- Oral presentation
- Open Access
T2-weighted MRI pulse sequences for imaging post-infarct edema in mice: comparison of spin echo and T2 preparation approaches
© Beyers et al; licensee BioMed Central Ltd. 2009
- Published: 28 January 2009
- Cardiac Magnetic Resonance
- Delayed Enhancement
- Phase Encode Gradient
- Gadolinium Delayed Enhancement
- Cardiac Magnetic Resonance Sequence
An ongoing diagnostic challenge exists in reliably differentiating non-salvageable, acutely infarcted myocardium from surrounding stunned, yet viable, myocardium that defines the area at risk. T2w cardiac magnetic resonance (CMR) imaging has previously been used to image the edema characterizing the area-at-risk region in post myocardial infarcted (MI) canine, porcine and human hearts. Similar techniques would be valuable in basic research studies of MI in mice, where they might be used jointly with gadolinium delayed enhancement (DE) imaging to non-invasively define infarct size as "% area-at-risk" in transgenic/knock-out mice. However, the rapid murine heart rate presents challenges to T2w CMR application in mice. The typical T2w echo time of 40–60 ms needed for the detection of edema occupies a significant portion of the murine cardiac cycle (100–120 ms) with significant periods of blood flow and cardiac motion.
Develop an effective T2w CMR sequence for mice that exhibits high immunity to flow and tissue motion artifacts while maintaining sufficient and consistent signal-to-noise (SNR) and contrast-to-noise (CNR) performance.
We developed two T2w sequences for murine CMR: a flow and motion desensitized spin-echo (SE) sequence and a T2 preparation (T2prep) sequence. The SE sequence employed a slice-selective excitation RF pulse and a thicker slice-selective refocusing RF pulse, and applied readout and phase encoding gradients after the refocusing pulse. The T2prep sequence employed non-selective MLEV-weighted composite RF pulses followed by a standard slice-selective gradient-echo readout. Each sequence was applied on an isoflurane-anesthetized mouse on Days 1 through 4 after reperfused MI induced by 60 min coronary occlusion, as described previously. Parameters for both sequences included TR = 1500 ms, TE = 40–60 ms, FOV = 25 × 25 mm, slice thickness = 1 mm, matrix = 128 × 128 and BW = 520 Hz/pixel. In addition, gadolinium-DTPA DE CMR was performed each day to define infarct location. All scans of each sequence were performed consecutively at four identical contiguous slice positions from mid-ventricular toward the apex. All scans were performed on a 7 T Bruker/Siemens ClinScan.
As shown (panel G), the T2prep yielded a consistently higher edema area percentage of 48.2 ± 2.5 compared to the infarct area percentage of 41.6 ± 1.8, which correlates well with previous canine and human studies. Meanwhile, the SE gave a slightly lower mean with higher variance edema area percentage of 47.0 ± 4.2 that was attributed to flow and motion artifacts. To our knowledge, this is the first study to demonstrate the feasibility of performing T2w CMR edema imaging in mice, which opens a variety of potential basic research applications investigating the role of individual genes in acute and chronic settings post-MI.
This article is published under license to BioMed Central Ltd.