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[特发性扩张型心肌病的新发病机制:冠状动脉微循环的变化]

[New pathogenetic mechanisms of idiopathic dilated cardiomyopathy: changes in coronary microcirculation].

作者信息

Neglia Danilo

机构信息

Laboratorio PET Clinico, Istituto di Fisiologia Clinica, Consiglio Nazionale delle Ricerche, Pisa.

出版信息

Recenti Prog Med. 2003 Jun;94(6):247-52.

PMID:12793095
Abstract

There is growing evidence of the presence and relevance of coronary microvascular abnormalities in many cardiac diseases. In particular, it has been recently shown that dilated cardiomyopathy is characterized by coronary microvascular dysfunction since its early onset. Abnormal coronary microcirculatory function is not an effect of myocardial damage but in turn seems to be able to cause progressive contractile dysfunction, ventricular dilatation and heart failure. The mechanisms are largely unknown but both myocardial hypoperfusion and myocardial ischaemia are most probably involved. It has been demonstrated that in patients with dilated cardiomyopathy the presence of severe coronary microcirculatory dysfunction is an independent and relevant prognostic factor. From these studies it is more and more evident that coronary microvascular dysfunction is a new pathogenetic mechanism in dilated cardiomyopathy and that the coronary microcirculation should be considered a new target of treatment in cardiac diseases at risk to evolve towards heart failure.

摘要

越来越多的证据表明,在许多心脏疾病中存在冠状动脉微血管异常且具有相关性。特别是,最近研究表明,扩张型心肌病从疾病早期起就具有冠状动脉微血管功能障碍的特征。冠状动脉微循环功能异常并非心肌损伤的结果,相反,它似乎能够导致进行性收缩功能障碍、心室扩张和心力衰竭。其机制在很大程度上尚不清楚,但心肌灌注不足和心肌缺血很可能都参与其中。已经证明,在扩张型心肌病患者中,严重冠状动脉微循环功能障碍的存在是一个独立且相关的预后因素。从这些研究中越来越明显的是,冠状动脉微血管功能障碍是扩张型心肌病的一种新的发病机制,并且冠状动脉微循环应被视为有发展为心力衰竭风险的心脏疾病治疗的新靶点。

相似文献

1
[New pathogenetic mechanisms of idiopathic dilated cardiomyopathy: changes in coronary microcirculation].[特发性扩张型心肌病的新发病机制:冠状动脉微循环的变化]
Recenti Prog Med. 2003 Jun;94(6):247-52.
2
Coronary microvascular dysfunction and idiopathic dilated cardiomyopathy.冠状动脉微血管功能障碍与特发性扩张型心肌病。
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Myocardial ischemia in patients with dilated cardiomyopathy.扩张型心肌病患者的心肌缺血
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Reduction of myocardial blood flow reserve in idiopathic dilated cardiomyopathy without overt heart failure and its relation with functional indices: an echo-Doppler and positron emission tomography study.无明显心力衰竭的特发性扩张型心肌病患者心肌血流储备的降低及其与功能指标的关系:一项超声多普勒和正电子发射断层扫描研究
J Cardiovasc Med (Hagerstown). 2008 Aug;9(8):778-82. doi: 10.2459/JCM.0b013e3282fa7007.
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[Coronary microvascular disease: from experimental models to clinical practice].[冠状动脉微血管疾病:从实验模型到临床实践]
Recenti Prog Med. 2012 Jul-Aug;103(7-8):288-96. doi: 10.1701/1127.12433.
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Increased plasma levels of osteopontin are associated with activation of the renin-aldosterone system and with myocardial and coronary microvascular damage in dilated cardiomyopathy.骨桥蛋白的血浆水平升高与肾素-血管紧张素系统的激活以及扩张型心肌病中心肌和冠状动脉微血管损伤有关。
Cytokine. 2010 Mar;49(3):325-30. doi: 10.1016/j.cyto.2009.11.018. Epub 2009 Dec 23.
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Depressed coronary flow reserve is associated with decreased myocardial capillary density in patients with heart failure due to idiopathic dilated cardiomyopathy.在特发性扩张型心肌病所致心力衰竭患者中,冠状动脉血流储备降低与心肌毛细血管密度降低有关。
J Am Coll Cardiol. 2008 Oct 21;52(17):1391-8. doi: 10.1016/j.jacc.2008.05.064.
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Who would be a candidate for bridge to recovery during prolonged mechanical left ventricular support in idiopathic dilated cardiomyopathy?在特发性扩张型心肌病患者接受长期左心室机械支持期间,谁会是恢复过渡治疗的合适人选?
J Thorac Cardiovasc Surg. 2005 Sep;130(3):699-704. doi: 10.1016/j.jtcvs.2005.05.016.
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The proposed new classification of coronary microcirculation as the predictor of the heart failure progression in idiopathic dilated cardiomyopathy.将冠状动脉微循环提议作为特发性扩张型心肌病心力衰竭进展预测指标的新分类。
Cardiovasc Pathol. 2015 Nov-Dec;24(6):351-8. doi: 10.1016/j.carpath.2015.08.001. Epub 2015 Aug 8.
10
The effects of cardiac resynchronization therapy on left ventricular function, myocardial energetics, and metabolic reserve in patients with dilated cardiomyopathy and heart failure.心脏再同步治疗对扩张型心肌病和心力衰竭患者左心室功能、心肌能量代谢及代谢储备的影响。
J Am Coll Cardiol. 2004 Mar 17;43(6):1027-33. doi: 10.1016/j.jacc.2003.10.044.

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Evid Based Complement Alternat Med. 2014;2014:323870. doi: 10.1155/2014/323870. Epub 2014 Dec 28.