BACKGROUND & AIMS: BACKGROUND:There is conflicting evidence as to whether achievement of cholesterol targets at the population level is dependent on the choice and cost of statin. AIM:To investigate the practice-level relationship between cholesterol quality indicators in patients with heart disease, stroke, and diabetes and prescribing of low-cost statins. DESIGN AND SETTING:Correlations and linear regression modelling of retrospective cross-sectional practice-level data with potential explanatory variables in 7909 (96.4%) general practices in England in 2008-2009. METHOD:Quality indicator data were obtained from the Information Centre and prescribing data from the NHS Business Authority. A 'cholesterol quality indicator' score was constructed by dividing the numbers of patients achieving the target for cholesterol control of ≤5 mmol/l in stroke, diabetes, and heart disease by the numbers on each register. A 'low-cost statin' ratio score was constructed by dividing the numbers of defined daily doses of simvastatin and pravastatin by the total numbers of defined daily doses of statins. RESULTS:Simvastatin accounted for 83.3% (standard deviation [SD] = 15.7%) of low-cost statins prescribed and atorvastatin accounted for 85.7% (SD = 14.8%) of high-cost statins prescribed. The mean cholesterol score was 73.7% (SD = 6.0%). Practices using a higher proportion of the low-cost statins were less successful in achieving cholesterol targets. An increase of 10% in the prescribing of low-cost statins was associated with a decrease of 0.46% in the cholesterol quality indicator score (95% confidence interval = -0.54% to -0.38%, P<0.001). CONCLUSION:Greater use of low-cost statins was associated with a small reduction in cholesterol control.

背景与目标：

BACKGROUND & AIMS: :The appearance of statins was key to our understanding of the pathologic effects of hypercholesterolemia. Before statins were available, physicians did not know whether cholesterol lowering improved cardiovascular health. Pioneering studies such as the Framingham Study and MR FIT identified high blood cholesterol as a risk factor for cardiovascular disease. However, because total cholesterol (TC) < or =300 mg/dL was common physicians were not convinced that this was abnormal. Cholesterol reduction by cholestyramine, nicotinic acid, and fibrates reduced the risk of coronary artery disease, but these treatments did not improve survival and quality of life. In 1987, the first statin arrived. This class of agents lowered cholesterol effectively with minimal side effects. Guidelines started to recognize the importance of cholesterol reduction. There followed a series of endpoint studies that emphatically demonstrated that statins improved cardiovascular outcomes. The WOSCOPS trial showed in a large cohort of men with TC >250 mg/dL and no prior MI that pravastatin dramatically reduced MI incidence, cardiovascular and total mortality, and revascularizations versus placebo over 5 years. WOSCOPS revealed for the first time that statin was effective for primary prevention. The benefits appeared early and persisted even after treatment ended. Statins also changed our perceptions with surprising ancillary effects.

背景与目标： : 他汀类药物的出现是我们理解高胆固醇血症的病理影响的关键。在他汀类药物问世之前，医生不知道降低胆固醇是否能改善心血管健康。弗雷明汉研究和FIT先生等开创性研究将高胆固醇确定为心血管疾病的危险因素。然而，由于总胆固醇 (TC) <或 = 300 mg/dL是常见的，因此医生不相信这是异常的。消胆胺，烟酸和贝特类药物降低胆固醇可降低冠心病的风险，但这些治疗方法并未改善生存率和生活质量。1987年，第一个他汀类药物到达。这类药物有效地降低了胆固醇，副作用最小。指南开始认识到降低胆固醇的重要性。随后进行了一系列终点研究，着重表明他汀类药物改善了心血管结局。WOSCOPS试验显示，与安慰剂相比，在5年内，普伐他汀显著降低了MI发病率、心血管和总死亡率以及血运重建的大队列中，TC >250 mg/dL且既往没有MI的男性队列中。WOSCOPS首次显示他汀类药物对一级预防有效。好处出现得很早，甚至在治疗结束后仍然存在。他汀类药物也以令人惊讶的辅助作用改变了我们的看法。

BACKGROUND & AIMS: :Statins belong to the most pre-scribed cholesterol lowering drugs in western countries. Their competitive inhibition of the HMG-CoA reductase causes a reduction in the mevalonate pool, resulting in reduced cholesterol biosynthesis, impaired protein prenylation and glycosylation. Recently, a cohort study showed a decreased mortality rate in humans between age 78-90 going along with statin therapy, which is independent of blood cholesterol levels. As C. elegans harbors the mevalonate pathway, but is cholesterol-auxotroph, it is particularly suitable to study cholesterol-independent effects of statins on aging-associated phenotypes. Here, we show that low doses of lovastatin or a mild HMG-CoA reductase knockdown via hmgr-1(RNAi) in C. elegans substantially attenuate aging pigment accumulation, which is a well-established surrogate marker for biological age. Consistently, for two statins we found dosages, which prolonged the lifespan of C. elegans. Together with an observed reduced fertility, slower developmental timing and thermal stress resistance this complex of outcomes point to the involvement of DAF-16/hFOXO3a, the master regulator of stress resistance and longevity. Accordingly, prolonged low-dose statin exposure leads to an increased expression of jnk-1, a known activator of DAF-16. Moreover, the beneficial effects of statins on aging pigments and lifespan depend on DAF-16 and JNK-1, as shown in epistasis analyses. These effects can be reverted by mevalonate supplementation. In conclusion, we describe a lifespan extension in C. elegans, which is conferred via two well-conserved stress-related factors (JNK-1, DAF-16) and results from mevalonate depletion.

背景与目标： : 他汀类药物属于西方国家最预先确定的降胆固醇药物。它们对HMG-CoA还原酶的竞争性抑制导致甲羟戊酸库减少，导致胆固醇生物合成减少，蛋白质异戊烯化和糖基化受损。最近，一项队列研究表明，与他汀类药物治疗 (与血液胆固醇水平无关) 一起，年龄在78-90岁之间的人死亡率降低。由于秀丽隐杆线虫具有甲羟戊酸途径，但具有胆固醇营养缺陷，因此特别适合研究他汀类药物对衰老相关表型的胆固醇依赖性作用。在这里，我们显示低剂量的洛伐他汀或温和的HMG-CoA还原酶通过hmgr-1敲除 (RNAi) 在秀丽隐杆线虫中显著减弱老化色素积累，这是一个公认的生物学年龄的替代标记。一致地，对于两种他汀类药物，我们发现了延长秀丽隐杆线虫寿命的剂量。再加上观察到的生育力降低，发育时间减慢和抗热应激性，这种复杂的结果表明，DAF-16/hFOXO3a是抗逆性和寿命的主要调节剂。因此，长时间的低剂量他汀类药物暴露导致jnk-1 (一种已知的DAF-16激活剂) 的表达增加。此外，如上位性分析所示，他汀类药物对老化色素和寿命的有益作用取决于DAF-16和JNK-1。这些作用可以通过补充甲羟戊酸来恢复。总之，我们描述了秀丽隐杆线虫的寿命延长，这是通过两个保守的压力相关因素 (JNK-1，DAF-16) 和甲羟戊酸耗竭的结果赋予的。

BACKGROUND & AIMS: :Beyond lipid lowering, statins are supposed to exert pleiotropic effects positively influencing the progression of atherosclerotic lesions. The development of such lesions is associated with increased release of angiopoietin-2 (Ang-2), an endothelial cell-specific protein growth factor stored in Weibel-Palade bodies (WPBs). The aim of our study was to examine whether statin pretreatment influences the release of Ang-2 from endothelial cells. Stimulation of HUVECs and HMVECs with PMA, thrombin or histamine resulted in significant release of Ang-2, as evidenced by ELISA. Pretreatment with simvastatin and mevastatin suppressed this release to basal level, while pravastatin had no effect. Simvastatin itself increased nitric oxide (NO, EC number 1.14.13.39) synthesis, measured by Griess reaction. Combining the statin pretreatment with the eNOS inhibitor L-NNA as well as bypassing the HMG-CoA reductase (EC number: 1.1.1.34) by adding mevalonic acid or geranyl pyrophosphate restored the exocytotic effect of PMA. Immunofluorescence microscopy showed that depletion of WPBs upon PMA stimulation ceased after pretreatment with simvastatin. This study demonstrates a potent suppressive effect of statins on the release of Ang-2 from endothelial cells. Regarding its harmful effects in the development of atherosclerotic lesions, our data provide further insight into the mechanisms of the anti-atherogenic potential of statins.

背景与目标： : 除降脂外，他汀类药物还应发挥多效性作用，积极影响动脉粥样硬化病变的进展。这种病变的发展与angiopoietin-2 (Ang-2) 的释放增加有关，后者是储存在Weibel-Palade body (WPBs) 中的内皮细胞特异性蛋白生长因子。我们研究的目的是检查他汀类药物预处理是否影响内皮细胞Ang-2的释放。用PMA，凝血酶或组胺刺激huvec和hmvec导致Ang-2的显着释放，如ELISA所证明。辛伐他汀和美伐他汀预处理可将这种释放抑制到基础水平，而普伐他汀则没有作用。辛伐他汀本身增加了一氧化氮 (NO，EC号1.14.13.39) 的合成，通过Griess反应测量。将他汀类药物预处理与eNOS抑制剂l-nna相结合，并通过添加甲羟戊酸或香叶基焦磷酸来绕过HMG-CoA还原酶 (EC号: 1.1.1.34)，可恢复PMA的胞外作用。免疫荧光显微镜显示，辛伐他汀预处理后，PMA刺激下WPBs的消耗停止。这项研究证明了他汀类药物对内皮细胞释放Ang-2的有效抑制作用。关于其在动脉粥样硬化病变发展中的有害作用，我们的数据为他汀类药物抗动脉粥样硬化潜力的机制提供了进一步的见解。

BACKGROUND & AIMS: :Statins are highly efficacious lipid modifying agents that reduce the risk for cardiovascular (CV) events in both primary and secondary prevention settings. However, statins affect molecular mechanisms which adversely impact on insulin sensitivity and β-cell function, thereby increasing risk for new onset diabetes mellitus (NOD). Defining the mechanisms involved is the focus of considerable current investigation. The statins reduce the risk for CV events in normoglycemic patients as well as in those with diabetes mellitus (DM) and their benefits outweigh the risk of inducing NOD. We review the clinical evidence for NOD with statin treatment, as well as the potential mechanisms involved. Our literature search was based on PubMed and Scopus listings. Further large studies are needed to elucidate both the association between NOD and statin use and the underlying mechanisms.

背景与目标： : 他汀类药物是高效的脂质调节剂，可降低一级和二级预防环境中心血管 (CV) 事件的风险。然而，他汀类药物会影响对胰岛素敏感性和 β 细胞功能产生不利影响的分子机制，从而增加了新发糖尿病 (NOD) 的风险。确定所涉及的机制是当前大量调查的重点。他汀类药物可降低正常血糖患者以及糖尿病 (DM) 患者的CV事件风险，其益处大于诱发NOD的风险。我们回顾了NOD与他汀类药物治疗的临床证据，以及涉及的潜在机制。我们的文献搜索基于PubMed和Scopus列表。需要进一步的大型研究来阐明NOD和他汀类药物使用之间的关联以及潜在的机制。

BACKGROUND & AIMS: :Osteoporosis increases dramatically with age. About 40 % of women in developed countries will experience an osteoporosis-related fracture in the course of their lifetime, with men experiencing approximately one-third to one-half the risk of women. The "lipid hypothesis of osteoporosis" claims for a role of oxidized lipids as a contributing factor in osteoporosis. On the other hand, statins are supposed to exert anabolic effects on the bone, either through their lipid-lowering action or signal pathways that are independent of their effects on lipid levels. The epidemiological evidence seems to suggest that higher triglycerides may give some protection against fracture, although no association with reduced fracture risk has been reported between lipid-lowering drug (except statins) users and non-users. The epidemiological evidence for a role of statins in osteoporosis is strong, with a lower fracture risk ranging from 30 to 40 % in statin users versus non-users. However, some pitfalls inherent to observational studies (high heterogeneity, residual confounding, potential publication bias) and the lack of association in randomized trials suggest caution. At the moment, the evidence for a role of statins in prevention of osteoporosis is insufficient to recommend starting statin therapy with the aim to prevent osteoporosis.

背景与目标： : 骨质疏松症随着年龄的增长而急剧增加。在发达国家中，约有40% 的女性在其一生中会经历骨质疏松症相关的骨折，其中男性的风险约为女性的3分之1至一半。“骨质疏松症的脂质假说” 声称氧化脂质在骨质疏松症中的作用。另一方面，他汀类药物应该通过其降脂作用或与脂质水平无关的信号途径对骨骼产生合成代谢作用。流行病学证据似乎表明，较高的甘油三酸酯可能对骨折有一定的保护作用，尽管降脂药物 (他汀类药物除外) 使用者和非使用者之间没有与骨折风险降低相关的报道。他汀类药物在骨质疏松症中的作用的流行病学证据很强，他汀类药物使用者与非使用者相比，骨折风险较低，范围为30至40%。然而，观察性研究固有的一些陷阱 (高度异质性，残留混杂，潜在的发表偏倚) 和随机试验中缺乏关联提示谨慎。目前，他汀类药物在预防骨质疏松症中的作用的证据不足以推荐开始他汀类药物治疗以预防骨质疏松症。

BACKGROUND & AIMS: Cyclooxygenase (COX)-2 and COX-1 play an important role in prostacyclin production in vessels and participate in maintaining vascular homeostasis. Statins are inhibitors of 3-hydroxy-3-methylglutaryl coenzyme A (HMG CoA) reductase, which is crucial in cholesterol biosynthesis. Recently, cholesterol-independent effects of statins have been described. In this study, we evaluated the effect of two inhibitors of HMG CoA reductase, mevastatin and lovastatin, on the production of prostacyclin and the expression of COX in human aortic smooth muscle cells. Treatment of cells with 25 microm mevastatin or lovastatin resulted in the induction of COX-2 and increase in prostacyclin production. Mevalonate, the direct metabolite of HMG CoA reductase, and geranylgeranyl-pyrophosphate reversed this effect. GGTI-286, a selective inhibitor of geranylgeranyltransferases, increased COX-2 expression and prostacyclin formation, thus indicating the involvement of geranylgeranylated proteins in the down-regulation of COX-2. Furthermore, Clostridium difficile toxin B, an inhibitor of the Rho GTP-binding protein family, the Rho selective inhibitor C3 transferase, and Y-27632, a selective inhibitor of the Rho-associated kinases, targets of Rho A, increased COX-2 expression whereas the activator of the Rho GTPase, the cytotoxic necrotizing factor 1, blocked interlukin-1alpha-dependent COX-2 induction. These results demonstrate that statins up-regulate COX-2 expression and subsequent prostacyclin formation in human aortic smooth muscle cells in part through inhibition of Rho.

背景与目标： 环氧化酶 (COX)-2和COX-1在血管中前列环素的产生中起重要作用，并参与维持血管稳态。他汀类药物是3-羟基-3-甲基戊二酰辅酶a (HMG CoA) 还原酶的抑制剂，这在胆固醇生物合成中至关重要。最近，已经描述了他汀类药物的胆固醇非依赖性作用。在这项研究中，我们评估了两种HMG CoA还原酶抑制剂美伐他汀和洛伐他汀对人主动脉平滑肌细胞中前列环素的产生和COX表达的影响。用25 microm甲伐他汀或洛伐他汀处理细胞可诱导COX-2并增加前列环素的产生。HMG CoA还原酶的直接代谢产物甲羟戊酸和香叶基焦磷酸逆转了这种作用。GGTI-286是香叶基转移酶的选择性抑制剂，可增加COX-2表达和前列环素的形成，因此表明香叶基化蛋白参与了COX-2的下调。此外，艰难梭菌毒素B (Rho GTP结合蛋白家族的抑制剂，Rho选择性抑制剂C3转移酶) 和Rho相关激酶的选择性抑制剂Y-27632 (Rho a的靶标) 增加了COX-2表达，而Rho GTPase的激活剂，细胞毒性坏死性因子1阻止了interlukin-1alpha-dependent COX-2的诱导。这些结果表明，他汀类药物部分通过抑制Rho来上调人主动脉平滑肌细胞中COX-2的表达和随后的前列环素形成。

BACKGROUND & AIMS: BACKGROUND:Polycystic ovary syndrome (PCOS) is an endocrine disorder affecting about 10% of women in reproductive age and associated with a variety of hormonal abnormalities, including hyperandrogenemia and infertility, all of which could lead to PCOS. Statins were previously introduced as a therapeutic option for reducing testosterone levels in women with PCOS, either alone or in combination. The aim of this study is to evaluate the effectiveness of different statins alone or in combination with metformin in reducing testosterone levels in women with PCOS. METHODS:Medline, Embase, and clinicaltrials.gov were searched for studies that investigated the efficacy of statins, metformin, spironolactone, or combined oral contraceptives (COCs), individually or in combination, in reducing the testosterone level in patients with PCOS. The search was limited to randomized clinical trials and conducted according to the preferred reporting items for systematic reviews and meta-analyses - extension statement for network meta-analyses (PRISMA-NMA). The quality of included studies was assessed using the Cochrane Collaboration risk of bias (RoB) assessment tool. A frequentist network meta-analysis using random-effects models was used to assess the efficacy in reducing testosterone level and were expressed as odds ratios (OR) and 95% credible interval (95%Crl). All statistical analyses were performed using netmeta Version 1.0 on R statistical package. RESULT:Nine RCTs involving 613 patients were included. Atorvastatin showed greater reduction in testosterone level compared to COC (MD -2.78, 95%CrI -3.60, -1.97), spironolactone plus metformin (MD -2.83, 95%CrI -3.80, -1.87), simvastatin (MD -2.88, 95%CrI -3.85, -1.92), spironolactone (MD -2.90, 95%CI -3.77, -2.02), simvastatin plus metformin (MD -2.93, 95%CrI -3.79, -2.06), metformin (MD -2.97, 95%CrI -3.69, -2.25), lifestyle modification (MD -3.02, 95%CrI -3.87, -2.18), and placebo (MD -3.04, 95%CrI -3.56, -2.53). CONCLUSION:Atorvastatin was found to be more effective than the other management strategies in reducing the total testosterone level for patients with PCOS. Future studies should focus on the optimal dose.

背景与目标：

BACKGROUND & AIMS: Background:The purpose of this cohort study was to investigate the independent relationship between preoperative statin therapy (PST) and postoperative severe multiorgan failure, measured by the Sequential Organ Failure Assessment (SOFA) maximum greater than 11, in high-risk patients undergoing isolated coronary artery bypass grafting (CABG). Methods:The present study is a perspective, single-center, cohort analysis enrolling high-risk patients undergoing CABG from Jan 1, 2018, to Dec 31, 2018, in Beijing Anzhen hospital. Results:Among a total of 880 high-risk patients undergoing isolated CABG included in this study, 503 (57.2%) experienced statin therapy before CABG. The SOFA maximum was significantly lower in the PST group compared with the control group (7.8 ± 3.0 v 9.2 ± 3.4, P < 0.0001). Multivariate logistic regression analysis demonstrated the incidence of the severe multiorgan dysfunction, measured by SOFA maximum ≥11, was dramatically reduced in the PST group (OR, 0.68, 95% CI 0.50-0.92, P=0.013). Furthermore, preoperative statin therapy (PST) might be associated with a decreased risk of postoperative major adverse cardiovascular and cerebral events and acute kidney injury, but an increased risk of postoperative hepatic inadequacy. Conclusion:SOFA maximum was significantly lower in the PST group compared with the control group and the incidence of the severe multiorgan dysfunction was dramatically reduced in the PST group. The findings of this study might shed new light on questions of positive or negative effects of PST on multiple organ function after high-risk CABG, so as to ultimately improve high-risk patient in-hospital outcomes from CABG.

背景与目标：

BACKGROUND & AIMS: OBJECTIVE:Statins are a group of medications that reduce cholesterol synthesis by inhibiting the activity of HMG-CoA reductase, a key enzyme in the mevalonate pathway. The clinical use of statins to lower excess cholesterol levels has revolutionized the cardiovascular field and increased the survival of millions, but some patients have adverse side effects. A growing body of data suggests that some of the beneficial and adverse effects of statins, including their anti-inflammatory, anti-tumorigenic, and myopathic activities, are cholesterol-independent. However, the underlying mechanisms for these effects of statins are not well defined. METHODS:Because Caenorhabditis elegans (C. elegans) lacks the cholesterol synthesis branch of the mevalonate pathway, this organism is a powerful system to unveil the cholesterol-independent effects of statins. We used genetic and biochemical approaches in C. elegans and cultured macrophage-derived murine cells to study the cellular response to statins. RESULTS:We found that statins activate a conserved p38-MAPK (p38) cascade and that the protein geranylgeranylation branch of the mevalonate pathway links the effect of statins to the activation of this p38 pathway. We propose that the blockade of geranylgeranylation impairs the function of specific small GTPases we identified as upstream regulators of the p38 pathway. Statin-mediated p38 activation in C. elegans results in the regulation of programs of innate immunity, stress, and metabolism. In agreement with this regulation, knockout of the p38 pathway results in the hypersensitivity of C. elegans to statins. Treating cultured mammalian cells with clinical doses of statins results in the activation of the same p38 pathway, which upregulates the COX-2 protein, a major regulator of innate immunity in mammals. CONCLUSIONS:Statins activate an evolutionarily conserved p38 pathway to regulate metabolism and innate immunity. Our results highlight the cytoprotective role of p38 activation under statin treatment in vivo and propose that this activation underlies many of the critical cholesterol-independent effects of statins.

背景与目标：

BACKGROUND & AIMS: Two in vitro and one in vivo assay were performed to study the endothelial pleiotropic actions of "tissue type" angiotensin converting enzyme inhibitors (ACE-Is) such as perindopril and quinapril, their active forms, that is, quinaprilat and peridoprilat, or of statins belonging to natural (lovastatin), semisynthetic (simvastatin), and synthetic enantiomeric (atorvastatin, cerivastatin) classes. Cytoplasmic [Ca2+]i levels in cultured bovine aortic endothelial cells and endothelium-dependent nitric oxide-mediated coronary vasodilatation in the Langendorff preparation of guinea pig heart constituted our in vitro assays. The in vivo assay consisted of study of PGI2-mediated thrombolytic response in arterial blood of rats after intravenous administration of drugs. In this last assay, perindopril and quinapril proved to be, by two orders of magnitude, more potent PGI2-dependent thrombolytics than the most potent statin (atorvastatin). However, in both in vitro assays we found a higher endothelial efficacy of statins as compared to ACE-Is. In particular, those statins that contain the lactone ring in their molecules (lovastatin, simvastatin) were the most potent coronary vasodilators. In summary, the in vivo profile of action of ACE-Is and statins contrasted with their reversed order of potency in vitro. We hypothesize that the endocrine-like function of the pulmonary circulation [28-31] may be responsible for the in vivo bradykinin-triggered, PGI2-mediated thrombolysis by ACE-Is, whereas the pleiotropic action of statins, possibly involving inhibition of prenylation [14-19], is diffused throughout many vascular beds.

背景与目标： 进行了两种体外和一种体内测定，以研究 “组织型” 血管紧张素转换酶抑制剂 (ACE-Is) (例如培哚普利和奎那普利) 的内皮多效性作用，它们的活性形式，即奎那普利拉和哌啶拉，或属于他汀类药物的内皮多效性作用天然 (洛伐他汀)，半合成 (辛伐他汀) 和合成对映体 (阿托伐他汀，西立伐他汀) 类。在豚鼠心脏的Langendorff制剂中，培养的牛主动脉内皮细胞中的细胞质 [Ca2] i水平和内皮依赖性一氧化氮介导的冠状动脉血管舒张作用构成了我们的体外测定。体内测定包括研究静脉给药后大鼠动脉血中的PGI2-mediated溶栓反应。在最后的测定中，培哚普利和喹普利被证明比最有效的他汀类药物 (阿托伐他汀) 具有两个数量级的PGI2-dependent溶栓药。然而，在两种体外测定中，我们发现他汀类药物与ACE-Is相比具有更高的内皮功效。特别是，那些在分子中含有内酯环的他汀类药物 (洛伐他汀，辛伐他汀) 是最有效的冠状动脉血管扩张剂。总而言之，ACE-Is和他汀类药物的体内作用曲线与它们在体外的效力顺序相反。我们假设肺循环的内分泌样功能 [28-31] 可能是体内缓激肽触发的，PGI2-mediated ACE-Is溶栓的原因，而他汀类药物的多效性作用，可能涉及抑制异戊二烯化 [14-19]，扩散到许多血管床。

BACKGROUND & AIMS: OBJECTIVE:To analyze the possible beneficial effects of statins on the disease activity of patients with rheumatoid arthritis (RA) using a database from a large observational cohort study. METHODS:We studied a total of 7512 patients enrolled in a single-institute based prospective observational cohort of RA patients (IORRA); their information was collected biannually. In this study, cross-sectional data of 4152 patients (female 83.3%, average age 58.4 yrs) in October 2003 were analyzed (Mann-Whitney U-test). RESULTS:Among 4152 patients with RA, 279 (6.7%) were taking statins; patients taking statins had lower C-reactive protein (0.85 vs 1.24 mg/dl, respectively) and lower swollen joint counts (1.80 vs 2.55), but more frequently used corticosteroids (2.88 vs 2.40 mg/day) compared to patients not taking statins. Serum cholesterol level was closely related to the use of corticosteroids. Thus, an adjustment with the dose of corticosteroid was conducted; even taking account of the effects of steroids, RA disease activity indicated by patient's assessment for pain, physician's assessment, and swollen joint counts was significantly lower in patients with statins compared to those without. CONCLUSION:This study indicates that statins have beneficial effects in reducing RA disease activity in the daily practice of rheumatology.

背景与目标：

BACKGROUND & AIMS: :Age-related macular degeneration (AMD) is the leading cause of irreversible central vision loss in patients over the age of 65 years in industrialized countries. Epidemiologic studies suggest that high dietary fat intake is a risk factor for the development and progression of both vascular and retinal disease. These, and other associations, suggest a hypothesis linking elevated cholesterol and AMD progression. It follows, therefore, that cholesterol-lowering medications, such as statins, may influence the onset and progression of AMD. However, the findings have been inconclusive as to whether statins play a role in AMD. Due to the significant public health implications of a potential inhibitory effect of statins on the onset and progression of AMD, it is important to continually evaluate emerging findings germane to this question.

背景与目标： : 年龄相关性黄斑变性 (AMD) 是工业化国家65岁以上患者不可逆的中枢视力丧失的主要原因。流行病学研究表明，高饮食脂肪摄入量是血管和视网膜疾病发生和发展的危险因素。这些以及其他关联表明，胆固醇升高与AMD进展相关的假说。因此，降胆固醇药物，如他汀类药物，可能会影响AMD的发病和进展。然而，对于他汀类药物是否在AMD中发挥作用，研究结果尚无定论。由于他汀类药物对AMD发病和进展的潜在抑制作用对公共健康的重大影响，因此不断评估与该问题密切相关的新兴发现非常重要。

BACKGROUND & AIMS: :Hypertension and hyperlipidemia, two powerful risk factors of cardiovascular disease (CVD), often coexist. Therefore, treatment should consider the beneficial properties of drugs used to treat either condition. Statins, the mainstay of lipid-lowering therapy, result in a significant clinical benefit both in primary and secondary CVD prevention. In addition to their hypolipidemic capacity, other properties may contribute to statin-induced benefits. Clinical and experimental evidence indicates that statins may modulate blood pressure (BP). The mechanisms by which statins reduce BP seem to be largely independent of their lipid effects. Although small, reductions in BP are possibly clinically relevant. Large landmark studies confirm that statins can reduce CVD risk in hypertensive patients. These findings suggest that statins could be prescribed as an adjunct in treating hypertension with dyslipidemia or even in patients with "normal" cholesterol levels. Whether the effect of statins on BP is accompanied by an additional decrease in clinical outcomes needs to be investigated in long-term, large-scale trials.

背景与目标： 高血压和高脂血症是心血管疾病 (CVD) 的两个重要危险因素，通常并存。因此，治疗应考虑用于治疗任何一种疾病的药物的有益特性。他汀类药物是降脂治疗的主要手段，在原发性和继发性CVD预防中均具有显着的临床益处。除了降血脂能力外，其他特性可能有助于他汀类药物诱导的益处。临床和实验证据表明，他汀类药物可能调节血压 (BP)。他汀类药物降低血压的机制似乎在很大程度上与其脂质作用无关。尽管血压降低幅度很小，但可能与临床相关。大型标志性研究证实，他汀类药物可以降低高血压患者的CVD风险。这些发现表明，他汀类药物可以作为治疗血脂异常的高血压甚至胆固醇水平正常的患者的辅助药物。他汀类药物对血压的影响是否伴随着临床结局的额外降低，需要在长期的大规模试验中进行研究。

BACKGROUND & AIMS: BACKGROUND:There is an increasing body of evidence to support the benefits of reducing low-density lipoprotein cholesterol (LDL-C) levels and this has been reflected in a lowering of LDL-C goals recommended by international guidelines. Therefore, there is a growing need for effective lipid-modifying therapies to optimise the achievement of these more stringent LDL-C goals. OBJECTIVE:A meta-analysis of data pooled from five studies participating in the DISCOVERY (DIrect Statin COmparison of LDL-C Values: an Evaluation of Rosuvastatin therapY) Programme was performed to compare the effect of rosuvastatin treatment with other statins in real-life clinical practice. RESULTS:These studies included 6743 patients with hypercholesterolaemia from different ethnicities, countries and cultural environments. The meta-analysis showed that significantly more patients receiving rosuvastatin 10 mg achieved the 2003 European LDL-C goals compared with those who received atorvastatin 10 mg or simvastatin 20 mg (p < 0.001 for both comparisons). A significantly greater proportion of patients receiving rosuvastatin 10 mg also achieved the 2003 European total cholesterol goal compared with those on atorvastatin 10 mg (p < 0.001). CONCLUSIONS:The meta-analysis showed that rosuvastatin was more effective than comparator statins at lowering LDL-C levels and enabling patients to achieve lipid goals at recommended start doses. In addition, all statins studied were well tolerated and confirmed that rosuvastatin had a similar safety profile to other statins.

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