• 文献检索
  • 文档翻译
  • 深度研究
  • 学术资讯
  • Suppr Zotero 插件Zotero 插件
  • 邀请有礼
  • 套餐&价格
  • 历史记录
应用&插件
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
定价
高级版会员购买积分包购买API积分包
服务
文献检索文档翻译深度研究API 文档MCP 服务
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利：CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2026

文献检索

告别复杂PubMed语法，用中文像聊天一样搜索，搜遍4000万医学文献。AI智能推荐，让科研检索更轻松。

立即免费搜索

文件翻译

保留排版，准确专业，支持PDF/Word/PPT等文件格式，支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述，25分钟生成高质量综述，智能提取关键信息，辅助科研写作。

立即免费体验

他汀类药物：经皮冠状动脉介入治疗中降低心血管风险——他汀类药物超急性使用的基础与临床证据

Statins: cardiovascular risk reduction in percutaneous coronary intervention-basic and clinical evidence of hyperacute use of statins.

作者信息

Morales-Villegas Enrique C, Di Sciascio Germano, Briguori Carlo

机构信息

Centro de Investigación Cardiometabólica, Quinta Avenida 702-210, Frac. Agricultura, Aguascalientes, 20234 México, AGS, Mexico.

出版信息

Int J Hypertens. 2011 Mar 28;2011:904742. doi: 10.4061/2011/904742.

DOI:10.4061/2011/904742
PMID:21461336
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3065660/
Abstract

Reduction of LDL-cholesterol concentration in serum, blocking the isoprenylation of GTPases and the activation of myocyte-protective enzyme systems are three mechanisms that currently explain the lipid and non-lipid effects of statins. However, the decrease of LDL-cholesterol, the reduction of inflammation biomarkers and even the atheroregresion, as surrogate effects to the mechanisms of action of statins would be irrelevant if not accompanied by a significant decrease in the incidence of cardiovascular events. Statins like no other pharmacological group have proven to reduce the incidence of cardiovascular events and prolong life in any clinical scenario. This article review the basic and clinical evidence that support a new indication for HMG-CoA reductase inhibitors "pharmacological myocardial preconditioning before anticipated ischemia" or hyperacute use of statins in subjects with any coronary syndrome eligible for elective, semi-urgent or primary percutaneous coronary intervention: ARMYDA-Original, NAPLES I-II, ARMYDA-ACS, ARMYDA-RECAPTURE, Non-STEMI-Korean, Korean-STEMI trials.

摘要

降低血清中低密度脂蛋白胆固醇浓度、阻断GTP酶的异戊二烯化以及激活心肌保护酶系统是目前解释他汀类药物脂质和非脂质作用的三种机制。然而，如果不伴随心血管事件发生率的显著降低，作为他汀类药物作用机制的替代效应，低密度脂蛋白胆固醇的降低、炎症生物标志物的减少甚至动脉粥样硬化的消退都将是无关紧要的。与其他任何药物类别不同，他汀类药物已被证明在任何临床情况下都能降低心血管事件的发生率并延长寿命。本文回顾了支持HMG-CoA还原酶抑制剂新适应症的基础和临床证据，即“预期缺血前的药理学心肌预处理”或在符合择期、半紧急或直接经皮冠状动脉介入治疗的任何冠状动脉综合征患者中他汀类药物的超急性使用：ARMYDA-Original、NAPLES I-II、ARMYDA-ACS、ARMYDA-RECAPTURE、非ST段抬高型心肌梗死-韩国、韩国ST段抬高型心肌梗死试验。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c475/3065660/8de4d1f2a01c/IJHT2011-904742.009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c475/3065660/8a562cf83699/IJHT2011-904742.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c475/3065660/e6c3c013a45d/IJHT2011-904742.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c475/3065660/32679c4f8e6a/IJHT2011-904742.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c475/3065660/e1d6846a75a7/IJHT2011-904742.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c475/3065660/5165020bc739/IJHT2011-904742.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c475/3065660/5a421dd03516/IJHT2011-904742.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c475/3065660/087d87ac0d42/IJHT2011-904742.007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c475/3065660/00a0db3aa53d/IJHT2011-904742.008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c475/3065660/8de4d1f2a01c/IJHT2011-904742.009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c475/3065660/8a562cf83699/IJHT2011-904742.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c475/3065660/e6c3c013a45d/IJHT2011-904742.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c475/3065660/32679c4f8e6a/IJHT2011-904742.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c475/3065660/e1d6846a75a7/IJHT2011-904742.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c475/3065660/5165020bc739/IJHT2011-904742.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c475/3065660/5a421dd03516/IJHT2011-904742.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c475/3065660/087d87ac0d42/IJHT2011-904742.007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c475/3065660/00a0db3aa53d/IJHT2011-904742.008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c475/3065660/8de4d1f2a01c/IJHT2011-904742.009.jpg

相似文献

1
Statins: cardiovascular risk reduction in percutaneous coronary intervention-basic and clinical evidence of hyperacute use of statins.他汀类药物：经皮冠状动脉介入治疗中降低心血管风险——他汀类药物超急性使用的基础与临床证据
Int J Hypertens. 2011 Mar 28;2011:904742. doi: 10.4061/2011/904742.
2
Atorvastatin efficacy in the primary and secondary prevention of cardiovascular events.阿托伐他汀在心血管事件一级和二级预防中的疗效。
Drugs. 2007;67 Suppl 1:29-42. doi: 10.2165/00003495-200767001-00004.
3
Pleiotropic effects of statins: evidence against benefits beyond LDL-cholesterol lowering.他汀类药物的多效性作用：证据表明其益处不仅限于降低 LDL 胆固醇。
Am J Cardiovasc Drugs. 2010;10 Suppl 1:10-7. doi: 10.2165/1158822-S0-000000000-00000.
4
Policosanol safely down-regulates HMG-CoA reductase - potential as a component of the Esselstyn regimen.聚廿八醇可安全下调HMG-CoA还原酶——作为埃塞尔斯坦疗法组成部分的潜力。
Med Hypotheses. 2002 Sep;59(3):268-79. doi: 10.1016/s0306-9877(02)00226-8.
5
Pharmacodynamics and pharmacokinetics of the HMG-CoA reductase inhibitors. Similarities and differences.HMG-CoA还原酶抑制剂的药效学与药代动力学。异同点。
Clin Pharmacokinet. 1997 May;32(5):403-25. doi: 10.2165/00003088-199732050-00005.
6
Percutaneous coronary interventions and statins therapy.
Ther Adv Cardiovasc Dis. 2008 Apr;2(2):101-7. doi: 10.1177/1753944708089983.
7
Pretreatment with statins may reduce cardiovascular morbidity and mortality after elective surgery and percutaneous coronary intervention: clinical evidence and possible underlying mechanisms.他汀类药物预处理可能降低择期手术和经皮冠状动脉介入治疗后的心血管发病率和死亡率：临床证据及潜在机制
Am Heart J. 2007 Aug;154(2):391-402. doi: 10.1016/j.ahj.2007.04.029.
8
Real-World Effectiveness of High- Versus Moderate-Intensity Statin Therapy in Thai Patients With Acute Coronary Syndrome and Who Had Undergone Primary Percutaneous Coronary Intervention.
J Pharm Pract. 2020 Oct;33(5):640-646. doi: 10.1177/0897190019825915. Epub 2019 Feb 18.
9
High-Intensity Versus Non-High-Intensity Statins in Patients Achieving Low-Density Lipoprotein Cholesterol Goal After Percutaneous Coronary Intervention.经皮冠状动脉介入治疗后 LDL-C 达标患者中高强度与非高强度他汀类药物的比较。
J Am Heart Assoc. 2018 Nov 6;7(21):e009517. doi: 10.1161/JAHA.118.009517.
10
PCSK9 inhibitors and ezetimibe for the reduction of cardiovascular events: a clinical practice guideline with risk-stratified recommendations.PCSK9 抑制剂和依折麦布降低心血管事件风险的临床实践指南：基于风险分层的推荐意见。
BMJ. 2022 May 4;377:e069066. doi: 10.1136/bmj-2021-069066.

引用本文的文献

1
Role of statins in the management of dyslipidaemia.他汀类药物在血脂异常管理中的作用。
Indian Heart J. 2024 Mar;76 Suppl 1(Suppl 1):S33-S37. doi: 10.1016/j.ihj.2023.11.267. Epub 2024 Apr 8.
2
An overview of protective strategies against ischemia/reperfusion injury: The role of hyperbaric oxygen preconditioning.缺血/再灌注损伤防护策略概述：高压氧预处理的作用。
Brain Behav. 2018 Mar 30;8(5):e00959. doi: 10.1002/brb3.959. eCollection 2018 May.
3
The challenge of translating ischemic conditioning from animal models to humans: the role of comorbidities.

本文引用的文献

1
Beyond LDL cholesterol, a new role for PCSK9.除了低密度脂蛋白胆固醇，前蛋白转化酶枯草溶菌素9的新作用。
Arterioscler Thromb Vasc Biol. 2010 Jul;30(7):1279-81. doi: 10.1161/ATVBAHA.110.209007.
2
Statin loading for acute coronary syndromes.他汀类药物负荷剂量用于急性冠脉综合征。
Curr Opin Cardiol. 2010 Jul;25(4):373-8. doi: 10.1097/HCO.0b013e32833987ca.
3
Cell membrane repair as a mechanism for ischemic preconditioning?细胞膜修复作为缺血预处理的一种机制？
从动物模型到人体转化缺血预处理的挑战：合并症的作用。
Dis Model Mech. 2014 Dec;7(12):1321-33. doi: 10.1242/dmm.016741.
4
Differences in statin usage and target-goal achievement between departments at the same hospital.同一医院不同科室之间他汀类药物使用和目标达成的差异。
PLoS One. 2012;7(12):e50466. doi: 10.1371/journal.pone.0050466. Epub 2012 Dec 10.
5
Poor maternal nutrition programmes a pro-atherosclerotic phenotype in ApoE-/- mice.不良的母体营养会导致 ApoE-/- 小鼠出现动脉粥样硬化表型。
Clin Sci (Lond). 2012 Aug 1;123(4):251-7. doi: 10.1042/CS20110487.
6
Statins for COPD: a challenge to conventional beliefs?他汀类药物用于慢性阻塞性肺疾病：对传统观念的挑战？
Prim Care Respir J. 2012 Mar;21(1):5-7. doi: 10.4104/pcrj.2012.00020.
Circulation. 2010 Jun 15;121(23):2547-9. doi: 10.1161/CIRCULATIONAHA.110.958462. Epub 2010 Jun 1.
4
Regulation of bone marrow-derived vascular progenitor cell mobilization and maintenance.骨髓源性血管祖细胞动员和维持的调控。
Arterioscler Thromb Vasc Biol. 2010 Jun;30(6):1088-93. doi: 10.1161/ATVBAHA.109.191668. Epub 2010 May 7.
5
Effect of hydroxymethylglutaryl coenzyme-a reductase inhibitors on the long-term progression of rheumatic mitral valve disease.羟甲基戊二酰辅酶 A 还原酶抑制剂对风湿性二尖瓣疾病长期进展的影响。
Circulation. 2010 May 18;121(19):2130-6. doi: 10.1161/CIRCULATIONAHA.109.891598. Epub 2010 May 3.
6
Efficacy of high-dose atorvastatin loading before primary percutaneous coronary intervention in ST-segment elevation myocardial infarction: the STATIN STEMI trial.大剂量阿托伐他汀在 ST 段抬高型心肌梗死患者直接经皮冠状动脉介入治疗前的疗效：STIN 试验。
JACC Cardiovasc Interv. 2010 Mar;3(3):332-9. doi: 10.1016/j.jcin.2009.11.021.
7
Comparison of 80 versus 10 mg of atorvastatin on occurrence of cardiovascular events after the first event (from the Treating to New Targets [TNT] trial).阿托伐他汀 80 毫克与 10 毫克对首次事件后心血管事件发生的比较（来自治疗新靶点[TNT]试验）。
Am J Cardiol. 2010 Feb 1;105(3):283-7. doi: 10.1016/j.amjcard.2009.09.025. Epub 2009 Dec 22.
8
Meta-analysis of comparative efficacy of increasing dose of Atorvastatin versus Rosuvastatin versus Simvastatin on lowering levels of atherogenic lipids (from VOYAGER).阿托伐他汀、瑞舒伐他汀和辛伐他汀增加剂量对降低致动脉粥样硬化脂质水平的疗效比较的荟萃分析（来自 VOYAGER）。
Am J Cardiol. 2010 Jan 1;105(1):69-76. doi: 10.1016/j.amjcard.2009.08.651.
9
Reduction in recurrent cardiovascular events with intensive lipid-lowering statin therapy compared with moderate lipid-lowering statin therapy after acute coronary syndromes from the PROVE IT-TIMI 22 (Pravastatin or Atorvastatin Evaluation and Infection Therapy-Thrombolysis In Myocardial Infarction 22) trial.与急性冠脉综合征后的中等强度降脂他汀治疗相比，强化降脂他汀治疗可降低复发性心血管事件：来自 PROVE IT-TIMI 22（普伐他汀或阿托伐他汀评估与感染治疗-心肌梗死 22 试验）的结果。
J Am Coll Cardiol. 2009 Dec 15;54(25):2358-62. doi: 10.1016/j.jacc.2009.10.005.
10
Reperfusion injury, microvascular dysfunction, and cardioprotection: the "dark side" of reperfusion.再灌注损伤、微血管功能障碍与心脏保护：再灌注的“阴暗面”
Circulation. 2009 Nov 24;120(21):2105-12. doi: 10.1161/CIRCULATIONAHA.108.814640.