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. 2014 Dec 20;16(1):104.
doi: 10.1186/s12968-014-0104-y.

Endogenous assessment of chronic myocardial infarction with T(1ρ)-mapping in patients

Affiliations

Endogenous assessment of chronic myocardial infarction with T(1ρ)-mapping in patients

Joep W M van Oorschot et al. J Cardiovasc Magn Reson. .

Abstract

Background: Detection of cardiac fibrosis based on endogenous magnetic resonance (MR) characteristics of the myocardium would yield a measurement that can provide quantitative information, is independent of contrast agent concentration, renal function and timing. In ex vivo myocardial infarction (MI) tissue, it has been shown that a significantly higher T(1ρ) is found in the MI region, and studies in animal models of chronic MI showed the first in vivo evidence for the ability to detect myocardial fibrosis with native T(1ρ)-mapping. In this study we aimed to translate and validate T(1ρ)-mapping for endogenous detection of chronic MI in patients.

Methods: We first performed a study in a porcine animal model of chronic MI to validate the implementation of T(1ρ)-mapping on a clinical cardiovascular MR scanner and studied the correlation with histology. Subsequently a clinical protocol was developed, to assess the feasibility of scar tissue detection with native T(1ρ)-mapping in patients (n = 21) with chronic MI, and correlated with gold standard late gadolinium enhancement (LGE) CMR. Four T1ρ-weighted images were acquired using a spin-lock preparation pulse with varying duration (0, 13, 27, 45 ms) and an amplitude of 750 Hz, and a T(1ρ)-map was calculated. The resulting T(1ρ)-maps and LGE images were scored qualitatively for the presence and extent of myocardial scarring using the 17-segment AHA model.

Results: In the animal model (n = 9) a significantly higher T(1ρ) relaxation time was found in the infarct region (61 ± 11 ms), compared to healthy remote myocardium (36 ± 4 ms) . In patients a higher T(1ρ) relaxation time (79 ± 11 ms) was found in the infarct region than in remote myocardium (54 ± 6 ms). Overlap in the scoring of scar tissue on LGE images and T(1ρ)-maps was 74%.

Conclusion: We have shown the feasibility of native T(1ρ)-mapping for detection of infarct area in patients with a chronic myocardial infarction. In the near future, improvements on the T(1ρ)-mapping sequence could provide a higher sensitivity and specificity. This endogenous method could be an alternative for LGE imaging, and provide additional quantitative information on myocardial tissue characteristics.

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Figures

Figure 1
Figure 1
Spin lock pulse sequence used to obtain T weighted images. The pulse sequence consists of 2 continuous RF pulses with opposite phase to compensate for B1 variations, and a refocusing pulse between the spin-locking halves to compensate for B0 errors, followed by the readout.
Figure 2
Figure 2
In vivo T relaxation time versus ex vivo histology. A: T relaxation time measured in vivo in a porcine animal model is significantly higher in infarct area (57 ± 11 ms) compared to healthy myocardium (37 ± 4 ms) (p < 0.001) B: The amount of fibrosis in the infarct area (44.9 ± 13.2%) was also significantly higher compared to the remote myocardium (6.6 ± 7.1%) (p < 0.0001).
Figure 3
Figure 3
Short axis in vivo T -maps of two different animals with corresponding LGE images and ex vivo TTC staining in a porcine animal model 8 weeks after MI. In the top T-map artefacts can be observed in the left ventricular free wall, which are likely caused by the effect of B0 and B1 inhomogeneities on the spin-lock pulse.
Figure 4
Figure 4
T dispersion measured in ex vivo porcine hearts (n = 5) 8 weeks after MI. Errorbars indicate standard deviation.
Figure 5
Figure 5
T relaxation time measured in patients with chronic MI is significantly higher in the infarct area (79 ± 11 ms) compared to healthy myocardium (54 ± 6 ms) (p < 0.0005), and compared to myocardium in healthy young volunteers (50 ± 3 ms) (p < 0.0005).
Figure 6
Figure 6
Short axis T -maps with corresponding LGE images in 3 different patients. Arrows indicate the infarcted area.

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