Journal of Cardiovascular Magnetic Resonance最新文献

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.

Background: Sodium-glucose cotransporter 2 (SGLT2) inhibitors improve metabolic and cardiovascular outcomes, but the mechanisms remain incompletely understood. We utilized cardiovascular magnetic resonance (CMR) and complementary methods to investigate whether preventive SGLT2 inhibitor administration attenuates the development of metabolic heart disease in a high-fat, high-sucrose diet (HFHSD) mouse model.

Methods: Male wild-type (WT) C57BL/6 J mice were fed an HFHSD for 18 weeks to induce obesity, coronary microvascular disease, and diastolic dysfunction. WT mice treated preventively with an SGLT2 inhibitor, empagliflozin (EMPA), were compared to untreated WT mice, and mice fed either an HFHSD or standard chow diet with myeloid cell-specific knockout of the Nos2 gene (Nos2^LysMCre) were compared to floxed controls (Nos2^fl/fl). CMR assessed epicardial adipose tissue (EAT) volume, fatty acid composition (FAC), proton density fat fraction (PDFF), and T1, and myocardial perfusion, and strain. EAT FAC, PDFF, and T1 were quantified using an inversion-recovery multi-echo gradient-echo sequence and a multi-resonance triglyceride model. EAT volume was quantified using cine images. Myocardial perfusion reserve (MPR) and strain were measured using arterial spin labeling, and displacement encoding with stimulated echoes (DENSE), respectively. Histology and flow cytometry assessed EAT remodeling and macrophage polarization.

Results: EMPA treatment reduced EAT volume (0.36±0.18 µL/g vs 0.61±0.25 µL/g, p<0.01) and saturated fatty acid fraction (38.81 [32.83-47.71]% vs 48.06 [43.82-52.65]%, p<0.05), increased EAT T1 (0.799 [0.764-0.859] s vs 0.755 [0.678-0.772] s, p<0.05), and decreased EAT NOS2⁺ macrophages (34.74 [21.38-42.098^]% vs 46.36 [38.08-61.30]%, p<0.05) compared to controls. EMPA improved diastolic strain rate (2.96 [2.61-3.99] s^-1 vs 1.68 [1.21-2.80] s^-1, p<0.01) and adenosine MPR (2.00±0.54 vs 1.37±0.40, p<0.01) compared to controls. Myeloid cell NOS2 knockout mice fed an HFHSD exhibited improved adenosine MPR (1.90±0.47 vs 1.39±0.38, p<0.01) compared to floxed controls.

Conclusions: In this obesity-related metabolic heart disease model, EMPA treatment prevents cardiometabolic dysfunction by improving EAT quantity and quality, coronary microvascular function, and diastolic function. These benefits are mediated in part through macrophage NOS2.

Background: Heart failure (HF) is a leading cause of morbidity and mortality in the United States and is projected to increase in the next decade. Left ventricular ejection fraction (LVEF) is used to guide optimal medical therapy and is typically quantified using two-dimensional transthoracic echocardiography (TTE) due to ease of accessibility and cost. However, LVEF measurements by cardiovascular magnetic resonance (CMR) are considered the gold standard due to their accuracy and precision. Despite this, CMR is not the first imaging modality selected for LVEF evaluation due to perceptions of long study time, high cost, and inaccessibility. Our study aims to determine the cost of imaging studies (e.g., CMR, TTE) relative to the overall HF-related health care costs and associated outcomes.

Methods: A retrospective single-center cohort study of 420 participants with same-day TTE and CMR from 2009-2019, including participants >18 years of age with good image quality with or at risk for cardiovascular disease. Primary outcome was a composite outcome defined as HF admission, left ventricular assist device, cardiovascular disease-related death, heart transplantation, and implantable cardioverter defibrillator implantation. HF risk groups were determined based on clinically relevant LVEF cutoffs. All costs were calculated and adjusted to 2022 US$.

Results: Participants were 49 ± 17 years old, 52% (219/420) female, 50% (209/420) White, and 41% (174/420) Black. Median follow-up was 4 years. HF was the most common co-morbidity (31%). LVEF measured by CMR predicted HF outcomes better than TTE (p = 0.005). Continuous net reclassification index of CMR LVEF was 0.36 (95% confidence interval: 0.16-0.56); p = 0.001 due to predominant reclassification to lower risk groups. On an individual level, HF health care cost increased from low- to high-risk groups irrespective of modality. High-risk individuals classified by CMR had lower average per-person HF health care costs compared to TTE counterparts. Cost of CMR and TTE was <1% of the total HF health care cost.

Conclusion: The cost of non-invasive imaging studies accounted for <1% of the cost compared to other components of HF care. Downstream cost prediction based on LVEF classification using CMR has the potential to better predict cost burden compared to TTE in patients with HF.

Background: Cardiac functional metrics such as ejection fraction, strain, and valve excursion are important diagnostic and prognostic measures of cardiac disease. However, they ignore a large amount of systolic shape change information available from modern cardiovascular magnetic resonance (CMR) examinations. We aimed to automatically quantify multidimensional shape and motion scores from CMR, investigate covariates, and test their discrimination of disease in the UK Biobank compared against standard functional metrics.

Methods: An automated analysis pipeline was used to obtain quality-controlled three-dimensional left and right ventricular shape models in 38,858 UK Biobank participants, 5149 of whom had one or more diagnoses of cardiovascular or cardiometabolic disease. Principal component analysis was used to obtain a statistical shape atlas and quantify each participant's left and right ventricular shape at both end-diastole and end-systole simultaneously. Systolic strain was obtained from arc length changes computed from the shape model, and mitral/tricuspid annular plane systolic excursion (MAPSE/TAPSE) was computed from the displacement of the valves. Discrimination for prevalent disease was quantified using linear discriminant analysis area under the receiver operating characteristic curve.

Results: The first 25 principal component scores captured >90% of the total shape variance. Significantly stronger discrimination for atrial fibrillation, heart failure, diabetes, ischemic disease, and conduction disorders (p<0.001 for each) was obtained using shape scores compared with volumes, ejection fractions, strains, MAPSE, and TAPSE.

Conclusion: Automatically derived shape and motion z-scores capture more discriminative information on disease effects than standard metrics, including volumes, ejection fraction, strain and valve excursions.