Single breath-hold co-registered T1-rho and T2 mapping for efficient myocardial dispersion index assessment

Presenting Author(s)

• 

  Kalvin Narceau, MSc

  Phd student
  Bordeaux University - INSERM U1045
  Pessac, Aquitaine, France

Primary Author(s)

• 

  Kalvin Narceau, MSc

  Phd student
  Bordeaux University - INSERM U1045
  Pessac, Aquitaine, France

Co-Author(s)

• 

  Thaïs Genisson, MSc

  PhD student
  IHU Liryc, Université de Bordeaux
  Bordeaux, Aquitaine, France
• 

  Victor de Villedon de Naide, MSc

  PhD student
  Bordeaux University - INSERM U1045
  Bordeaux, Aquitaine, France
• TR

  Théo Richard, MSc

  Engineer
  IHU LIRYC, Heart rhythm disease institute, Université de Bordeaux – INSERM U1045, Avenue du Haut Lévêque, 33604, Pessac, France
  Bordeaux, Aquitaine, France
• 

  Alexis Jacquier, MD, PhD

  Prof
  Aix Marseille Univ, CNRS, CRMBM, Marseille, France; APHM, Hôpital Universitaire Timone, Radiology Dept, Marseille, France
  Marseille, Provence-Alpes-Cote d'Azur, France
• AB

  Axel Bartoli, MD

  Medical doctor
  Aix-Marseille Université, France
• SS

  Salim Si-Mohamed, MD

  Medical Doctor
  Louis Pradel Hospital, Hospices Civils de Lyon; University of Lyon, France
• MS

  Matthias Stuber, PhD

  Professor/Director
  CIBM/CHUV/UNIL
  Lausanne, Switzerland
• HC

  Hubert Cochet, MD, PhD

  Professor
  Bordeaux University - INSERM U1045
  Bordeaux, Aquitaine, France
• 

  Aurelien Bustin, FSCMR

  Research Associate
  Department of Cardiovascular Imaging, Hôpital Cardiologique du Haut-Lévêque, CHU de Bordeaux, Avenue de Magellan, Pessac, France; IHU LIRYC, Electrophysiology and Heart Modeling Institute, Université de Bordeaux – INSERM U1045, Avenue du Haut Lévêque, Pessac, France; Department of Diagnostic and Interventional Radiology, Lausanne University Hospital and University of Lausanne, Lausanne, Switzerland
  Bordeaux, Aquitaine, France

Background: T1-rho (T1ρ) mapping has shown promise for detecting ischemic and non-ischemic cardiomyopathies without contrast agents (1). However, its precision can be compromised by the influence of T2 relaxation time (2). Myocardial T1ρ dispersion addresses this limitation by combining two sequences—a T1ρ and a T2 mapping sequence—which, when subtracted from each other, isolates the dispersion effect and yields the myocardial dispersion index (MDI) map (3). MDI acquisition thus requires two separate sequences, yielding image misalignment and complex image analysis, which hampers the use of MDI in practice. We sought i) to develop a novel MDI sequence that acquires co-registered T1ρ and T2 maps in a single acquisition, and ii) to evaluate its preliminary clinical feasibility in patients with structural heart disease.

Methods: The proposed MDI sequence interleaves single-shot T1ρ-prepared bSSFP images with a spin-lock frequency (FSL) of 500Hz (even heartbeats) and 0Hz (odd heartbeats), the latter corresponding to a T2-prepared acquisition. This scheme is repeated by varying the spin-lock times (TSL) [0,10,20,35,50] ms (Fig.1), with the first heartbeat shared between them (TSL=0ms). This allowed complete co-registered T1ρ and T2 mapping in only 9 heartbeats per slice (vs. 13 heartbeats for each conventional mapping). Pixel-wise two-parameter fitting yielded T1ρ and T2 maps, from which MDI maps were generated by subtraction.

Nine patients (1 CMR-negative, 2 diffuse myocarditis, 2 amyloidosis, 2 hypertrophic cardiomyopathy, 2 chronic myocardial infarction) underwent 1.5T CMR (Siemens Aera). Acquisitions included pre-contrast MDI, reference T1ρ maps (FSL 500Hz and 0Hz), conventional T2 maps, and post-contrast late gadolinium enhancement (LGE). Three short-axis slices were acquired per sequence (1.5x1.5x8 mm, multiple breath-holds). Regions of interest were drawn in remote and injured myocardium for quantitative analysis.

Results: Images were successfully collected in all 9 patients, yielding co-registered T1ρ, T2, and MDI maps (Fig.2). In all LGE-positive patients, the anatomical distribution of LGE corresponded to regions with elevated T1ρ values. Chronic infarction cases demonstrated marked T1ρ elevation in scar versus remote myocardium (P8: 64.9ms vs. 34.5ms; P9: 66.7ms vs. 44.1ms; Fig.3). MDI values in remote myocardium ranged from 1.0-2.8ms, whereas injured regions ranged from 4.3-8.5ms, except in one diffuse myocarditis case (P2) where values overlapped. Reference T1ρ and T2 values closely matched those from the proposed MDI method.

Conclusion: We present a novel contrast-agent-free MDI technique that enables rapid, co-registered T1ρ and T2 acquisition in a single sequence, overcoming major limitations of conventional MDI. This approach shows promise for detecting focal and diffuse myocardial injury in various cardiomyopathies. Larger studies are warranted to assess its clinical utility in acute and chronic myocardial disease.

Figure 1: Proposed 9-heartbeat T1rho dispersion sequence for myocardial dispersion index (MDI) mapping. The sequence alternates between a T1rho-prepared module with a spin-lock frequency (FSL) of 500Hz and a module with FSL = 0Hz, corresponding to T2 preparation. The T1rho module shape is preserved, with only the FSL varied between modules. Images were acquired with a 2D bSSFP readout.
Figure 2: Visual comparison of LGE, T1rho (500Hz), T1rho (0Hz), and MDI maps in 9 patients. For each patient, three short-axis slices (1.5x1.5x8 mm) were acquired. The MDI maps derived from the proposed sequence show clear regional elevations corresponding to LGE-positive regions, despite visible noise influence in some cases.
Figure 3: ROI-based comparison of remote and injured myocardium across mapping techniques. T2 maps (when available), T1rho (500Hz and 0Hz) maps, MDI maps from the proposed sequence, and reference T1rho maps were analyzed. With the exception of P2 (diffuse myocarditis, unusually high remote values) and diffuse amyloidosis cases (no true remote myocardium), remote myocardium values clustered around 1.0-2.8 ms, while injured myocardium ranged from 4.3-8.5 ms.