他汀类药物干预冠脉事件发生的机制

本文论述了他汀类药物通过稳定斑块、诱导平滑肌细胞凋亡，改善凝血及血小板功能等机制以预防冠脉事件的发生。     

他汀类药物的抗炎效应

他汀类药物的临床获益远大于单纯降低低密度脂蛋白(LDL)胆固醇的预期获益。近年来的许多研究结果显示，他汀类药物具有抗炎效应，独立于降脂作用，可有效减少心脑血管事件。     

他汀类药物的抗炎效应

他汀类药物的临床获益远大于单纯降低低密度脂蛋白(LDL)胆固醇的预期获益.近年来的许多研究结果显示,他汀类药物具有抗炎效应,独立于降脂作用,可有效减少心脑血管事件.     

他汀类药物对急性冠脉综合征早期的影响

急性冠脉综合征 (ＡＣＳ)是指急性心肌梗死(ＡＭＩ)、不稳定性心绞痛和心脏缺血性猝死。由于急性冠脉综合征死亡率和心血管事件发生率较高 ,因此近年来引起医务工作者的高度重视 ,已完成了一系列相关的实验和临床研究。ＷＯＳＣＯＰＳ(ＷｅｓｔＯｆＳｃｏｔｌａｎｄＣｏｒｏｎａｒｙＰｒｅｖｅｎｔｉｏｎＳｔｕｄｙ)和ＡＦＣＡＰＳ/Ｔｅｘ ＣＡＰＳ(ＡｉｒＦｏｒｃｅ/ＲｅｘａｓＣｏｒｏｎａｒｙＡｔｈｅｒｏｓｃｌｅｒｏｓｉｓＰｒｅｖｅｎ ｔｉｏｎＳｔｕｄｙ)研究确立了他汀类药物在急性冠脉综合征一级预防中的地位。ＣＡＲＥ (Ｃｈｏｌ…     

急性冠状动脉综合征他汀类药物治疗的抗炎机制

急性冠状动脉综合征（ACS）是冠心病的特殊疾病谱，ACS的发生机制是由于动脉粥样硬化斑块的溃蚀、破裂，并在此基础上导致血栓形成。在冠状动脉事件发生前对易损斑块进行预测及发生后进行有效治疗，已成为临床医生和研究人员的重要研究目标。     

急性冠脉综合征患者停用他汀类药物导致意外事件发生率增高

HMG-CoA降解酶抑制剂(他汀类药物)能使病情稳定的冠心病患者心脏事件发生率降低。有假设认为,急性冠脉综合征时,撤除原来持续应用的他汀类药物会导致与其降脂作用无关的血管功能损害,使心脏事件增多。因而有必要对这种假设作进一步的验证。 方法与结果 利用缺血综合征治疗试验中研     

他汀类药物在急性冠脉综合征中的非降脂作用

20世纪90年代进行的他汀类药物试验充分肯定了降脂治疗的临床益处,长期应用具有良好的安全性.本文就他汀类药物的非降脂作用(如稳定斑块、改善内皮功能、减少炎症反应和抑制血栓形成等),在急性冠脉综合征中的应用作一综述.     

阿托伐他汀序贯治疗急性冠脉综合症临床观察

目的观察和分析应用阿托伐他汀序贯治疗急性冠脉综合征患者的临床疗效及价值。方法选取于2011年12月-2013年07月在我院接受治疗的急性冠脉综合症患者84例为研究对象,采取数字标记法随机将上述选取对象分成对照组和观察组,对照组42例给予常规剂量他汀类药物进行治疗,观察组给予阿托伐他汀序贯进行治疗,观察和记录两组患者在4个月内严重心血管事件发生率。结果通过采取上述治疗,观察组42例患者恶性心血管事件的发生率较对照组患者明显的降低,两组该项指标对比有显著性差异和统计学意义(P0.05)。结论采取阿托伐他汀序贯治疗急性冠状动脉综合征,治疗效果良好,有助于心血管临床症状的改善和心血管事件发生率的降低,这对与患者预后的改善和生活质量的提升有着积极的影响。     

86例急性冠脉综合征患者他汀类药物治疗对肝功能的影响病例分析

摘 要 目的：探讨他汀类药物治疗急性冠脉综合征对肝功能的影响及安全性。方法：收集2014年2月至2014年7月于我院心内科住院治疗的86例急性冠脉综合征患者病例资料,入院即刻给予常规剂量他汀类药物治疗,检测24h内、7天、15天的肝脏转氨酶,根据服用他汀类药物后7天后肝功能(丙氨酸氨基转移酶)正常与否分成两组:肝功能正常组与肝功能异常组;分析两组肝脏转氨酶变化趋势。结果：两组入院后7天、15天无肝脏转氨酶超过正常高限3倍以上的病例;两组肝脏天门冬氨酸氨基转移酶（AST）入院24小时内均数明显增高,入院后7天、15天降至正常范围内;肝功能异常组入院24小时内丙氨酸氨基转移酶(ALT)均数呈轻中度增高,入院后7天、15天呈轻度增高;肝功能正常组入院24小时内丙氨酸氨基转移酶(ALT)均数呈轻中度增高,入院后7天、15天降至正常;结论：部分患者服用他汀类药物后肝功能ALT轻度增高,AST降至正常范围,急性冠脉综合征患者服用常规剂量他汀是安全的。     

早期强化他汀类药物对急性冠脉综合征的影响

急性冠状动脉综合征（acute coronary svndrome．ACS）是在冠状动脉粥样硬化斑块破裂基础上继发血栓形成而引起的一组急性缺血性心脏病,包括不稳定型心绞痛（UAP）、非sT段抬高型心肌梗死（NSTEMI）、ST段抬高型心肌梗死（STEMI）和缺血性心脏猝死。ACS是目前发达国家和我国致死、致残的主要疾病之一。     

Early statin therapy in acute coronary syndromes

Patients who survive an acute coronary syndrome of unstable angina or myocardial infarction are at much higher risk of a recurrent event within the following year than patients with stable coronary syndromes. Statin therapy is justified for many of these patients, not only for long-term benefit but also to reduce the risk of recurrent events within weeks of the primary event. The mechanisms that underlie this benefit are probably related to improvements in endothelial function, a decrease in vascular inflammation, and reduced prothrombotic factors. The effects of statins may be mediated by cholesterol reduction, cholesterol-independent effects (particularly decreasing isoprenoids), and mechanisms that are independent of inhibiting 3-hydroxy-3-methylglutaryl coenzyme A (HMG CoA) reductase. Observational studies consistently show an early reduction in mortality with statin therapy started before discharge from hospital after an acute coronary syndrome. Several randomized controlled trials also support an early benefit of risk reduction from statins started during the hospital admission for an acute coronary syndrome. Early statin therapy is also related to improved compliance and use of statins several years after a coronary event. Thus, early statin therapy may improve both early and long-term secondary prevention efforts.     

Early statin therapy in acute coronary syndromes

Patients who survive an acute coronary syndrome are at much higher risk of a recurrent event within the following year than patients with stable coronary syndromes. Risk factor modification, including statin therapy, lowers the risk of recurrent events over many years, but also to reduces the high risk of an another event within the weeks to months following the initial acute coronary syndrome. The mechanisms that contribute to this benefit are likely related to improvements in endothelial function, a decrease in vascular inflammation, and reduced prothrombotic factors. The effects of statins may be mediated by cholesterol reduction, cholesterol-independent effects (particularly by decreasing isoprenoids), and mechanisms that are independent of inhibiting HMG CoA reductase. Observational studies show an early reduction in mortality with statin therapy started before discharge from hospital after an acute coronary syndrome. Several randomized controlled trials also support a rapid reduction in the risk of recurrent events after starting statins during the hospital admission for an acute coronary syndrome. Early statin therapy is also related to improved compliance and use of statins several years after a coronary event. Thus early statin therapy may improve both early and long-term secondary prevention efforts.     

Intensive statin therapy in acute coronary syndromes

Acute coronary syndromes (ACS) represent an enormous disease burden, especially in the Western world, where they are one of the largest causes of mortality and morbidity. Patients suffering an acute coronary event are at very high risk of further coronary events, and although improvements in medical therapy over the past two decades have significantly reduced the risk, it remains high. 3-Hydroxy-3-methylglutaryl coenzyme A reductase inhibitors (statins) are now fully established in the primary and secondary prevention of stable coronary heart disease, and recently a substantial body of evidence has proven their efficacy in ACS. This paper examines the evidence for statin use in ACS.     

The case for early statin therapy in acute coronary syndromes

Three large secondary prevention studies have shown that, in patients with a history of cardiovascular disease, statin treatment reduces the risk of further events and lowers overall mortality. In these studies, total mortality was reduced by as much as 30% in high-risk groups and 22% in average-risk groups. However, these studies did not include patients immediately after the coronary event. There are many benefits to early intervention with statin therapy in patients with acute coronary syndromes, including reduction of the risk of a subsequent event, which is highest immediately after the index event. Early treatment may reduce this likelihood in the first months after a coronary event by stabilizing atherosclerotic plaques and improving endothelial function in addition to lowering low-density lipoprotein cholesterol levels. This article reviews the case for early statin therapy in patients with a history of coronary heart disease. Results of clinical studies have now shown early statin therapy to be safe and cost-effective in reducing in-hospital and 6-month mortality.     

Role of statin drugs in acute coronary syndromes

Conclusions The statin class of drugs has demonstrated clinical efficacy in reducing long-term recurrence of myocardial infarction, ischemic events, and sudden death. The drugs have now been shown to exert beneficial influences on the vascular endothelium, monocytes/macrophages, platelets, smooth muscle cells, and the inflammatory process. Recent experimental studies have documented protection during myocardial ischemia, preservation of post-infarction left ventricular function, and reduction of hypertensive-induced hypertrophy of the myocardium. Several of these pleiotropic effects have been documented before a decline in lipid levels was observed. Recent clinical trials have suggested efficacy of the statin drugs in acute coronary syndromes of unstable angina and acute myocardial infarction. Thus, a promising future for the statin drugs will involve administration to patients with acute coronary syndromes.     

Aggressive statin therapy for acute coronary syndromes

Acute coronary syndromes (ACS) account for an enormous disease burden, especially in the Western world. Patients suffering acute coronary events are now understood to carry a very high risk of further coronary events and although improvements in conventional medical therapy over the past two decades have significantly reduced the risk, it remains high. Therapy with HMG CoA reductase inhibitors (statins) have now been well established for the primary and secondary prevention of stable coronary heart disease, but recently a substantial body of evidence has proven their efficacy in the treatment of ACS. This article examines this emerging evidence for the use of statins in ACS.     

普罗布考对急性冠脉综合征患者抗氧化、抗炎作用的研究

目的:观察普罗布考对急性冠脉综合征(ACS)患者血氧化低密度脂蛋白抗体(oxLDL-Ab)、高敏C反应蛋白(hs-CRP)和白介素18(IL-18)水平的影响。方法:ACS患者81例,随机分为普罗布考组(41例)和常规治疗组(40例),用药治疗前检测外周血oxLDL-Ab、hs-CRP和IL-18的水平,用药治疗1周后复查hs-CRP和IL-18,治疗4周后复查oxLDL-Ab,观察治疗前后各指标变化。并分析两组治疗结束前一周心绞痛发作的频率。结果:治疗后普罗布考组较常规治疗组oxLDL-Ab[(56.20±14.56)U/ml∶(88.65±11.23)U/ml]、hs-CRP[(8.78±5.61)mg/L∶(14.23±9.79)mg/L]及IL-18[(88.54±17.74)pg/ml∶(141.83±19.52)pg/ml]浓度明显降低(P均0.05)。普罗布考组治疗第4周平均心绞痛发作频率较常规治疗组显著降低[(2.5±1.5)次/周∶(4.7±1.7)次/周,P0.05],次数减少与oxLDL-Ab减少有明显相关性(r=0.60,P0.05)。结论:普罗布考对急性冠脉综合征患者具有抗氧化、抗炎作用,可减少心绞痛发作频率。     

In-hospital initiation of statin therapy in patients with acute coronary events

After acute coronary events, patients remain at high risk for recurrent cardiovascular events and mortality. Despite the compelling scientific and clinical trial evidence that statin therapy reduces mortality in patients after acute coronary events, this life-saving therapy continues to be underutilized. It is now recognized that the setting in which statin therapy is initiated has a major impact on patient adherence. In-hospital initiation of statin therapy has been demonstrated to result in a markedly increased treatment rate, improved long-term patient compliance, more patients reaching low-density lipoprotein levels less than 100 mg/dL, and improved long-term clinical outcomes. As long-term risk reduction is seen with statin therapy irrespective of baseline low-density lipoprotein cholesterol, virtually all acute coronary event patients are candidates for statin treatment. In-hospital initiation of statin therapy may also reduce early clinical events in acute coronary syndrome patients, but further research is required before this is fully established. The adoption of in-hospital initiation of statin therapy as the standard of care for patients hospitalized with acute coronary events will dramatically improve treatment rates and thus substantially reduce the risk of future coronary events and prolong life in the large number of patients hospitalized each year.     

强化降脂治疗对急性冠脉综合征患者经皮冠状动脉介入治疗效果的影响

目的 探讨强化他汀治疗对急性冠脉综合征患者PCI术后心肌灌注的影响及可能机制.方法 行择期PCI的急性冠脉综合征患者228例,随机分为标准他汀组(n=115)和强化他汀组(n=113).于PCI术前7 d,纪录PCI后的TIMI血流、纠正的TIMI计桢数(CTFC)以及TIMI心肌灌注分级(TMPG)等.于PCI前后测量肌酸磷酸激酶(CK)、CK同工酶MB(CPK-MB)、肌钙蛋白I(TnI)、高敏C反应蛋白(hs-CRP)、P选择素和细胞间黏附分子(ICAM)水平.结果 强化他汀组支架置入后TIMI血流0～1级显著少于标准他汀组,3级显著多于标准他汀组(P<0.05).强化他汀组无复流发生率显著低于标准他汀组(P<0.001).CTFC在强化他汀组显著低于标准他汀组(P<0.001).强化他汀组的TMPG也显著优于标准他汀组(P=0.001).PCI术后24 h,CPK-MB和TnI在强化他汀组显著低于标准他汀组[CPK-MB:(18.74±8.41) ng/ml vs (21.78±10.64) ng/ml,P=0.018;TnI:(0.99±1.07) ng/ml vs (1.47±1.54) ng/ml,P=0.006].标准治疗组CK-MB升高者占27.8% (32/115),强化他汀组则只有15.9%(18/113)(P=0.030).标准他汀组TnI升高者显著多于强化他汀组[36.5% (42/115) vs 19.5%(22/113),P=0.04],其中,标准他汀组的心肌坏死发生率为13%(15/115),而在强化他汀组仅为4.4%(5/113)(P=0.021).PCI术后24 h,强化他汀组的hs-CRP、P选择素及ICAM水平均显著低于标准他汀组(P<0.001).结论 PCI术前使用强化他汀治疗比标准他汀治疗能更有效改善急性冠脉综合征患者的心肌灌注、减轻心肌损伤.同时伴有hs-CRP、P选择素和ICAM-1水平显著降低.