Journal of Cardiovascular Magnetic Resonance最新文献

Background: Quantitative perfusion cardiovascular magnetic resonance (QP-CMR) allows the generation of pixel-wise myocardial blood flow (MBF) maps using model-based deconvolution with several models including Tofts, modified-Tofts, and Fermi function models. However, the accuracy of pixel-wise MBF mapping has not been fully investigated in humans. The aim of this study was to evaluate the accuracy of advanced QP-CMR using ¹⁵O-water positron emission tomography (PET) as a reference.

Methods: Thirty-nine patients (29 men, 68±11years) with known or suspected coronary artery disease underwent both CMR including stress and rest QP-CMR and ¹⁵O-water PET at a median interval of 13 days. QP-CMR was performed using dual-sequence technique and a single bolus of gadolinium contrast agent during adenosine triphosphate stress and at rest. MBF maps were generated using three different model-based deconvolution techniques as follows: Tofts, modified-Tofts, and Fermi function models. Agreement of MBF and myocardial perfusion reserve (MPR) between QP-CMR and ¹⁵O-water PET was evaluated using Pearson's correlation, Bland-Altman analysis, and intraclass correlation (ICC). The ability of CMR-derived stress MBF and MPR to detect PET-defined abnormal myocardial perfusion (stress MBF ≤2.3 mL/min/g and MPR ≤2.5) was evaluated by receiver operating characteristic (ROC) analysis.

Results: CMR-derived MBF showed a good linear correlation with ¹⁵O-water PET-derived MBF in each of the Tofts, modified-Tofts, and Fermi function models (r = 0.776, 0.752, 0.784, respectively; p<0.001 each) at the patient level. Bland-Altman analysis demonstrated measurement biases for MBF between CMR and ¹⁵O-water PET of 0.31±0.70, 0.05±0.63, and 0.26±0.68 mL/min/g for the Tofts, modified-Tofts, and Fermi function models, respectively. ICCs were 0.734, 0.747, and 0.750, respectively. The area under the ROC curves for stress MBF derived from the Tofts and Fermi function models (0.921 and 0.914, respectively) was significantly higher than that derived from the modified-Tofts model (0.861; p = 0.003 for both). However, there was no significant difference between the Tofts and Fermi function models (p = 0.618).

Conclusion: Advanced QP-CMR using three different model-based deconvolution techniques demonstrated strong agreement with ¹⁵O-water PET. Of these techniques, the Fermi function and Tofts models were more effective in detecting abnormal myocardial perfusion as determined by ¹⁵O-water PET. Considering our results, the model complexity, and its technical availability, the Fermi function model may possess a practical advantage.

Background: Commercial 0.55T low-field magnetic resonance imaging (MRI) systems have recently become available, offering the potential to enhance global accessibility to MRI. T1ρ mapping is an emerging quantitative cardiac MR imaging technique capable of detecting myocardial disease without the need for contrast administration. However, experience with cardiac T1ρ mapping at low-field strength remains limited. This study aims to develop and validate an efficient, free-breathing three-dimensional (3D) high-resolution adiabatic T1ρ mapping sequence for non-contrast whole-heart tissue characterization at 0.55T.

Methods: The proposed 3D T1ρ mapping research sequence acquires four interleaved volumes with different contrast weightings using saturation and adiabatic spin-lock preparation pulses, and a 3-parameter fitting method is used to calculate T1ρ maps. Two-dimensional (2D) image navigators are acquired for non-rigid motion-compensated image reconstruction, enabling 100% respiratory scan efficiency. Phantom and in-vivo experiments in 10 healthy volunteers were conducted to evaluate the accuracy and precision of the proposed 3D sequence in comparison with 2D T1ρ mapping sequences.

Results: Phantom T1ρ values measured using the proposed 3D sequence showed strong agreement with the 2D reference (R² = 0.997), demonstrating high accuracy and reduced sensitivity to heart rate variations. In-vivo experiments in healthy subjects demonstrated that the proposed sequence is feasible for acquiring whole-heart T1ρ maps with 2 mm isotropic resolution in an efficient scan time of 6.6±0.5 min. The mean myocardial T1ρ value obtained with the 3D sequence was slightly higher than that of a conventional 2D breath-hold sequence (112.8±16.7 vs. 106.1±15.1%, p<0.01), while coefficient of variation (CV) was slightly lower (10.2±5.2 vs. 11.4±4.4%, p = 0.02).

Conclusion: The proposed sequence enables 3D free-breathing high-resolution adiabatic T1ρ mapping and shows promising potential for non-contrast whole-heart tissue characterization at 0.55T.

Purpose: Free-running five-dimensional (5D) whole-heart magnetic resonance imaging (MRI) simplifies image acquisition by eliminating the need for external gating, breath-holding, and prospective scan planning. However, it remains vulnerable to patient movement in pediatric populations, which may require sedation or general anesthesia. We present a retrospective motion correction approach using the automatic respiratory and bulk patient motion correction (ACROBATIC) framework to detect, estimate, and correct for bulk motion, thereby improving image quality in pediatric cardiac MRI.

Methods: Free-running Ferumoxytol-enhanced three-dimensional (3D) radial gradient-echo (GRE) data from 210 pediatric patients were manually categorized by the amount of bulk motion within each acquisition, based on retrospective reconstructions. From this cohort, 25 cases with the highest and 25 with the lowest detected bulk motion were selected, forming the moving and reference cohorts, respectively, for subsequent analysis and evaluation of the proposed framework. Respiratory motion was estimated using focused navigation. Bulk motion events were automatically detected from the variation in repeated radial readouts. The data were divided into four-dimensional (4D) arrays with timepoints spanning single respiratory cycles and reconstructed into retrospective real-time images using compressed sensing. Bulk motion was corrected via 3D rigid registration and poorly aligned images were excluded using an outlier-rejection algorithm. Final reconstruction was performed using a previously established 5D cardiac and respiratory motion-resolved compressed sensing approach. ACROBATIC's performance was evaluated by a Dice coefficient (automatic detection), sharpness metrics at the blood-myocardium interface and within the pulmonary vessels, as well as qualitative grading by two expert reviewers.

Results: The ACROBATIC framework successfully differentiated between moving and non-moving patients relative to manual evaluation (Dice = 0.96). Image sharpness significantly improved after motion correction, for analyses of the blood-myocardium interfaces and pulmonary veins. Expert evaluations supported the quantitative findings with average grade improvements of 0.44 and 0.54, respectively for Reviewer 1 and Reviewer 2.

Conclusion: The ACROBATIC framework effectively reduces motion-related artifacts in pediatric cardiac MRI, particularly in patients with significant movement. This method supports the broader goal of achieving high-quality, dynamic whole-heart imaging in children without the need for sedation or general anesthesia.

Background: Cardiovascular magnetic resonance is promising for non-invasive assessment of various cardiac diseases with the ability to provide multi-contrast images, including late gadolinium enhancement (LGE) for myocardial tissue characterization and coronary magnetic resonance angiography (CMRA) for anatomical imaging. However, LGE and CMRA are usually acquired separately in clinical routine with unmatched spatial resolution and slice positions. In this proof of concept study, we aim to achieve a one-stop imaging of 3D gray-blood phase-sensitive inversion recovery (PSIR) LGE and 3D CMRA by proposing a free-breathing simultaneous Gray-Blood and Bright-blOOd phase SensiTive inversion recovery (GB-BOOST) sequence.

Methods: The proposed research sequence acquires two interleaved 3D volumes with inversion recovery and T2 preparation pulses to obtain gray-blood PSIR and CMRA, respectively. Two-dimensional image navigator (iNAV) is performed before the acquisition of each volume to detect respiratory motion, enabling free-breathing acquisition with 100% respiratory scan efficiency. The GB-BOOST framework is compatible with both Dixon gradient echo (GRE) and balanced steady-state free precession (bSSFP) sequences for the application at 3T and 1.5T. In-vivo validation experiments included in total 23 patients for GB-BOOST, which were performed on either a 3T or a 1.5T clinical scanner. The performance of the proposed sequence was compared with clinical 2D gray-blood PSIR and free-breathing 3D CMRA.

Results: GB-BOOST was successfully performed on all 23 patients and was able to efficiently acquire intrinsically co-registered 3D PSIR and CMRA images with 1.2 mm³ resolution in 9.4±1.3 min. Compared with 2D gray-blood PSIR, 3D PSIR GB-BOOST had comparable scar area detection performance without significant differences in image contrast of scar-to-blood (0.42±0.40 vs. 0.30±0.43, p = 0.38), scar-to-myocardium (1.09±0.27 vs. 1.02±0.32, p = 0.30), and blood-to-myocardium (0.67±0.19 vs. 0.72±0.23, p = 0.56). Compared with single-contrast 3D CMRA sequence, 3D T2prep GB-BOOST showed comparable image quality and quantitative vessel metrics of coronary arteries.

Conclusion: The proposed GB-BOOST sequence can achieve simultaneous co-registered 3D whole-heart gray-blood PSIR and CMRA in a single scan with image contrast and image quality comparable with separately acquired images.

Background: Wilson's disease (WD) causes intracellular copper accumulation due to a genetic defect in the copper-transporting protein ATP7B. Cardiac involvement has been reported even in young WD patients; however, pathophysiological mechanisms remain unclear. This study aimed to comprehensively assess the myocardium in WD patients without cardiac symptoms using multiparametric cardiovascular magnetic resonance imaging (CMR), including quantitative stress perfusion mapping and strain analysis.

Methods: WD patients and healthy volunteers underwent multiparametric 1.5T CMR, including cine, native T1, native T2, extracellular volume (ECV), adenosine stress perfusion mapping, and late gadolinium enhancement (LGE) imaging. Left and right ventricle (LV, RV) mass and volumes, global native T1, native T2, ECV, rest and stress perfusion, myocardial perfusion reserve (MPR), strain measures and liver native T1 were compared. LGE images were assessed visually. Disease type and duration, medications, and cardiovascular risk factors were recorded. Symptoms of myocardial ischemia were quantified with Seattle Angina Questionnaire-7.

Results: WD patients (n = 17, 34 [29-55] years, 8/17 (47%) female) and healthy volunteers (n = 17, 33 [29-52] years, 8/17 (47%) female, p = ns for both) were included. There were no differences in cardiovascular risk factors or medications. LV ejection fraction was lower in WD patients (57 [55-61] vs 62 [57-67] %, p = 0.02), and LV global circumferential strain was mildly worse (-18 [-19 to (-17)] vs -20 [-21 to (-18)] %, p = 0.005), otherwise there were no differences in LV or RV mass or function. WD patients had lower stress perfusion and MPR (2.95 [2.74-3.29] vs 3.81 [2.67-4.45] mL/min/g, and 3.3 [3.1-3.8] vs 5.0 [2.9-5.4]), while ECV was higher (29 [28-30] vs 26 [26-29] %), p<0.05 for all, but there were no other differences in multiparametric mapping results. ECV did not correlate with strain parameters. ECV was associated with WD and sex but not age (WD β = 2.58%, male sex β = -0.03%, model R² 0.41, p<0.05 for all). LGE was present in the RV insertion point in 12/17 (71%) of WD patients.

Conclusions: In this study, stable WD patients without apparent cardiac symptoms have early signs of diffuse fibrosis, coronary microvascular dysfunction, and worse systolic function. However, this study is limited by small sample size limiting further subgroup analysis, lack of both longitudinal clinical data and biopsies, not allowing for correlation of CMR findings to histopathology.

Background: Carotid atherosclerosis is a major contributor to the etiology of ischemic stroke. Although intraplaque hemorrhage (IPH) is known to increase stroke risk and plaque burden, its long-term effects on plaque dynamics remain unclear. This study aimed to evaluate the long-term impact of IPH on carotid plaque burden progression using deep learning-based segmentation on multi-contrast magnetic resonance vessel wall imaging (VWI).

Methods: 28 asymptomatic subjects with carotid atherosclerosis underwent an average of 4.7±0.6 VWI scans over 5.8±1.1 years. Deep learning pipelines were used to segment the carotid vessel walls and IPH. Bilateral plaque progression was analyzed using correlation coefficients and generalized estimating equations. Associations between IPH occurrence, IPH volume, and plaque burden (%WV) progression were evaluated using linear mixed-effect models.

Results: IPH was detected in 23/50 of the arteries at any time point. Of arteries without IPH at baseline, 11/39 developed new IPH that persisted, while 5/11 arteries with baseline IPH exhibited it throughout the study. Bilateral plaque growth was significantly correlated (r = 0.54, p<0.001), but this symmetry was weakened in cases with IPH (r = 0.1, p = 0.62). Moreover, IPH presence or development at any point was associated with a 2.3% absolute increase in %WV on average within the affected artery (p<0.001). The volume of IPH was also positively associated with increased %WV (p = 0.005).

Conclusion: Deep learning-based segmentation pipelines were utilized to identify IPH, quantify IPH volume, and measure their effects on carotid plaque burden during long-term follow-up. Findings demonstrated that IPH may persist for extended periods. While arteries without IPH demonstrated minimal progression under contemporary treatment, the presence of IPH and greater IPH volume significantly accelerated long-term plaque growth.

Background: Late gadolinium enhancement (LGE) imaging is considered the imaging reference standard for the diagnosis of myocardial infarction and scarring. The aim of this study is to evaluate a free-breathing high-resolution three-dimensional (3D) Dixon LGE imaging prototype with image navigation (iNAV) in chronic myocardial infarction on a 3T system.

Methods: Consecutive myocardial infarction patients were enrolled to undergo CMR examination between February 2024 and January 2025. LGE protocols included breath-hold two-dimensional (2D) phase-sensitive inversion recovery (PSIR) and free-breathing iNAV 3D Dixon acquisitions. Radiologist image quality scoring, contrast ratio (CR), quantitative LGE assessment, and scan time were obtained and reported. Paired t-tests, Wilcoxon signed-rank tests, and repeated-measures ANOVA were used for the comparison.

Results: A total of 32 participants (50 years ± 11; 31 male, 1 female) were included. 3D LGE reduced scan time by 2m9s (3D: 4m34s [3m50s, 5m17s], 2D: 6m43s [5m17s, 7m41s], P<0.001). Overall image quality showed no difference (3D: 4 [3, 4], 2D: 4 [3, 5], P = 0.474). 3D LGE showed a trend toward higher image quality scores (3D: 4 [3, 4], 2D: 3 [2, 4], P = 0.053) in patients with respiratory motion artifacts on 2D images. LGE-to-blood CR was significantly higher in the 3D LGE than the 2D LGE images (P<0.001). LGE mass (P = 0.11) and LGE extent (P = 0.02) showed no significant difference between the 3D and 2D LGE datasets.

Conclusion: Free-breathing iNAV 3D Dixon LGE is feasible at 3T, achieving comparable image quality and scar quantification to 2D PSIR within shorter scan times. It improves CR and enables simultaneous assessment of myocardial fibrosis and fat infiltration.

Background: Cardiovascular magnetic resonance (CMR) is the principal non-invasive imaging modality used to diagnose idiopathic/viral myocarditis. The revised Lake Louise criteria (LLC) stipulate that a diagnosis can be made in the presence of one T1-based and one T2-based criterion. While the LLC have been extensively validated in viral myocarditis, their utility for the diagnosis of myocarditis due to an active autoimmune rheumatic disease is unknown. This study sought to assess the performance of the revised LLC in patients with clinically suspected myocarditis due to active systemic autoimmune disease.

Methods: Patients with clinically active autoimmune rheumatic disease, symptoms of myocarditis, and elevated troponin levels were recruited and compared with controls with autoimmune rheumatic disease but no suspicion of autoimmune myocarditis. All patients underwent CMR at 1.5T including T1 and T2 mapping.

Results: Thirty-seven patients with suspected myocarditis due to an active autoimmune rheumatic disease were recruited with a median (interquartile [IQR]) troponin level of 121 ng/L (72-318 ng/L). Overall, 65% (24/37) of patients met either of the two revised LLC resulting in a sensitivity (95% confidence interval) of 65% (49-78%) and specificity of 76% (57-89%). Only 32% (12/37) of patients fulfilled both of the main LLC (i.e., non-ischemic myocardial injury/edema with elevated T1 values or presence of late gadolinium enhancement and myocardial edema detected by increased T2 values or positive T2-STIR), resulting in a sensitivity of 32% (20-49%) and specificity of 100% (87-100%). Among controls, 24% (6/25) of patients had elevated native T1 values, but all had normal T2.

Conclusion: In patients with suspected myocarditis due to autoimmune rheumatic disease, who are receiving immunosuppressive therapy, the LLC have a high specificity, but a lower sensitivity than in patients with viral myocarditis. Additional tests should therefore be used to improve disease detection in this population. Where the pre-test probability is high, in patients with suspected myocarditis due to autoimmune rheumatic disease who are undergoing immunosuppression, there may need to be greater reliance on one T1-based criterion rather than both LLC, with the recognition that there is an appreciable rate of raised T1 in controls without myocarditis.

Background: Alpha-protein kinase 3 (ALPK3) was recently identified as a candidate gene associated with hypertrophic cardiomyopathy (HCM). However, clinical data regarding carriers of ALPK3 variants are limited. Therefore, this study amied to evaluate the prevalence of heterozygous ALPK3 variants in adult patients with HCM and to elucidate the phenotypes of individuals harboring these variants.

Methods: 575 consecutive patients diagnosed with HCM who underwent 3T cardiovascular magnetic resonance (CMR) imaging and whole-exome sequencing genetic testing were recruited. Patients harboring ALPK3 rare missense variants (minor allele frequency < 0.0005) or truncating variants were considered genotype-positive.

Results: Among the 575 included patients (65.0% [374/575] male; median age: 50 [40-61] years), 37 (6.43%) showed heterozygous ALPK3 variants. In comparison with sarcomere variant carriers, ALPK3 heterozygotes showed a higher prevalence of apical hypertrophy (59.5% [22/37] vs 20.2% [66/326], P < 0.001) and a lower fibrosis burden, with a two-fold reduction in the incidence of extensive fibrosis (≥15% left ventricle [LV] mass: 8.1% [3/37] vs 14.7% [48/326], P < 0.001). Patients with single ALPK3 variants were more likely to present with apical HCM (ApHCM; 80.0% [16/20]vs 35.3% [6/17], P, 0.006) and show a lower extent of late gadolinium enhancement (LGE; 1.26 [0.00-5.77] % vs 6.00 [3.63-8.50] %, P, 0.011) than those with both ALPK3 and sarcomere variants. CMR characteristics showed no significant differences between carriers with truncating and missense ALPK3 variants. Moreover, among patients with ApHCM, those with single ALPK3 variants were more likely to present with mixed ApHCM (87.5% [14/16] vs 55.2% [16/29] vs 14.3% [1/7], P < 0.05), a lower extent of LGE (0.67 [0-5.77] % vs 6.32 [2.39-10.90] % vs 3.32 [0.00-4.68] %, P < 0.05), and greater free-wall and apex LGE involvement (85.7% [6/7] vs 41.6% [10/24] vs 50% [2/4]) than those with myosin-binding protein C or β-myosin heavy chain variants.

Conclusion: The clinical phenotype of individuals harboring heterozygous ALPK3 variants showed distinct characteristics, characterized by apical hypertrophy, especially mixed apical hypertrophy, and a lower extent of fibrosis.

Background and purpose: Epicardial adipose tissue (EAT) plays a crucial role in the progression of heart failure (HF). This study employs cardiovascular magnetic resonance (CMR) imaging to investigate potential differences in EAT between patients with heart failure with reduced ejection fraction (HFrEF) and those with heart failure with preserved ejection fraction (HFpEF), as well as the correlation between EAT and biventricular function (myocardial strain).

Methods: We collected data from patients diagnosed with HF at the Second Affiliated Hospital of Kunming Medical University between January 2021 and December 2023. All patients underwent CMR imaging and were categorized into two groups based on left ventricular ejection fraction (LVEF): the HFrEF group and the HFpEF group. Patients without heart failure served as the control group. We gathered clinical baseline data and utilized CVI-42 post-processing software to obtain parameters related to cardiac structure and function, including LVEF, global radial strain (GRS), global longitudinal strain (GLS), EAT, pericardial adipose tissue (PeAT), paracardial adipose tissue (PaAT), and wall stress. We compared differences in parameters among the three groups and conducted pairwise comparisons. Additionally, we performed correlation analyses of EAT and PeAT with GLS and body mass index (BMI) within the HFrEF and HFpEF cohorts.

Results: A total of 104 patients with HFrEF, 226 patients with HFpEF, and 172 patients without heart failure were ultimately included in the study. Significant statistical differences were observed among the three groups regarding age, smoking status, diabetes, brain natriuretic peptide (BNP) levels, BMI, EAT, PeAT, PaAT, wall stress, GLS, and GRS of both ventricles (p<0.05). The EAT volume in HFrEF patients (32±14 mL) was lower than that in HFpEF patients (51±21 mL) and the control group (33±19 mL). Additionally, PeAT and PaAT levels were higher in HFpEF patients compared to those in HFrEF and the control group. Correlation analysis revealed that in HFrEF patients, EAT accumulation was associated with better left ventricular (LV) function (LVGLS, r=0.85, p<0.01) and right ventricular (RV) function (RVGLS, r=0.73, p<0.01). Conversely, in HFpEF patients, EAT accumulation correlated with poorer LV (LVGLS, r=-0.67, p<0.01) and RV (RVGLS, r=0.55, p<0.01) function.

Conclusion: EAT was greater in patients with HFpEF compared to HFrEF. In the HFpEF group, increased EAT was correlated with worsening biventricular function, while the opposite trend was observed in the HFrEF group.