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T2-based BOLD effect in myocardial infarction: a study at 3 T

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Journal of Cardiovascular Magnetic Resonance201012(Suppl 1):P204

https://doi.org/10.1186/1532-429X-12-S1-P204

Published: 21 January 2010

Keywords

  • Dipyridamole
  • Remote Region
  • Myocardial Perfusion Reserve
  • Remote Myocardium
  • Myocardial Infarct Model

Introduction

Coronary vasodilator dysfunction has been demonstrated in infarcted as well as remote myocardium in patients with acute coronary syndrome. Recently, blood-oxygen-level-dependent (BOLD) approaches have been employed to probe myocardial perfusion reserve using T2, T2* and characterize stenosis using SSFP signal contrast. We extended the T2-based BOLD approach to a myocardial infarct model, exploring the advantages of 3 T to evaluate regional vasodilatory function using a stress agent.

Purpose

The aim of the study was two-fold, 1) to evaluate oxygen-sensitive T2 changes in normal myocardium at 3 T, 2) to apply this BOLD effect in assessing serial changes in vasodilatory reserve in infarct and remote zones after myocardial infarction (MI).

Methods

7 pigs underwent MRI before LAD occlusion (control) with subgroups studied at 2,7,14 and 30-42 days post-infarction. Histology was performed upon sacrifice at either Day 14 (N = 3) or 30-42 (N = 4). Imaging was performed on a 3 T MRI scanner (MR 750, GE Healthcare). T2 quantification was performed using a previously validated T2-prepared spiral sequence (interecho-spacing, 6 ms). The sequences were repeated after coronary vasodilation with intravenous injection of Dipyridamole. A contrast-enhanced (CE) IR-GRE sequence was used for infarct delineation.

Results

Table 1 compares the theoretical and experimental values of oxygen-sensitive T2, demonstrating the advantage of higher field strength with respect to changes observed (15% vs 2%). Figure 1 demonstrates T2 maps and CE images of mid-ventricular (infarct-slice) and basal regions (remote-slice) of representative pig myocardium at 2 weeks post-MI. Figure 2 shows the cumulative evolution of T2 in infarct and remote regions under rest and stress state. In remote regions, stress-induced T2 elevations were statistically significant at all time points (P < 0.04) except at week-1,2. We also noted a subtle but significant T2 elevation in the rest state (42.4 vs 40.3 ms control, P < 0.03) at week-1. In the infarct territory, rest and stress T2's were both elevated compared to remote tissue, particularly after week-1, however differences between the two were not significant.
Table 1

Oxygen-sensitive T2 changes

Bo = 1.5 T

T2 (ms, rest)

T2 (ms, stress)

% change

Theory

44.1

45.1

2.3

Experiment

43.2

44.1

2.1

Bo = 3 T

T2 (ms, rest)

T2 (ms, stress)

% change

Theory

40.2

46.3

15.2

Experiment

40.4

46.6

15.3*

* - P < 0.0001

Theory - Two-compartment tissue model

Resting blood volume was assumed to be 5%, which increases by 30% in stress state

Figure 1
Figure 1

Row 1 shows T2 maps while 2 shows CE images of representative porcine myocardium in infarcy (mid) and remote (base) slices. ROI in anterio-septal infarct region indicated edema as reflected by eleveated T2 (bright). (Note that this animal also developed an inferio0lateral infarct). Indicated ROIs were chosen for T2 analysis.

Figure 2
Figure 2

Plots demonstrate evolution of T2 after MI in remote and infarct zones under rest and stress states.

Conclusion

We have demonstrated the utility of the T2-based BOLD effect in probing regional myocardial oxygenation after MI on a 3 T system. Suppressed stress response in remote region between day-2 and week-4 could be suggestive of an already-vasodilated state resulting from a systemic acute inflammatory response, which eventually resolves. T2 changes with stress seen in infarct zones of some animals could be attributed to salvageable myocardium. T2 at 3 T appears to be a sensitive indicator of vasodilatory alterations in remote myocardium following MI.

Authors’ Affiliations

(1)
Sunnybrook Health Sciences Center, Toronto, Canada
(2)
St Michael's Hospital, Toronto, Canada

Copyright

© Ghugre et al; licensee BioMed Central Ltd. 2010

This article is published under license to BioMed Central Ltd.

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