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Endogenous assessment of myocardial injuries using T1-rho mapping: comparison to T1 mapping, T2 mapping and late gadolinium enhancement imaging
Aurelien Bustin1,2,3, Xavier Pineau2, Soumaya Sridi2, Pierre Jaïs1,4, Matthias Stuber1,3,5, and Hubert Cochet1,2
1IHU LIRYC, Electrophysiology and Heart Modeling Institute, Université de Bordeaux – INSERM U1045, Bordeaux, France, 2Department of Cardiovascular Imaging, Hôpital Cardiologique du Haut-Lévêque, CHU de Bordeaux, Bordeaux, France, 3Department of Diagnostic and Interventional Radiology, Lausanne University Hospital and University of Lausanne, Lausanne, Switzerland, 4Department of Cardiac Electrophysiology, Hôpital Cardiologique du Haut-Lévêque, CHU de Bordeaux, Bordeaux, France, 5CIBM Center for Biomedical Imaging, Lausanne, Switzerland

Synopsis

Myocardial T1-rho (T1ρ) mapping is a promising technique which reveals new insights about the macromolecular content of biological tissues. The idea that T1ρ mapping can be used to quantify myocardial fibrosis without contrast agent opens the door to new clinical capabilities. Yet, the tissue determinants driving T1ρ changes are still unclear, and the applicability of the technique to the broad spectrum of myocardial injuries remains uncharted territory. In the present study, we aim to identify clinical correlates of myocardial T1ρ and to examine how myocardial T1ρ values change under various clinical scenarios.

INTRODUCTION

Magnetic resonance myocardial T1-rho (T1ρ) mapping has emerged as a promising tool for detecting myocardial injuries without exogenous contrast agents.1,2,3 Yet, the tissue determinants driving T1ρ changes remain unclear, and the applicability of the technique to the broad spectrum of acute and chronic myocardial injuries uncharted territory. The aims of this study were to identify clinical correlates of myocardial T1ρ, and to examine how myocardial T1ρ values change under various clinical scenarios.

METHODS

Image Acquisition: A total of 113 subjects were enrolled between October 2020 and December 2020. The population comprised 69 patients (51 males, age 54±16yo) with known ischemic (N=18) and non-ischemic (N=51) heart disease and 44 healthy controls (22 males, age 44±16yo). CMR was performed using a 1.5T Siemens MAGNETOM Aera scanner. Breath-held T1ρ mapping (pre-contrast, Fig.1), conventional T2 mapping (T2-prepared bSSFP, pre-contrast), T1 mapping (MOLLI, pre- and post-contrast), extracellular volume (ECV) quantification, and late gadolinium enhancement (LGE, 15min after injection of 0.2mmol/kg gadoteric acid) were performed in short-axis.2
Image Analysis: Injured areas were defined by an expert as regions with LGE, while remote areas were defined as regions with no LGE. The agreement between T1ρ map, T2 map, ECV and LGE was assessed at a segmental level on the left ventricle (LV). In healthy subjects, relations of T1ρ with age, native T1 and T2 were compared using Pearson’s r correlation coefficient. In patients, quantitative analysis was achieved by tracing regions of interest on T1ρ, T2, and ECV maps within remote and injured areas. Paired t-tests were used to compare T1ρ measurements. All statistical tests were 2-tailed, with p values <0.05 considered to indicate statistical significance.

RESULTS

In healthy controls, mean myocardial T1ρ was 47±2ms. Compared to males, females had higher T1ρ (48±2ms vs. 46±2ms, P<0.01), T2 (47±2ms vs. 45±3ms, P=0.03) and ECV (26±2% vs. 24±2%, P<0.01). T1ρ correlated positively with age (R=0.4, P=0.003) and T2 (R=0.6, P<0.001), and significantly increased from basal to apical LV levels (P<0.01). In patients with acute focal myocardial injuries (N=9 with focal T2 elevation), T1ρ significantly increased (69±7ms vs. 48±2ms in remote, P<0.01). In patients with focal fibrosis (N=27 with positive LGE and negative T2), T1ρ significant increased (64±5ms vs. 47±2ms in remote, P<0.01). In patients with diffuse myocardial involvement (N=8 with ECV>30%), T1ρ significantly increased (52±6ms vs. 47±2 in controls, P<0.01) with a moderate positive correlation with ECV (R=0.3, P<0.01). Examples of patients with ischemic and non-ischemic cardiomyopathies are shown in Figures 2 and 3.

CONCLUSION

Myocardial T1ρ values are gender and age dependent and are slightly higher in the apical segments. The technique appears to be equally sensitive to acute, chronic, focal, and diffuse myocardial injuries, and may thus be a contrast-free adjunct to LGE for gaining new and quantitative insight into acute and chronic myocardial structural disorders.

Acknowledgements

This research was supported by funding from the French National Research Agency under grant agreements ANR-21-CE17-0034-01, Equipex MUSIC ANR-11-EQPX-0030 and Programme d’Investissements d’Avenir ANR-10-IAHU04-LIRYC, and from the European Council under grant agreement ERC n715093. AB acknowledges a Lefoulon-Delalande Foundation fellowship administered by the Institute of France.

References

1. Witschey WE, et al. In vivo chronic myocardial infarction characterization by spin locked cardiovascular magnetic resonance. J. Cardiovasc. Magn. Reson. 14, 37 (2012). https://doi.org/10.1186/1532-429X-14-37.2.

2. Bustin A, et al. Endogenous assessment of myocardial injury with single-shot model-based non-rigid motion-corrected T1 rho mapping, J. Cardiovasc. Magn. Reson. 23, 119 (2021). https://doi.org/10.1186/s12968-021-00781-w.

3. Van Oorschot JWM, et al. Single breath-hold T1r -mapping of the heart for endogenous assessment of myocardial fibrosis. Invest. Radiol. 51(8):505-12 (2016). https//doi.org/10.1097/RLI.0000000000000261.

Figures

Figure 1. Schematic of the proposed 2D myocardial T1ρ mapping sequence (A) with joint T1ρ fitting and model-based non-rigid motion correction (B). T1ρ mapping is performed using a single-shot ECG-triggered balanced steady-state free precession acquisition where five images with different spin lock times (TSL) are acquired over 13 heartbeats within a single breath-hold.

Figure 2. 57-year-old female patient with CMR findings consistent with Takotsubo cardiomyopathy. T2-weighted images and T2 maps exhibit myocardial edema at the medial and apical short-axis levels (T2=67ms) with a clear T1ρ elevation at these locations (T1ρ=71ms) whereas LGE images show a lack of ischemia and delayed hyperenhancement.

Figure 3. Top: 21-year-old male (control) with normal T2 (45 ms), T1ρ (44 ms), native T1 (1006 ms), and normal LGE. Middle: 33-year-old male patient with ischemic cardiomyopathy reflected by basal anteroseptal hyperenhancements on LGE with T2 (67ms) and T1ρ (80ms) elevations. Bottom: 59-year-old male patient with non-ischemic dilated cardiomyopathy with subepicardial inferobasal hyperenhancement on LGE with a clear T1ρ elevation in the same segment (79ms) and normal T2 on T2 mapping (48ms).

Proc. Intl. Soc. Mag. Reson. Med. 30 (2022)
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DOI: https://doi.org/10.58530/2022/1108