Suppr超能文献

用99mTc标记的膜联蛋白A5对心力衰竭中程序性细胞丢失进行无创检测。

Noninvasive detection of programmed cell loss with 99mTc-labeled annexin A5 in heart failure.

作者信息

Kietselaer Bas L J H, Reutelingsperger Chris P M, Boersma Hendrikus H, Heidendal Guido A K, Liem Ing Han, Crijns Harry J G M, Narula Jagat, Hofstra Leo

机构信息

Department of Cardiology, University Hospital of Maastricht, Maastricht, The Netherlands.

出版信息

J Nucl Med. 2007 Apr;48(4):562-7. doi: 10.2967/jnumed.106.039453.

Abstract

UNLABELLED

Apoptosis, or programmed cell death (PCD), contributes to the decline in ventricular function in heart failure. Because apoptosis comprises a programmed cascade of events, it is potentially reversible, and timely intervention should delay the development of cardiomyopathy. (99m)Tc-Labeled annexin A5 has successfully been used for the noninvasive detection of PCD in myocardial infarction and heart transplant rejection. The present study evaluated the role of annexin A5 imaging for detection of PCD in heart failure patients.

METHODS

Annexin A5 imaging was performed on 9 consecutive heart failure patients with advanced nonischemic cardiomyopathy (dilated, n = 8; hypertrophic, n = 1) and in 2 relatives having the same genetic background as the hypertrophic cardiomyopathy patient but no heart failure.

RESULTS

Four of the patients with dilated cardiomyopathy and the 1 with hypertrophic cardiomyopathy and heart failure showed focal, multifocal, or global left ventricular uptake of annexin A5. No uptake was visualized in the remaining 4 patients or in the 2 controls. All cases showing annexin A5 uptake within the left ventricle experienced significant reduction in left ventricular function or functional class. In cases with no annexin A5 uptake, left ventricular function and clinical status remained stable.

CONCLUSION

These data indicate the feasibility of noninvasive PCD detection with annexin imaging in heart failure patients. Annexin A5 uptake is associated with deterioration in left ventricular function, and this association may lend itself to the development of novel management strategies.

摘要

未标记

细胞凋亡,即程序性细胞死亡(PCD),是导致心力衰竭时心室功能下降的原因之一。由于细胞凋亡包含一系列程序性事件,因此它可能是可逆的,及时干预应能延缓心肌病的发展。(99m)锝标记的膜联蛋白A5已成功用于心肌梗死和心脏移植排斥反应中PCD的无创检测。本研究评估了膜联蛋白A5成像在心力衰竭患者中检测PCD的作用。

方法

对9例晚期非缺血性心肌病(扩张型,n = 8;肥厚型,n = 1)的连续心力衰竭患者以及2名与肥厚型心肌病患者具有相同遗传背景但无心力衰竭的亲属进行膜联蛋白A5成像。

结果

8例扩张型心肌病患者中的4例以及1例肥厚型心肌病合并心力衰竭患者显示左心室有局灶性、多灶性或整体摄取膜联蛋白A5。其余4例患者和2名对照者未观察到摄取。所有左心室内显示有膜联蛋白A5摄取的病例,左心室功能或心功能分级均显著降低。在无膜联蛋白A5摄取的病例中,左心室功能和临床状态保持稳定。

结论

这些数据表明在心力衰竭患者中通过膜联蛋白成像进行无创PCD检测是可行的。膜联蛋白A5摄取与左心室功能恶化相关,这种关联可能有助于开发新的治疗策略。

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验