Legacy effects of statins on cardiovascular and all-cause mortality: a meta-analysis.
Legacy effects of statins on cardiovascular and all-cause mortality: a meta-analysis.
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DOI：
10.1136/bmjopen-2017-020584
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发表时间：
2018-10-04
期刊：
影响因子：
2.9
通讯作者：
Bell K
中科院分区：
文献类型：
--
作者：
Nayak A;Hayen A;Zhu L;McGeechan K;Glasziou P;Irwig L;Doust J;Gregory G;Bell K
评估他汀类药物安慰剂对照随机对照试验（RCT）成年受试者心血管疾病（CVD）死亡率和全因死亡率的“遗留”（试验后）效应的证据。汇总数据的荟萃分析。安慰剂对照的他汀类RCTS用于一级和二级CVD预防。数据来源：PubMed、Embase，从胆固醇治疗试验者合作者RCT的开始和转发引用到2016年6月16日。研究选择：两名独立审查员确定了所有他汀类药物RCT随访报告，包括≥1000例受试者，以及心血管和全因死亡率。数据提取和综合：两名独立评审员根据系统性综述和荟萃分析指南的首选报告项目提取数据。主要结局：试验后CVD和全因死亡率。我们纳入了8项试验，平均试验后随访时间为1.6 - 15.1年，包括13781例试验后死亡（6685例CVD）。试验中他汀类药物的直接效应大于试验后的遗留效应。所有8项研究的汇总数据显示，总体上没有证据表明对CVD死亡率有遗传效应，但有一些证据表明对全因死亡率有遗传效应（p=0.01）。探索性亚组分析发现，与二级预防试验相比，一级预防试验的CVD死亡率（p=0.15）和全因死亡率（p=0.02）的遗留效应可能存在差异。三项一级预防研究的试验后HR汇总显示，试验后可能对CVD死亡率（HR=0.87; 95% CI 0.79 - 0.95）和全因死亡率（HR=0.90; 95% CI 0.85 - 0.96）产生遗留效应。试验后他汀类药物对全因死亡率的可能影响似乎是由一级预防研究驱动的。尽管这些相对获益小于试验中观察到的获益，但两个时间段的绝对获益可能相似。在低风险人群中进行安慰剂对照的他汀类药物RCT后，对随访研究中的个体患者数据进行分析，可能会为亚临床动脉粥样硬化的早期治疗是否可能有益提供更明确的证据。
To assess evidence for ‘legacy’ (post-trial) effects on cardiovascular disease (CVD) mortality and all-cause mortality among adult participants of placebo-controlled randomised controlled trials (RCTs) of statins. Meta-analysis of aggregate data. Placebo-controlled statin RCTS for primary and secondary CVD prevention. Data sources: PubMed, Embase from inception and forward citations of Cholesterol Treatment Trialists’ Collaborators RCTs to 16 June 2016. Study selection: Two independent reviewers identified all statin RCT follow-up reports including ≥1000 participants, and cardiovascular and all-cause mortality. Data extraction and synthesis: Two independent reviewers extracted data in accordance with the Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines. Main outcomes: Post-trial CVD and all-cause mortality. We included eight trials, with mean post-trial follow-up ranging from 1.6 to 15.1 years, and including 13 781 post-trial deaths (6685 CVD). Direct effects of statins within trials were greater than legacy effects post-trials. The pooled data from all eight studies showed no evidence overall of legacy effects on CVD mortality, but some evidence of legacy effects on all-cause mortality (p=0.01). Exploratory subgroup analysis found possible differences in legacy effect for primary prevention trials compared with secondary prevention trials for both CVD mortality (p=0.15) and all-cause mortality (p=0.02). Pooled post-trial HR for the three primary prevention studies demonstrated possible post-trial legacy effects on CVD mortality (HR=0.87; 95% CI 0.79 to 0.95) and on all-cause mortality (HR=0.90; 95% CI 0.85 to 0.96). Possible post-trial statin legacy effects on all-cause mortality appear to be driven by the primary prevention studies. Although these relative benefits were smaller than those observed within the trial, the absolute benefits may be similar for the two time periods. Analysis of individual patient data from follow-up studies after placebo-controlled statin RCTs in lower-risk populations may provide more definitive evidence on whether early treatment of subclinical atherosclerosis is likely to be beneficial.
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影响因子：
168.9
作者：
Mihaylova, B.;Emberson, J.;Blackwell, L.;Keech, A.;Simes, J.;Barnes, E. H.;Voysey, M.;Gray, A.;Collins, R.;Baigent, C.;de Lemos, J.;Braunwald, E.;Blazing, M.;Murphy, S.;Downs, J. R.;Gotto, A.;Clearfield, M.;Holdaas, H.;Gordon, D.;Davis, B.;Koren, M.;Dahlof, B.;Poulter, N.;Sever, P.;Knopp, R. H.;Fellstrom, B.;Holdaas, H.;Jardine, A.;Schmieder, R.;Zannad, F.;Goldbourt, U.;Kaplinsky, E.;Colhoun, H. M.;Betteridge, D. J.;Durrington, P. N.;Hitman, G. A.;Fuller, J.;Neil, A.;Wanner, C.;Krane, V.;Sacks, F.;Moye, L.;Pfeffer, M.;Hawkins, C. M.;Braunwald, E.;Kjekshus, J.;Wedel, H.;Wikstrand, J.;Barter, P.;Keech, A.;Tavazzi, L.;Maggioni, A.;Marchioli, R.;Tognoni, G.;Franzosi, M. G.;Maggioni, A.;Bloomfield, H.;Robins, S.;Collins, R.;Armitage, J.;Keech, A.;Parish, S.;Peto, R.;Sleight, P.;Pedersen, T. R.;Ridker, P. M.;Holman, R.;Meade, T.;Simes, J.;Keech, A.;MacMahon, S.;Marschner, I.;Tonkin, A.;Shaw, J.;Serruys, P. W.;Nakamura, H.;Knatterud, G.;Furberg, C.;Byington, R.;Macfarlane, P.;Cobbe, S.;Ford, I.;Murphy, M.;Blauw, G. J.;Packard, C.;Shepherd, J.;Kjekshus, J.;Pedersen, T.;Wilhelmsen, L.;Braunwald, E.;Cannon, C.;Murphy, S.;Collins, R.;Armitage, J.;Bowman, L.;Parish, S.;Peto, R.;Sleight, P.;Baigent, C.;Landray, M.;Collins, R.;La Rosa, J.;Rossouw, J.;Probstfield, J.;Shepherd, J.;Cobbe, S.;Macfarlane, P.;Ford, I.
通讯作者：
Ford, I.
影响因子：
168.9
作者：
Holdaas, H;Fellström, B;Pedersen, TR
通讯作者：
Pedersen, TR
影响因子：
8
作者：
通讯作者：
--
影响因子：
16.2
作者：
Knopp, Robert H.;D'Emden, Michael;Pocock, Stuart J.
通讯作者：
Pocock, Stuart J.
影响因子：
168.9
作者：
Baigent, C;Keech, A;Simes, J
通讯作者：
Simes, J