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钆增强心血管磁共振成像高估人类急性心肌梗死面积的机制:一项定量与动力学研究。

Mechanisms for overestimating acute myocardial infarct size with gadolinium-enhanced cardiovascular magnetic resonance imaging in humans: a quantitative and kinetic study.

作者信息

Hammer-Hansen Sophia, Bandettini W Patricia, Hsu Li-Yueh, Leung Steve W, Shanbhag Sujata, Mancini Christine, Greve Anders M, Køber Lars, Thune Jens Jakob, Kellman Peter, Arai Andrew E

机构信息

Laboratory for Advanced Cardiovascular Imaging, National Heart, Lung, and Blood Institute, Department of Health and Human Services, National Institutes of Health, Building 10, Room B1D416, MSC 1061, 10 Center Drive, Bethesda, MD 20892-1061, USA Department of Medicine B, The Heart Center, Rigshospitalet, Copenhagen, Denmark.

Laboratory for Advanced Cardiovascular Imaging, National Heart, Lung, and Blood Institute, Department of Health and Human Services, National Institutes of Health, Building 10, Room B1D416, MSC 1061, 10 Center Drive, Bethesda, MD 20892-1061, USA.

出版信息

Eur Heart J Cardiovasc Imaging. 2016 Jan;17(1):76-84. doi: 10.1093/ehjci/jev123. Epub 2015 May 16.

Abstract

AIMS

It remains controversial whether cardiovascular magnetic resonance imaging with gadolinium only enhances acutely infarcted or also salvaged myocardium. We hypothesized that enhancement of salvaged myocardium may be due to altered extracellular volume (ECV) and contrast kinetics compared with normal and infarcted myocardium. If so, these mechanisms could contribute to overestimation of acute myocardial infarction (AMI) size.

METHODS AND RESULTS

Imaging was performed at 1.5T ≤ 7 days after AMI with serial T1 mapping and volumetric early (5 min post-contrast) and late (20 min post-contrast) gadolinium enhancement imaging. Infarcts were classified as transmural (>75% transmural extent) or non-transmural. Patients with non-transmural infarctions (n = 15) had shorter duration of symptoms before reperfusion (P = 0.02), lower peak troponin (P = 0.008), and less microvascular obstruction (P < 0.001) than patients with transmural infarcts (n = 22). The size of enhancement at 5 min was greater than at 20 min (18.7 ± 12.7 vs. 12.1 ± 7.0%, P = 0.003) in non-transmural infarctions, but similar in transmural infarctions (23.0 ± 10.0 vs. 21.9 ± 9.9%, P = 0.21). ECV of salvaged myocardium was greater than normal (39.5 ± 5.8 vs. 24.1 ± 3.1%) but less than infarcted myocardium (50.5 ± 6.0%, both P < 0.001). In kinetic studies of non-transmural infarctions, salvaged and infarcted myocardium had similar T1 at 4 min but different T1 at 8-20 min post-contrast.

CONCLUSION

The extent of gadolinium enhancement in AMI is modulated by ECV and contrast kinetics. Image acquisition too early after contrast administration resulted in overestimation of infarct size in non-transmural infarctions due to enhancement of salvaged myocardium.

摘要

目的

钆增强心血管磁共振成像是否仅能增强急性梗死心肌,还是也能增强存活心肌,目前仍存在争议。我们推测,与正常心肌和梗死心肌相比,存活心肌的强化可能是由于细胞外容积(ECV)和对比剂动力学改变所致。如果是这样,这些机制可能导致急性心肌梗死(AMI)面积的高估。

方法与结果

在1.5T场强下,于AMI后≤7天进行成像,采用连续T1mapping以及容积早期(注射对比剂后5分钟)和晚期(注射对比剂后20分钟)钆增强成像。梗死灶分为透壁性(透壁范围>75%)或非透壁性。与透壁梗死患者(n = 22)相比,非透壁梗死患者(n = 15)再灌注前症状持续时间更短(P = 0.02),肌钙蛋白峰值更低(P = 0.008),微血管阻塞更少(P < <0.001)。在非透壁梗死中,5分钟时的强化面积大于20分钟时(18.7±12.7%对12.1±7.0%,P = 0.003),但在透壁梗死中相似(23.0±10.0%对21.9±9.9%,P = 0.21)。存活心肌的ECV大于正常心肌(39.5±5.8%对24.1±3.1%)但小于梗死心肌(50.5±6.0%,P均<0.001)。在非透壁梗死的动力学研究中,存活心肌和梗死心肌在注射对比剂后4分钟时T1相似,但在8 - 20分钟时T1不同。

结论

AMI中钆增强的范围受ECV和对比剂动力学调节。对比剂注射后过早进行图像采集,由于存活心肌的强化,导致非透壁梗死中梗死面积被高估。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c3bb/4684160/d7077d767d30/jev12301.jpg

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