Volume 10 Supplement 1

Abstracts of the 11th Annual SCMR Scientific Sessions - 2008

Open Access

111 Detection of changes in myocardial blood flow and volume: a CMR study in a canine model of coronary artery stenosis

  • Kyle S McCommis1,
  • Thomas A Goldstein1,
  • Robert J Gropler1 and
  • Jie Zheng1
Journal of Cardiovascular Magnetic Resonance200810(Suppl 1):A12

DOI: 10.1186/1532-429X-10-S1-A12

Published: 22 October 2008

Introduction

Quantification of both myocardial blood flow (MBF) and myocardial blood volume (MBV) may provide critical information on coronary artery diseases. We have recently developed fast mapping techniques for quantifying both perfusion parameters with the CMR first-pass dynamic imaging approach and an intravascular contrast agent. The purpose of this study is to evaluate the techniques in the assessment of changes in MBF and MBV that occur with differing severities of coronary artery stenosis during Dipyridamole or Dobutamine induced hyperemia.

Methods

25 dogs were divided into six groups (Table in Figure 1). Stenosis was created by using an occluder in the proximal left anterior descending coronary artery (LAD) in an open-chest model. First-pass CMR perfusion scans were performed at rest and during the pharmacologically induced hyperemia for all dogs. Gadomer (Schering AG, Berlin), an intravascular contrast agent, was injected (0.015 mmol/kg) as a bolus during each perfusion. CMR images were pre-denoised with a wavelet method [1]. A validated perfusion quantification method designed in our lab [2] was applied to obtain MBF (Figure 2) and MBV maps (Figure 3). The regional data from both LAD perfused anterior and left circumflex artery (LCX) perfused inferior myocardial beds were determined.
Figure 1

Table of dog groups and results. A quantitative CMR perfusion technique was performed in a canine stenosis model during Dipyridamole or Dobutamine-induced hyperemia to assess changes in both myocardial blood flow and volume. Hyperemia caused different responses in stenotic and normal vessel perfused myocardial regions.

Figure 2

Myocardial blood flow maps from different dogs. Short axis images showing the left ventricle, right ventricle, and myocardial ring with example regions of interest in the LAD bed (white) and LCX bed (yellow).

Figure 3

Myocardial blood volume maps from different dogs.

Results

The percentage changes of MBF and MBV before and after the hyperemia are presented in Table in Figure 1. For the normal dogs, global MBF and MBV values are given. In normal dogs, Dipyridamole increases MBF more than Dobutamine, whereas MBV increases more with Dobutamine hyperemia. As expected, in stenotic dogs, increased MBF values during the hyperemia were proportionally attenuated with the stenosis degrees (negative correlation) in the LAD region (Figure 4). Interestingly, the flow reserve in the normal region decreased with stenosis severity as well, which agrees with other studies [36]. The same finding was observed in MBV during Dobutamine hyperemia. However, Dipyridamole vasodilation showed slight increases in blood volume reserve with increased stenosis severity in both the LAD and LCX regions (Figure 5). This may reflect adaptive auto-regulation, but further study is needed on this observation.
Figure 4

Myocardial flow reserve during Dipyridamole or Dobutamine for varying stenosis severities.

Figure 5

Myocardial volume reserve during Dipyridamole or Dobutamine for varying stenosis severities.

Conclusion

First-pass perfusion CMR allows for fast evaluation of MBF/MBV changes during pharmacologically induced hyperemia. Measurements of both MBF and MBV may allow for more comprehensive diagnoses of coronary artery stenosis and better treatment planning.

Authors’ Affiliations

(1)
Mallinckrodt Institute of Radiology, Washington University School of Medicine

References

  1. Goldstein TA: Magn Reson Med. 2006, 56: 439-45. 10.1002/mrm.20950.View ArticlePubMedGoogle Scholar
  2. Goldstein TA: Proceedings of the International Society of Magnetic Resonance in Medicine, Seattle, WA. 2006, 3573-Google Scholar
  3. Sambuceti G: Am J of Cardiol. 1993, 72: 538-43. 10.1016/0002-9149(93)90348-G.View ArticleGoogle Scholar
  4. Sambuceti G: Circulation. 1994, 90: 1696-1705.View ArticlePubMedGoogle Scholar
  5. Wu JC: J Nucl Cardiol. 2000, 7: 43-52. 10.1067/mnc.2000.99189.View ArticlePubMedGoogle Scholar
  6. Pacella JJ: Circulation. 2006, 114: 1940-7. 10.1161/CIRCULATIONAHA.106.641779.View ArticlePubMedGoogle Scholar

Copyright

© McCommis et al; licensee BioMed Central Ltd. 2008

This article is published under license to BioMed Central Ltd.

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