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Novel Approach for In Vivo Detection of Vulnerable Coronary Plaques Using Molecular 3-T CMR Imaging With an Albumin-Binding Probe

  • Leif Christopher Engel
  • , Ulf Landmesser
  • , Kevin Gigengack
  • , Thomas Wurster
  • , Constantina Manes
  • , Georg Girke
  • , Milosz Jaguszewski
  • , Carsten Skurk
  • , David M. Leistner
  • , Alexander Lauten
  • , Andreas Schuster
  • , Bernd Hamm
  • , Rene M. Botnar
  • , Marcus R. Makowski
  • , Boris Bigalke
  • Charité – Universitätsmedizin Berlin
  • Charite Universitätsmedizin Berlin
  • Partner Site Munich Heart Alliance
  • Kolling Institute of Medical Research
  • King's College London
  • Pontificia Universidad Católica de Chile

Research output: Contribution to journalArticlepeer-review

21 Scopus citations

Abstract

Objectives: This study sought to investigate the potential of the noninvasive albumin-binding probe gadofosveset-enhanced cardiac magnetic resonance (GE-CMR) for detection of coronary plaques that can cause acute coronary syndromes (ACS). Background: ACS are frequently caused by rupture or erosion of coronary plaques that initially do not cause hemodynamically significant stenosis and are therefore not detected by invasive x-ray coronary angiography (XCA). Methods: A total of 25 patients with ACS or symptoms of stable coronary artery disease underwent GE-CMR, clinically indicated XCA, and optical coherence tomography (OCT) within 24 h. GE-CMR was performed approximately 24 h following a 1-time application of gadofosveset-trisodium. Contrast-to-noise ratio (CNR) was quantified within coronary segments in comparison with blood signal. Results: A total of 207 coronary segments were analyzed on GE-CMR. Segments containing a culprit lesion in ACS patients (n = 11) showed significant higher signal enhancement (CNR) following gadofosveset-trisodium application than segments without culprit lesions (n = 196; 6.1 [3.9 to 16.5] vs. 2.1 [0.5 to 3.5]; p < 0.001). GE-CMR was able to correctly identify culprit coronary lesions in 9 of 11 segments (sensitivity 82%) and correctly excluded culprit coronary lesions in 162 of 195 segments (specificity 83%). Additionally, segmented areas of thin-cap fibroatheroma (n = 22) as seen on OCT demonstrated significantly higher CNR than segments without coronary plaque or segments containing early atherosclerotic lesions (n = 185; 9.2 [3.3 to 13.7] vs. 2.1 [0.5 to 3.4]; p = 0.001). Conclusions: In this study, we demonstrated for the first time the noninvasive detection of culprit coronary lesions and thin-cap fibroatheroma of the coronary arteries in vivo by using GE-CMR. This method may represent a novel approach for noninvasive cardiovascular risk prediction.

Original languageEnglish
Pages (from-to)297-306
Number of pages10
JournalJACC: Cardiovascular Imaging
Volume12
Issue number2
DOIs
StatePublished - Feb 2019
Externally publishedYes

Keywords

  • CMR
  • atherosclerosis
  • endothelial dysfunction
  • molecular imaging
  • vulnerable plaque

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