Browsing by Author "Botnar, René M."

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    Advances in molecular imaging of atherosclerosis and myocardial infarction: shedding new light on in vivo cardiovascular biology
    (2012) Phinikaridou, Alkystis; Andía Kohnenkampf, Marcelo Edgardo; Shah, Ajay M.; Botnar, René M.
    Molecular imaging of the cardiovascular system heavily relies on the development of new imaging probes and technologies to facilitate visualization of biological processes underlying or preceding disease. Molecular imaging is a highly active research discipline that has seen tremendous growth over the past decade. It has broadened our understanding of oncologic, neurologic, and cardiovascular diseases by providing new insights into the in vivo biology of disease progression and therapeutic interventions. As it allows for the longitudinal evaluation of biological processes, it is ideally suited for monitoring treatment response. In this review, we will concentrate on the major accomplishments and advances in the field of molecular imaging of atherosclerosis and myocardial infarction with a special focus on magnetic resonance imaging.
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    Cardiac Magnetic Resonance Fingerprinting for Simultaneous T1, T2, and Fat-Fraction Quantification at 0.55 T
    (2025) Pedraza, Diego; Castillo-Passi, Carlos; Kunze, Karl; Botnar, René M.; Prieto, Claudia
    Cardiac magnetic resonance fingerprinting (cMRF) has been shown to allow for simultaneous quantitative characterization of myocardial tissue in a single scan. While cMRF has been assessed at 1.5 T and 3 T, its application at 0.55 T has not been demonstrated yet. This study introduces an adapted version of a previously implemented Dixon cMRF sequence designed for simultaneous quantification of T1, T2, and fat fraction (FF) at 1.5 T, to be employed at 0.55 T within a single breath-hold scan. The sequence was developed using the Pulseq environment and employs a radial tiny golden angle acquisition with bipolar readout. Reconstruction was performed using low-rank inversion in combination with a high-dimensional patch-based regularization. The Dixon cMRF technique at 0.55 T was tested on standardized phantoms and 15 healthy volunteers (HVs). cMRF at 0.55 T was compared to spin-echo (SE) and proton density references from phantoms, as well as conventional T1, T2, and FF mapping sequences at 0.55 T. Intrasession and intersession variability was assessed in phantoms and a representative HV. Results showed a good correlation between the proposed cMRF T1, T2, and FF at 0.55 T and the phantom IR-SE references (R 2  ≥ 0.98 for T1 and T2, R 2  ≥ 0.97 for FF). Intrasession variability was low (8.9 ± 13.8 ms for T1, 0.1 ± 1 ms for T2, and 0.02 ± 0.03% for FF), as was intersession variability (8.2 ± 8.5 ms, 0.4 ± 1.1 ms, and 0.02 ± 0.25%, respectively). In vivo assessments yielded good map quality, with mean myocardial values of 714 ± 24 ms for T1, 49 ± 5.9 ms for T2, and 2.6 ± 0.9% for FF in comparison to 672 ± 40 for T1-MOLLI, 60 ± 5.4 for T2prep-bSSFP, and 4.7 ± 2.4% for 2-echo PDFF, respectively. The technique demonstrated good agreement for T1 and FF, but T2 was underestimated, which is consistent with findings at higher field strengths. Further investigation in a larger cohort of healthy subjects and in patients with cardiovascular disease is warranted.
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    Free‐breathing 3D whole‐heart joint T1/T2 mapping and water/fat imaging at 0.55 T
    (2024) Si, Dongyue; Crabb, Michael G.; Kunze, Karl P.; Littlewood, Simon J.; Prieto Vasquez, Claudia Del Carmen; Botnar, René M.
    To develop and validate a highly efficient motion compensated free-breathingisotropic resolution 3D whole-heart joint T 1 /T2 mapping sequence with anatomicalwater/fat imaging at 0.55 T.Methods: The proposed sequence takes advantage of shorter T1 at 0.55 T to acquirethree interleaved water/fat volumes with inversion-recovery preparation, no prepara-tion, and T 2 preparation, respectively. Image navigators were used to facilitate nonrigidmotion-compensated image reconstruction. T1 and T2 maps were jointly calculated bya dictionary matching method. Validations were performed with simulation, phantom,and in vivo experiments on 10 healthy volunteers and 1 patient. The performance ofthe proposed sequence was compared with conventional 2D mapping sequences includ-ing modified Look-Locker inversion recovery and T2 -prepared balanced steady-SSFPsequence.Results: The proposed sequence has a good T1 and T2 encoding sensitivity in simula-tion, and excellent agreement with spin-echo reference T 1 and T2 values was observedin a standardized T1 /T2 phantom (R2 = 0.99). In vivo experiments provided good-qualityco-registered 3D whole-heart T1 and T2 maps with 2-mm isotropic resolution in ashort scan time of about 7 min. For healthy volunteers, left-ventricle T1 mean andSD measured by the proposed sequence were both comparable with those of modi-fied Look-Locker inversion recovery (640 ± 35 vs. 630 ± 25 ms [p = 0.44] and 49.9 ± 9.3vs. 54.4 ± 20.5 ms [p = 0.42]), whereas left-ventricle T2 mean and SD measured by theproposed sequence were both slightly lower than those of T2 -prepared balanced SSFP(53.8 ± 5.5 vs. 58.6 ± 3.3 ms [p < 0.01] and 5.2 ± 0.9 vs. 6.1 ± 0.8 ms [p = 0.03]). MyocardialT 1 and T2 in the patient measured by the proposed sequence were in good agreementwith conventional 2D sequences and late gadolinium enhancement.Conclusion: The proposed sequence simultaneously acquires 3D whole-heart T1 and T2mapping with anatomical water/fat imaging at 0.55 T in a fast and efficient 7-min scan.Further investigation in patients with cardiovascular disease is now warranted
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    Motion corrected 3D whole-heart SAVA T 1 mapping at 0.55 T.
    (2025) De la Sotta, Rafael I.; Crabb, Michael G.; Kunze, Karl P.; Botnar, René M.; Prieto, Claudia
    PURPOSE: To propose a novel highly efficient isotropic-resolution 3D whole-heart saturation-recovery and variable-flip-angle (SAVA) T 1 mapping sequence at 0.55 T, incorporating image navigator (iNAV)-based non-rigid motion correction and dictionary matching. METHODS: The proposed iNAV-based isotropic-resolution 3D whole-heart SAVA T 1 mapping sequence at 0.55 T acquires three gradient echo T 1-weighted volumes sequentially: an equilibrium contrast with 4° flip angle, and two saturation recovery T 1-weighted contrasts with 10° flip angles and different saturation delays. Sequence parameters were optimized for the lower field strength by simulations and phantom experiments. Two-dimensional iNAVs are acquired at each heartbeat to enable respiratory motion estimation and correction and 100% respiratory scan efficiency. The T 1 mapping is computed by dictionary matching, using subject-specific dictionaries based on Bloch equations simulations. Non-rigid motion correction is implemented based on respiratory bins reconstructed by iterative-SENSE and subsequent patch-based low-rank denoising, for each contrast separately. The proposed approach was evaluated in a standardized T 1 phantom and 10 healthy subjects, in comparison to spin-echo reference and 2D MOLLI, respectively. RESULTS: Excellent agreement is observed between iNAV-based SAVA T 1 mapping at 0.55 T and spin echo reference in phantom, with a R 2 = 0.998 $$ {R}^2=0.998 $$ for all phantom vials. Good image quality was obtained in vivo for the contrast images and corresponding T 1 maps in a scan time of 6:30 min ±40 s. Average and SD of myocardial T 1 values across subjects and segments was 706 ± 41 ms, which is comparable to acquired 2D MOLLI values of 681 ± 26 ms, and previously reported 2D MOLLI values of 701 ± 24 ms. Coefficient of variation values (12%) are higher than those previously reported for diaphragmatic navigator-based non-isotropic SAVA T 1 mapping at 3 T (7.4%). CONCLUSION: The proposed iNAV-based SAVA approach achieves free-breathing motion-corrected 3D whole-heart T 1 mapping at 0.55 T in approximately 7 min scan time for an isotropic resolution of 2 mm. In vivo experiments showed that the proposed sequence achieves good map quality, with comparable T 1 values and spatial variability compared to 2D MOLLI T 1 mapping. Further evaluation is warranted in patients with cardiovascular disease.