• 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

心肌梗死后心室扩大与生存率降低

Ventricular enlargement and reduced survival after myocardial infarction.

作者信息

Pfeffer M A, Pfeffer J M

出版信息

Circulation. 1987 May;75(5 Pt 2):IV93-7.

PMID:2952370
Abstract

Increased ventricular volume is one of the most powerful predictors of reduced survival in patients with heart disease. Despite its well-documented prognostic significance, the magnitude of the progression of ventricular dilatation from the acute to the chronic phase of myocardial infarction has only recently been appreciated. In an experimental preparation of myocardial infarction in rats, left ventricular cavitary volume increased progressively even after histologic resolution of the infarct region. We hypothesized that this remodeling of the infarcted left ventricle was a response to an increase in both systolic and diastolic wall stresses and that captopril, by reducing wall stress, would attenuate the process. For comparably sized infarcts, the captopril-treated rats had smaller ventricular volumes at common distending pressures, yet they had maintained or improved cardiac output. Most importantly, long-term captopril therapy also prolonged the survival of these rats with experimental myocardial infarction. The implication of these animal studies is that the potential exists for the attenuation of progressive ventricular enlargement and improvement of survival of patients recovering from a myocardial infarction. At the present time, no information is available in patients as to the therapeutic potential of interrupting this insidious process of ventricular dilatation in order to improve survival. Clinical trials are required to determine whether salutary benefits similar to those observed in animals can be provided to patients recovering from a myocardial infarction.

摘要

心室容量增加是心脏病患者生存率降低的最强有力预测因素之一。尽管其预后意义已得到充分证明,但直到最近人们才认识到从心肌梗死急性期到慢性期心室扩张进展的程度。在大鼠心肌梗死的实验模型中,即使梗死区域在组织学上已愈合,左心室腔容量仍在逐渐增加。我们推测,梗死左心室的这种重塑是对收缩期和舒张期壁应力增加的一种反应,而卡托普利通过降低壁应力将减弱这一过程。对于大小相当的梗死灶,接受卡托普利治疗的大鼠在相同的扩张压力下心室容量较小,但它们维持或改善了心输出量。最重要的是,长期卡托普利治疗还延长了这些实验性心肌梗死大鼠的生存期。这些动物研究表明,有可能减轻进行性心室扩大,并改善心肌梗死后恢复患者的生存率。目前,关于中断这种隐匿性心室扩张过程以提高生存率的治疗潜力,在患者中尚无相关信息。需要进行临床试验来确定,能否为心肌梗死后恢复的患者提供与在动物中观察到的类似的有益效果。

相似文献

1
Ventricular enlargement and reduced survival after myocardial infarction.心肌梗死后心室扩大与生存率降低
Circulation. 1987 May;75(5 Pt 2):IV93-7.
2
The extent of regional wall motion abnormalities identifies patients at risk of extensive left ventricular remodeling: implications for the design of post myocardial infarction trials.局部室壁运动异常的程度可识别有广泛左心室重构风险的患者:对心肌梗死后试验设计的启示。
G Ital Cardiol. 1999 Jan;29(1):20-6.
3
A role of fatty acid oxidation in cardiac hypertrophy.脂肪酸氧化在心肌肥大中的作用。
Cardioscience. 1993 Sep;4(3):133-42.
4
Hemodynamic benefits and prolonged survival with long-term captopril therapy in rats with myocardial infarction and heart failure.长期卡托普利治疗对心肌梗死和心力衰竭大鼠的血流动力学益处及生存期延长作用。
Circulation. 1987 Jan;75(1 Pt 2):I149-55.
5
Development and prevention of congestive heart failure following myocardial infarction.心肌梗死后充血性心力衰竭的发展与预防
Circulation. 1993 May;87(5 Suppl):IV120-5.
6
Ventricular remodeling after myocardial infarction. Experimental observations and clinical implications.心肌梗死后的心室重构。实验观察与临床意义。
Circulation. 1990 Apr;81(4):1161-72. doi: 10.1161/01.cir.81.4.1161.
7
[Expansion and remodelling of the left ventricle after myocardial infarction].[心肌梗死后左心室的扩张与重塑]
Ann Cardiol Angeiol (Paris). 1990 Nov;39(9):541-6.
8
Changes in ventricular size and function in patients treated with valsartan, captopril, or both after myocardial infarction.心肌梗死后接受缬沙坦、卡托普利或两者联合治疗的患者心室大小和功能的变化。
Circulation. 2005 Jun 28;111(25):3411-9. doi: 10.1161/CIRCULATIONAHA.104.508093. Epub 2005 Jun 20.
9
Plasma brain natriuretic peptide correlates with infarct size but not with subsequent remodeling in the rat heart.血浆脑钠肽与大鼠心脏梗死面积相关,但与随后的心脏重塑无关。
Cardiovasc Pathol. 2007 Mar-Apr;16(2):79-84. doi: 10.1016/j.carpath.2006.11.003. Epub 2006 Dec 18.
10
Thickening of the infarcted wall by collagen injection improves left ventricular function in rats: a novel approach to preserve cardiac function after myocardial infarction.通过注射胶原蛋白使梗死心肌壁增厚可改善大鼠左心室功能:一种心肌梗死后保留心脏功能的新方法。
J Am Coll Cardiol. 2005 Aug 16;46(4):714-9. doi: 10.1016/j.jacc.2005.04.056.

引用本文的文献

1
Mechanical response of cardiac microtissues to acute localized injury.心肌微组织对急性局部损伤的力学反应。
Am J Physiol Heart Circ Physiol. 2022 Oct 1;323(4):H738-H748. doi: 10.1152/ajpheart.00305.2022. Epub 2022 Sep 2.
2
Clinical Assessment of Ventricular Wall Stress in Understanding Compensatory Hypertrophic Response and Maladaptive Ventricular Remodeling.心室壁应力的临床评估在理解代偿性肥厚反应和适应性不良的心室重构中的作用
J Cardiovasc Dev Dis. 2021 Sep 29;8(10):122. doi: 10.3390/jcdd8100122.
3
Reverse Cardiac Remodeling and ARNI Therapy.
心脏逆向重构与ARNI治疗
Curr Heart Fail Rep. 2021 Apr;18(2):71-83. doi: 10.1007/s11897-021-00501-6. Epub 2021 Jan 22.
4
Reverse Cardiac Remodeling: A Marker of Better Prognosis in Heart Failure.逆向心脏重塑:心力衰竭预后较好的一个标志
Arq Bras Cardiol. 2015 Jun;104(6):502-6. doi: 10.5935/abc.20150025. Epub 2015 Mar 27.
5
Recurrence of left ventricular dysfunction in patients with restored idiopathic dilated cardiomyopathy.特发性扩张型心肌病恢复后左心室功能障碍的复发
Clin Cardiol. 2014 Apr;37(4):222-6. doi: 10.1002/clc.22243. Epub 2014 Jan 22.
6
Innate immune response after acute myocardial infarction and pharmacomodulatory action of tacrolimus in reducing infarct size and preserving myocardial integrity.急性心肌梗死后的固有免疫反应和他克莫司在减少梗死面积和保护心肌完整性方面的药物调节作用。
J Biomed Sci. 2013 Oct 29;20(1):82. doi: 10.1186/1423-0127-20-82.
7
Cardiac wound healing post-myocardial infarction: a novel method to target extracellular matrix remodeling in the left ventricle.心肌梗死后心脏伤口愈合:一种针对左心室细胞外基质重塑的新方法。
Methods Mol Biol. 2013;1037:313-24. doi: 10.1007/978-1-62703-505-7_18.
8
Systematic characterization of myocardial inflammation, repair, and remodeling in a mouse model of reperfused myocardial infarction.在再灌注心肌梗死的小鼠模型中对心肌炎症、修复和重塑进行系统表征。
J Histochem Cytochem. 2013 Aug;61(8):555-70. doi: 10.1369/0022155413493912. Epub 2013 May 28.
9
Endogenous IRAK-M attenuates postinfarction remodeling through effects on macrophages and fibroblasts.内源性 IRAK-M 通过对巨噬细胞和成纤维细胞的作用来减轻梗死后的重构。
Arterioscler Thromb Vasc Biol. 2012 Nov;32(11):2598-608. doi: 10.1161/ATVBAHA.112.300310. Epub 2012 Sep 20.
10
Tunable hydrogel-microsphere composites that modulate local inflammation and collagen bulking.可调谐水凝胶-微球复合材料,可调节局部炎症和胶原增生。
Acta Biomater. 2012 Sep;8(9):3218-27. doi: 10.1016/j.actbio.2012.05.027. Epub 2012 May 29.