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  • Meeting abstract
  • Open Access

231 Alternation of myocardial oxygen consumption during hyperemia: detection with a CMR method

  • 1,
  • 1 and
  • 1
Journal of Cardiovascular Magnetic Resonance200810 (Suppl 1) :A92

https://doi.org/10.1186/1532-429X-10-S1-A92

  • Published:

Keywords

  • Cardiovascular Magnetic Resonance
  • Dobutamine
  • Dipyridamole
  • Myocardial Blood Flow
  • Myocardial Oxygen Consumption

Introduction

Myocardial oxygen consumption (MVO2) directly reflects myocardial oxygen supply and demand. The purpose of this study is to test the ability of a cardiovascular magnetic resonance (CMR) method to determine changes in myocardial MVO2 during pharmacologically-induced hyperemia in a canine stenosis model.

Methods

13 dogs were divided into four groups, which can be seen in Table 1. Stenosis was created by an occluder around the proximal left-anterior descending (LAD) and stenosis severity was confirmed via Doppler flow reduction. MVO2 was calculated by the Fick principle: MVO2 OEF × MBF, in which OEF is the oxygen extraction fraction and MBF represents myocardial blood flow.

Table 1

Dog groups

Group (n)

Stenosis

Stress

1 (4)

70%

Dipyridamole

2 (3)

90%

Dipyridamole

3 (3)

50%

Dobutamine

4 (3)

70–90%

Dobutamine

OEF during hyperemia was determined by a two compartment model with measured myocardial T2 that is measured with a 2-D segmented turbo spin-echo (TSE) sequence [1]. This sequence was performed several times at rest and during either Dipyridamole-induced vasodilation or Dobutamine-induced hyperemia. Rest OEF was assumed to be 0.6, which is based on values measured in normal dogs using an arterial and coronary sinus blood sampling approach at rest [2]. MBF values, both at rest and during pharmaceutical stress, were determined with the quantitative first-pass perfusion CMR method. First-pass images were denoised and MBF maps were created with an algorithm that was developed and validated in our laboratory [3]. MVO2 values were determined in the stenotic LAD perfused anterior region and the remote left-circumflex (LCX) perfused inferior region.

Results

MVO2 results can be seen in Figure 1. As expected, Dobutamine causes a dramatic increase in MVO2, while injection of Dipyridamole shows only a moderate effect.
Figure 1
Figure 1

Changes in MVO2 during dipyridamole or dobutamine with various LAD stenosis. A quantitative CMR method is introduced to detect changes in myocardial MVO2 during hyperemia in a canine stenosis model. While severe stenosis attenuated MVO2 increase in the stenosis subtended region, the remote region also showed reduced increase in MVO2.

In the anterior area with LAD stenosis, after the injection of Dipyridamole, a small increase in MVO2 was observed at 13.8% and 10.7% for the 70% and 90% stenosis groups, respectively. With Dobutamine, MVO2 increased significantly at 57.9% and 35% for the 50% and 70–90% stenosis groups, respectively.

In the remote normal LCX perfused region, Dipyridamole induced moderate increases in MVO2 at 49.9% and 17.3% in the 70% and 90% stenosis groups, respectively. This is different from conventional wisdom that Dipyridamole would induce no changes in MVO2, but is consistent with a report using adenosine injection in dogs [4]. As expected, Dobutamine induced much higher changes in MVO2, 183.7% and 79% increases in the 50% and 70–90% stenosis groups, respectively. It is interesting to note that severe single-vessel stenosis not only attenuated the increase in MVO2 in stenotic perfused region with both Dipyridamole and Dobutamine, but also attenuated MVO2 in the remote normal myocardial region.

Conclusion

Our CMR method can non-invasively quantify regional myocardial MVO2. Determination of the changes in MVO2 is important in the diagnosis and management of patients with coronary artery disease.

Authors’ Affiliations

(1)
Mallinckrodt Institute of Radiology, Washington University School of Medicine, St. Louis, MO, USA

References

  1. Zhang H, et al: J Magn Reson Imaging. 2007, 26: 72-9. 10.1002/jmri.20964.View ArticlePubMedGoogle Scholar
  2. Zheng J, et al: Magn Reson Med. 2004, 51: 718-26. 10.1002/mrm.20025.View ArticlePubMedGoogle Scholar
  3. Goldstein TA, et al: Proceedings of the International Society of Magnetic Resonance in Medicine, Seattle, WA. 2006, 3573-Google Scholar
  4. Hoffman WE, et al: J Cardiothoracic and Vascular Anesthesia. 2003, 17: 495-8. 10.1016/S1053-0770(03)00156-3.View ArticleGoogle Scholar

Copyright

© McCommis et al; licensee BioMed Central Ltd. 2008

This article is published under license to BioMed Central Ltd.

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