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  • Oral presentation
  • Open Access

'Splenic switch-off' to detect adenosine understress; a novel method to improve test sensitivity

  • 1,
  • 4,
  • 3,
  • 2,
  • 5,
  • 5,
  • 6,
  • 4 and
  • 3
Journal of Cardiovascular Magnetic Resonance201416 (Suppl 1) :O1

https://doi.org/10.1186/1532-429X-16-S1-O1

  • Published:

Keywords

  • Adenosine
  • Dobutamine
  • Pharmacological Stressor
  • Regadenoson
  • Adenosine Perfusion

Background

The sensitivity of adenosine perfusion CMR is reduced by false negative scans, with up to 50% resulting from inadequate pharmacological stress. Without a robust physiological marker for adequate myocardial hyperaemia, this false negative rate is difficult to address. We observed that splenic perfusion is markedly attenuated with adenosine - compared both to rest and to myocardial perfusion. In this collaborative multi-center study, we investigate the pharmacology of 'splenic switch-off', and evaluate its potential clinical utility as a marker of inadequate stress in adenosine perfusion imaging.

Methods

We assessed splenic perfusion in 4 cohorts acquired in 4 separate CMR units using 3 different pharmacological stressors. This study included: • Verification cohort of 50 adenosine perfusion scans (London, UK); to determine if splenic perfusion is consistently switched-off with adenosine. • 2 comparison cohorts using alternative pharmacological stressors (25 dobutamine scans; Southampton, UK and 25 regadenoson scans; Pittsburgh, USA); to assess whether generic stress (or only adenosine) causes splenic switch-off. • Clinical utility cohort of 100 adenosine scans (35 false and 65 true negative) from the CE-MARC trial (Leeds, UK); to assess whether failure of splenic switch-off could be a useful clinical indicator of inadequate stress.

Results

The spleen was visible in 98.5% of scans and grading of splenic perfusion was concordant between 2 blinded observers, κ = 0.84. Splenic switch-off occurred in 92% of adenosine studies acquired in London, but did not occur either with dobutamine or regadenoson perfusion studies, Figure 1. Measuring perfusion semi-quantitatively using signal intensity, splenic perfusion with adenosine stress was significantly lower than at rest (8.1 ± 9 versus 33.3 ± 19 arbitrary units, p < 0.0001), in contrast to with regadenoson where it increased significantly (123.7 ± 56.7 versus 144.6 ± 59.2 au, p = 0.003). With dobutamine (where only stress images were acquired), splenic perfusion was greater than myocardial (54.1 ± 1 versus 67.6 ± 25.2 au, p = 0.0005), again in contrast to adenosine. Within the CE-MARC cohort, patients with false negative CMR scans had a 36% rate of failed splenic switch-off. By contrast, the true negative group had a 9% rate (p = 0.0027 for difference), Figure 2. Splenic response to adenosine was concordant with haemodynamic response in 81% of subjects.
Figure 1
Figure 1

Splenic perfusion at stress and rest with adenosine (upper panels) and regadenoson (lower panels), showing splenic switch-off with adenosine only.

Figure 2
Figure 2

Data from CE-MARC trial to assess splenic and hemodynamic responses to adenosine There were significantly more patients with false negative CMR perfusion scans who failed to switch-off splenic perfusion with adenosine (indicating inadequate pharmacological stress) in comparison to those with true negative scans. Concordance was good between hemodynamic and splenic responses to adenosine. *p = 0.0027.

Conclusions

Splenic switch-off with adenosine is a new observation, and although a drug-specific effect, can be assessed in nearly all scans. Rescanning individuals with failure of splenic switch-off would reduce false negative scans by a third, but it may be that up to 1 in 11 of all adenosine perfusion patients are understressed. Further work is needed on this important sign.

Funding

CM is an NIHR Clinical Lecturer.

Authors’ Affiliations

(1)
Heart Hospital Imaging Centre and Imperial College, London, UK
(2)
University Hospital, Southampton, Southampton, UK
(3)
Heart Hospital Imaging Centre and University College, London, UK
(4)
Multidisciplinary Cardiovascular Research Centre (MCRC) & Leeds Institute of Genetics, Health and Therapeutics, University of Leeds, Leeds, UK
(5)
UPMC Cardiovascular Magnetic Resonance Center, Heart and Vascular Institute, University of Pittsburgh, Pittsburgh, Pennsylvania, USA
(6)
Heart Hospital Imaging Centre and Royal Free Hospital, London, UK

Copyright

© Manisty et al.; licensee BioMed Central Ltd. 2014

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/2.0), 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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