serum lipid comparison in patients treated by statins or fibrates: existence of bad HDL-C responders to statins

INTRODUCTION: Major cardiac events are strongly associated with high levels of low-density lipoprotein cholesterol (LDL-C) and low levels of high-density lipoprotein cholesterol (HDL-C). The HDL-C target level (40 mg/dl) is often not achieved with statins. The aim of this study was to compare the proportions of patients achieving the HDL-C target levels after one year of treatment with statins or fibrates. Furthermore, a subgroup with low HDL-C levels during statin treatment was investigated and suggestions are made for a better management of these patients. METHODS: A survey of lipid levels, cardiovascular disease and risk factors in 120 outpatients treated with a statin or a fibrate for hyperlipidaemia (total cholesterol (TC) > 250 mg/dl or triglycerides (TG) > 200 mg/dl after diet). After one year of treatment the proportions of patients achieving the target levels for TC, LDL-C, HDL-C,TG,TC/HDL-C and LDL-C/HDL-C are compared for statins and fibrates. RESULTS: The proportions of patients achieving the target lipid levels with statins or fibrates are comparable except for HDL-C. Compared to the baseline, the proportion of patients achieving the HDL-C target level of 40 mg/dl increases only by 8.3% for statins and by 42.9% for fibrates. In total, 38.5% of the statin group had low HDL-C-levels after one year of treatment. Among these patients, eight were treated with a fibrate before the statin and six were treated with a fibrate afterwards. In those 14 patients, mean HDL-C increased during fibrate treatment by 48.5% and TC/HDL-C and LDL-C/HDL-C decreased by 25.7 and 26.5%, respectively as compared with statins. CONCLUSIONS: Patients with low levels of HDL-C during statin treatment had far better levels of HDL-C, TC/HDL-C and LDL-C/HDL-C with fibrates. A randomised double-blind crossover trial with simvastatin and fenofibrate has been initiated to corroborate these findings.     

Effective use of combination lipid therapy

Despite the benefits of statin therapy, low-density lipoprotein cholesterol (LDL-C) management remains suboptimal and many patients do not achieve their recommended target goals. The aim of combination lipid drug therapy in high-risk patients is to achieve LDL-C and non-high-density lipoprotein cholesterol (HDL-C) goals with a minimum of serious adverse effects. Although statins are the drug of first choice, statin monotherapy may be limited by intolerance of dose escalation or failure to attain non-HDL-C goals in those with mixed hyperlipidemia. Statins plus bile acid resins or ezetimibe can achieve greater than 50% reduction in LDL-C, with little or no increase in adverse effects. Fibrates, niacin, and omega-3 fatty acids, when added to statins, can reduce triglycerides, increase HDL-C, and reduce non-HDL-C to a greater extent than statin monotherapy. The safety profile of combination lipid therapy is acceptable, if the global coronary heart disease risk of the patient is high, thus producing a favorable risk to benefit ratio. Careful surveillance of hepatic transaminases, avoidance of gemfibrozil in statin-fibrate combinations, and awareness of statin-concomitant drug interactions is key to safe and efficacious use of combination lipid drug therapy.     

Comprehensive Lipid Management in the Coronary Artery Disease Patient

Low-density lipoprotein cholesterol (LDL-C) is the lipoprotein most implicated in atherosclerosis, and aggressive statin therapy remains the cornerstone of treatment. Adjunct therapies are often required to reach LDL-C goals, and recent studies have only fueled the debate over ezetimibe versus niacin. Alternate dosing regimens of high-potency statins can be used in those who cannot tolerate side effects. Residual risk may remain after LDL-C goals are achieved. Non–high-density lipoprotein cholesterol (non–HDL-C) must be calculated in patients with elevated triglycerides. Omega-3 fatty acids are most effective in lowering non–HDL-C. Low HDL-C levels can be raised with niacin, but clinical events may not be significantly reduced. Newer therapeutic targets, such as cholesteryl ester transfer protein (CETP) inhibitors, raise HDL-C and are being evaluated for safety and efficacy. Several ongoing, randomized controlled trials are investigating the relative efficacy of adjunctive therapies for reducing coronary heart disease events in high-risk patients.     

HDL-C and triglyceride levels: relationship to coronary heart disease and treatment with statins

The association between low-density lipoprotein cholesterol (LDL-C) levels and risk of coronary heart disease (CHD) is well established and LDL-C-lowering is currently the primary target for the treatment of dyslipidemia. However, low levels of high-density lipoprotein cholesterol (HDL-C), and high levels of triglycerides (TG) are also risk factors for CHD and modifying levels of these lipid subfractions, in addition to LDL-C lowering, may have clinical benefits in many patients.Statins are the first-line drug therapy for the treatment of dyslipidemia because of their efficacy in lowering LDL-C and good tolerability. Statins also have beneficial effects on TG and HDL-C levels although they differ in the degree to which they modify the levels of these lipoproteins. Improvements across the atherogenic components of the lipid profile may be optimized by the co-administration of a statin with a fibrate, niacin or omega-3 fatty acids; however, particular combination therapies have been associated with side effects and may be poorly tolerated. Newer combinations with better tolerability, or new statins with improved efficacy on non-LDL-C lipid subfractions, would be welcome additions to the currently available therapies for the treatment of dyslipidemia.     

Treating mixed hyperlipidemia and the atherogenic lipid phenotype for prevention of cardiovascular events

Statins reduce cardiovascular events and cardiovascular and total mortality in persons at risk for and with coronary disease, but there remains a significant residual event rate, particularly in those with the atherogenic lipid phenotype that is characterized by a low high-density lipoprotein (HDL) cholesterol and increase in non-HDL cholesterol. Large outcome trials designed to assess the value of combining statins with other agents to target HDL cholesterol and non-HDL cholesterol will not be completed for a few years, but there is ample evidence for the clinician to consider combination therapy. The choices for therapies to supplement statins include niacin, fibrates, and omega-3 fatty acids. We present the argument that after therapeutic lifestyle changes, the first priority should be the maximally tolerated effective dose of a potent statin. Evidence supports the addition of niacin as the second agent. In some situations, high-dose omega-3 fatty acid therapy could be the first agent added to statins. Although fibrate monotherapy alone or in combination with non-statin low-density lipoprotein cholesterol-lowering agents can be effective in mixed hyperlipidemia when statins are not tolerated, the combination of statin + fibrate should be considered second-line therapy until the efficacy and safety are established.     

A review of trials evaluating nonstatin lipid-lowering therapies

Recently reported clinical trials raise doubts on the effectiveness of nonstatin lipid-lowering therapies in reducing the residual risk of cardiovascular events after statin monotherapy. Addition of torcetrapib to statin therapy increased overall mortality in coronary patients despite a marked increase in high-density lipoprotein cholesterol. Combining ezetimibe with statin therapy neither further reduces carotid atherosclerosis nor slows aortic stenosis, and it has not been shown to be superior to statin monotherapy in reducing cardiovascular events. Clinical trials currently in progress will more clearly delineate the cardiovascular effects of adding either ezetimibe or extended-release niacin/laropiprant to statin therapy.     

Effective use of combination lipid therapy

Despite the benefits of statin therapy, low-density lipoprotein (LDL) cholesterol management remains suboptimal and many patients do not achieve their recommended target goals. The aim of combination lipid drug therapy in high-risk patients is to achieve LDL cholesterol and non-high-density lipoprotein (HDL) cholesterol goals with a minimum of serious adverse effects. Although statins are the drug of first choice, statin monotherapy may be limited by intolerance of dose escalation or failure to attain non-HDL cholesterol goals in those with mixed hyperlipidemia. Statins plus bile acid resins or ezetimibe can achieve greater than 50% reduction in LDL cholesterol, with little or no increase in adverse effects. Fibrates, niacin, and omega-3 fatty acids, when added to statins, can reduce triglycerides, increase HDL cholesterol, and reduce non-HDL cholesterol to a greater extent than statin monotherapy. The safety profile of combination lipid therapy is acceptable if the global coronary heart disease risk of the patient is high, thus producing a favorable risk to benefit ratio. Careful surveillance of hepatic transaminases, avoidance of gemfibrozil in statin-fibrate combinations, and awareness of statin-concomitant drug interactions is key to safe and efficacious use of combination lipid drug therapy.     

Low HDL-C: a secondary target of dyslipidemia therapy

Current guidelines for the prevention of coronary heart disease (CHD) focus on lowering low-density lipoprotein cholesterol (LDL-C) as the primary target of lipid-modifying therapy. However, there is increasing interest in high-density lipoprotein cholesterol (HDL-C) as a secondary target of therapy. A wealth of epidemiologic data demonstrate that low levels of HDL-C are associated with an increased risk of CHD events, and data from large-scale clinical trials with statins and fibrates indicate that observed clinical benefits are related, at least in part, to improvements in HDL-C levels. Raising HDL-C levels with therapeutic lifestyle changes and pharmacologic intervention might afford opportunities to further reduce the risk of CHD beyond LDL-C lowering. Statins are first-line pharmacotherapy for dyslipidemia and can also improve HDL-C levels, although the extent to which they modify HDL-C varies. Combining a fibrate or niacin with statin therapy raises HDL-C more than a statin alone but might be associated with reduced tolerability and increased adverse reactions. Several new therapeutic approaches to raising HDL-C are in development, including an HDL mimetic and inhibitors of cholesteryl ester transfer protein. Although lowering LDL-C remains the primary target of lipid-modifying therapy, dyslipidemia therapies that are efficacious for both LDL-C reduction and raising HDL-C might offer further improvements in CHD risk reduction.