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Volume 18 Supplement 1

19th Annual SCMR Scientific Sessions

  • Poster presentation
  • Open Access

Automatic segmentation of myocardium at risk from contrast enhanced SSFP CMR: validation against expert readers and SPECT

  • 1, 2,
  • 1,
  • 1, 3,
  • 1,
  • 4,
  • 5,
  • 6,
  • 6,
  • 7,
  • 5,
  • 1 and
  • 1, 2
Journal of Cardiovascular Magnetic Resonance201618 (Suppl 1) :P222

https://doi.org/10.1186/1532-429X-18-S1-P222

  • Published:

Keywords

  • Cardiovascular Magnetic Resonance
  • Late Gadolinium Enhancement
  • Randomize Clinical Trial
  • Left Ventricular Mass
  • Automatic Segmentation

Background

Efficacy of reperfusion therapy can be assessed as myocardial salvage index (MSI) by determining the size of myocardium at risk (MaR) and myocardial infarction (MI), (MSI=1-MI/MaR). Cardiovascular magnetic resonance (CMR) can be used to assess MI by late gadolinium enhancement (LGE) and MaR by either T2-weighted imaging or contrast enhanced SSFP (CE-SSFP). Automatic segmentation algorithms have been developed and validated for MI by LGE as well as for MaR by T2-weighted imaging. There are, however, no algorithms available for CE-SSFP. Therefore, the aim of this study was to develop and validate automatic segmentation of MaR in CE-SSFP.

Methods

The automatic algorithm applies surface coil intensity correction and classifies myocardial intensities by Expectation Maximization to define a MaR region based on a priori regional criteria, and infarct region from LGE. Automatic segmentation was validated against manual delineation by expert readers in 183 patients with reperfused acute MI from two multi-center randomized clinical trials (RCT) (CHILL-MI and MITOCARE) and against myocardial perfusion SPECT in an additional set (n = 16). Endocardial and epicardial borders were manually delineated at end-diastole and end-systole. Manual delineation of MaR was used as reference and inter-observer variability was assessed for both manual delineation and automatic segmentation of MaR in a subset of patients (n = 15). MaR was expressed as percent of left ventricular mass (%LVM) and analyzed by bias (mean ± standard deviation). Regional agreement was analyzed by Dice Similarity Coefficient (DSC) (mean ± standard deviation).

Results

MaR assessed by manual and automatic segmentation were 36 ± 10 % and 37 ± 11 %LVM respectively with bias 1 ± 6 %LVM and regional agreement DSC 0.85 ± 0.08 (n = 183)(Figure 1). MaR assessed by SPECT and CE-SSFP automatic segmentation were 27 ± 10 %LVM and 29 ± 7 %LVM respectively with bias 2 ± 7 %LVM (Figure 1). Inter-observer variability was 0 ± 3 %LVM for manual delineation and -1 ± 2 %LVM for automatic segmentation.
Figure 1
Figure 1

Scatter plot of MaR as % of LVM (left column) and Bland-Altman plot of MaR bias as % of LVM (right column) for the automatic segmentation algorithm Segment MaR CE-SSFP against manual delineation in 183 patients (top row) and against SPECT in 16 patients (bottom row). The line of identity is shown as a solid line for both scatter plots and mean bias (solid line) and mean ± two standard deviations (dashed line) is shown for both Bland-Altman plots.

Conclusions

Automatic segmentation of MaR in CE-SSFP was validated against manual delineation in multi-center, multi-vendor studies with low bias and high regional agreement. Bias and variability was similar to inter-observer variability of manual delineation and inter-observer variability was decreased by automatic segmentation. Thus, the proposed automatic segmentation can be used to reduce subjectivity in quantification of MaR in RCT.

Authors’ Affiliations

(1)
Dept. of Clinical Physiology, Skåne University Hospital in Lund, Lund University, Lund, Sweden
(2)
Dept. of Biomedical Engineering, Faculty of Engineering, Lund University, Lund, Sweden
(3)
Laboratory of Medical Informatics, School of Medicine, Aristotle University of Thessaloniki, Thessaloniki, Greece
(4)
Dept. of Cardiology, Henri Mondor Hospital, Creteil, France
(5)
Dept. of Cardiology, Lund University, Lund, Sweden
(6)
Dept. of Medicine, Karolinska Institutet, Karolinska University Hospital, Stockholm, Sweden
(7)
Dept. of Cardiology B, Oslo, University Hospital Ullevål and Faculty of Medicine, University of Oslo, Oslo, Norway

Copyright

© Tufvesson et al. 2016

This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

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