[ 99m Tc]-PentixaTec SPECT/CT for Imaging of Chemokine Receptor 4 Expression After Myocardial Infarction

医学 骨髓 核医学 正电子发射断层摄影术 单光子发射计算机断层摄影术 灌注 心肌梗塞 CXCR4型 趋化因子受体 发射计算机断层扫描 Spect成像 脾脏 血运重建 炎症 病理 内科学 趋化因子
作者
Alessandro Liebich,Ralph Alexander Bundschuh,Christian Helmut Pfob,Malte Kircher,Georgine Wienand,Philip W J Raake,Stephan G. Nekolla,Margret Schottelius,Takahiro Higuchi,Maximilian Rieger,Constantin Lapa
出处
期刊:Circulation-cardiovascular Imaging [Lippincott Williams & Wilkins]
卷期号:17 (11): e016992-e016992 被引量:3
标识
DOI:10.1161/circimaging.124.016992
摘要

BACKGROUND: Accumulation of CXCR4 (C-X-C motif chemokine receptor 4)–positive immune cells after acute myocardial infarction (AMI) can be visualized by positron emission tomography. For a broader clinical application, there is a need for CXCR4-directed radiotracers labeled with isotopes that can be used with single-photon emission computed tomography (SPECT). We report on the detection of CXCR4 expression after AMI in humans using the novel tracer [ 99m Tc]-PentixaTec. METHODS: In this retrospective analysis, 9 patients with AMI after mechanical revascularization underwent myocardial inflammation imaging with [ 99m Tc]-PentixaTec SPECT/computed tomography and rest perfusion SPECT imaging. Tracer uptake in the infarcted area, spleen, bone marrow, and blood pool were used for semiquantitative analysis and calculation of signal-to-background ratios. The extent and intensity of SPECT-derived inflammatory changes were compared with serological markers and perfusion defects. RESULTS: CXCR4-directed SPECT was positive in all patients. Increased CXCR4 expression was only detected in areas with diminished perfusion corresponding to the affected vessel in coronary angiography, with a signal-to-background ratio (infarcted area-to-blood pool) of 2.36±0.74. Uptake in bone marrow and spleen showed a significant correlation with CXCR4 expression in the infarcted areas (r=0.73 and P =0.03 for spleen and r=0.81 and P =0.008 for bone marrow, respectively). The extent and intensity of SPECT-derived inflammatory changes showed no significant association with serum troponin, CK (creatine kinase), leukocyte, or CRP (C-reactive protein) levels. CONCLUSIONS: This is the first report of in vivo CXCR4 imaging after AMI using a 99m Tc-labeled tracer. Increased CXCR4 expression was observed locally in the infarcted region and was related to a systemic inflammatory response in the reticuloendothelial system. This proof-of-concept investigation demonstrates the general feasibility of evaluating the inflammation-related CXCR4 expression in the myocardium after AMI using conventional scintigraphy or SPECT and might, thus, broaden its worldwide application in clinical practice.
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