Cardiac α(V)β(3) integrin expression following acute myocardial infarction in humans.

Cardiac α(V)β(3) integrin expression following acute myocardial infarction in humans.
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人类急性心肌梗塞后心脏α(V)β(3)整联蛋白表达。

DOI:
10.1136/heartjnl-2016-310115
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发表时间:
2017-04
期刊:
Heart (British Cardiac Society)
影响因子:
--
通讯作者:
Newby DE
Newby DE
中科院分区:
其他
文献类型:
--
作者:
Jenkins WS;Vesey AT;Stirrat C;Connell M;Lucatelli C;Neale A;Moles C;Vickers A;Fletcher A;Pawade T;Wilson I;Rudd JH;van Beek EJ;Mirsadraee S;Dweck MR;Newby DE

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适应不良修复有助于心肌梗死后心力衰竭的发展。αvβ3整合素受体是心脏修复的关键介质和决定因素。我们的目的是确定α和β3整合素的表达是否决定心肌梗死后的心肌恢复。对21例ST段抬高心肌梗死患者(前壁16例,外侧壁4例,下壁壁1例)于ST段抬高后2 周行18F-氟尿嘧啶正电子发射断层扫描和增强扫描。心肌梗死后9个月复查 。7例冠状动脉主干慢性完全闭塞(CTO)稳定期患者和9例健康志愿者进行了单次PET/CT和CMR检查。与远隔心肌(组织-本底比)和健康志愿者心肌(组织-本底比分别为1.34±0.22vs0.70±0.03vs0.70±0.03;p<0.001)相比,急性心肌梗死部位18F-Fuciclade摄取增加。CTO患者在已建立的心肌梗死部位无18F-氟内酯摄取,其活动与健康志愿者心肌相似(TBR平均值为0.71±0.06 vs 0.70±0.03,p=0.83)。室壁运动功能减退(室壁运动指数≥为1vs0;TbR平均值分别为0.93±0.31vs0.80±0.26,p<0.001)和心内膜下心肌梗死部位均可摄取~(18)F-氟尿嘧啶。重要的是,尽管与梗塞面积(r=0.03,p=0.9)或炎症(C反应蛋白,r=−0.20,p=0.38)无相关性,但在显示功能恢复的节段,18F-氟内酯摄取增加(TBR平均值为0.95±0.33vs0.81±0.27,p=0.002),并与局部恢复的可能性增加有关。18F-FLuciclade摄取在最近的心肌梗死部位增加,作为心脏修复和预测恢复区域的生物标记物。NCT01813045;发布结果。
Maladaptive repair contributes towards the development of heart failure following myocardial infarction (MI). The αvβ3 integrin receptor is a key mediator and determinant of cardiac repair. We aimed to establish whether αvβ3 integrin expression determines myocardial recovery following MI. 18F-Fluciclatide (a novel αvβ3-selective radiotracer) positron emission tomography (PET) and CT imaging and gadolinium-enhanced MRI (CMR) were performed in 21 patients 2 weeks after ST-segment elevation MI (anterior, n=16; lateral, n=4; inferior, n=1). CMR was repeated 9 months after MI. 7 stable patients with chronic total occlusion (CTO) of a major coronary vessel and nine healthy volunteers underwent a single PET/CT and CMR. 18F-Fluciclatide uptake was increased at sites of acute infarction compared with remote myocardium (tissue-to-background ratio (TBRmean) 1.34±0.22 vs 0.85±0.17; p<0.001) and myocardium of healthy volunteers (TBRmean 1.34±0.22 vs 0.70±0.03; p<0.001). There was no 18F-fluciclatide uptake at sites of established prior infarction in patients with CTO, with activity similar to the myocardium of healthy volunteers (TBRmean 0.71±0.06 vs 0.70±0.03, p=0.83). 18F-Fluciclatide uptake occurred at sites of regional wall hypokinesia (wall motion index≥1 vs 0; TBRmean 0.93±0.31 vs 0.80±0.26 respectively, p<0.001) and subendocardial infarction. Importantly, although there was no correlation with infarct size (r=0.03, p=0.90) or inflammation (C reactive protein, r=−0.20, p=0.38), 18F-fluciclatide uptake was increased in segments displaying functional recovery (TBRmean 0.95±0.33 vs 0.81±0.27, p=0.002) and associated with increase in probability of regional recovery. 18F-Fluciclatide uptake is increased at sites of recent MI acting as a biomarker of cardiac repair and predicting regions of recovery. NCT01813045; Post-results.
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