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Background: Pulmonary hypertension (PH) results in right ventricular (RV) dysfunction, subsequently leading to left ventricular (LV) impairment. The mechanism underlying ventricular interdependence is largely uninvestigated., Purpose: To explore the biventricular dysfunction and the ventricular interdependence in PH patients., Study Type: Retrospective., Population: One hundred and seven PH patients (mean pulmonary artery pressure >20 mmHg) and 72 age- and sex-matched controls with cardiac magnetic resonance imaging (MRI) studies., Field Strength/sequence: 3.0 T/balanced steady-state free precession sequence., Assessment: LV and RV ejection fractions (EF) and RV and LV radial, circumferential, and longitudinal strains were assessed using commercial software. Strains were compared between controls, PH patients with preserved RVEF (RVEF ≥40%, N = 48), and PH patients with reduced RVEF (RVEF <40%, N = 59)., Statistical Tests: Chi-squared tests or Fisher's exact test, t tests or Mann-Whitney U test, one-way ANOVA with Bonferroni's post hoc correction or Kruskal-Wallis test, Pearson or Spearman correlation, and multivariable linear regression analysis. A two-tailed P < 0.05 was deemed statistically significant., Results: RV strain decreased sequentially from controls, through PH with preserved RVEF, to PH with reduced RVEF. PH patients with reduced RVEF had significantly lower LV strain, especially septal strain, and LV peak diastolic strain rate compared with both controls and PH patients with preserved RVEF. Multivariable analyses showed that RVEF was independently correlated with LV strain; furthermore, independent of RVEF, RV strain was significantly correlated with LV strain (LVGRS: β = 0.416; LVGCS: β = -0.371; LVGLS: β = 0.283)., Data Conclusion: Subclinical impairment of RV function was found in PH with preserved RVEF. LV strain was impaired when RV was dysfunctional, which was associated with worsening RV strain. Therefore, while focusing on improving RV function, LV dysfunction in PH patients should also be monitored and treated early in order to slow the progression of the disease., Level of Evidence: 3 TECHNICAL EFFICACY: Stage 3., (© 2023 The Authors. Journal of Magnetic Resonance Imaging published by Wiley Periodicals LLC on behalf of International Society for Magnetic Resonance in Medicine.)

Background: Functional mitral regurgitation (FMR) is one of the most common heart valve diseases in diabetes and may increase left ventricular (LV) preload and aggravate myocardial stiffness. This study aimed to investigate the aggravation of FMR on the deterioration of LV strain in type 2 diabetes mellitus (T2DM) patients and explore the independent indicators of LV peak strain (PS)., Materials and Methods: In total, 157 T2DM patients (59 patients with and 98 without FMR) and 52 age- and sex-matched healthy control volunteers were included and underwent cardiac magnetic resonance examination. T2DM with FMR patients were divided into T2DM patients with mild (n = 21), moderate (n = 19) and severe (n = 19) regurgitation. LV function and global strain parameters were compared among groups. Multivariate analysis was used to identify the independent indicators of LV PS., Results: The T2DM with FMR had lower LV strain parameters in radial, circumferential and longitudinal direction than both the normal and the T2DM without FMR (all P < 0.05). The mild had mainly decreased peak diastolic strain rate (PDSR) compared to the normal. The moderate had decreased peak systolic strain rate (PSSR) compared to the normal and PDSR compared to the mild and the normal. The severe FMR group had decreased PDSR and PSSR compared to the mild and the normal (all P < 0.05). Multiple linear regression showed that the regurgitation degree was independent associated with radial (β = - 0.272), circumferential (β = - 0.412) and longitudinal (β = - 0.347) PS; the months with diabetes was independently associated with radial (β = - 0.299) and longitudinal (β = - 0.347) PS in T2DM with FMR., Conclusion: FMR may aggravate the deterioration of LV stiffness in T2DM patients, resulting in decline of LV strain and function. The regurgitation degree and months with diabetes were independently correlated with LV global PS in T2DM with FMR., (© 2021. The Author(s).)

Background: Diabetic peripheral neuropathy (DPN) is the most prevalent complication of diabetes, and has been demonstrated to be independently associated with cardiovascular events and mortality. This aim of this study was to investigate the subclinical left ventricular (LV) myocardial dysfunction in type 2 diabetes mellitus (T2DM) patients with and without DPN. Methods: One hundred and thirty T2DM patients without DPN, 61 patients with DPN and 65 age and sex-matched controls who underwent cardiovascular magnetic resonance (CMR) imaging were included, all subjects had no symptoms of heart failure and LV ejection fraction ≥ 50%. LV myocardial non-infarct late gadolinium enhancement (LGE) was determined. LV global strains, including radial, circumferential and longitudinal peak strain (PS) and peak systolic and diastolic strain rates (PSSR and PDSR, respectively), were evaluated using CMR feature tracking and compared among the three groups. Multivariable linear regression analyses were performed to determine the independent factors of reduced LV global myocardial strains in T2DM patients. Results: The prevalence of non-infarct LGE was higher in patients with DPN than those without DPN (37.7% vs. 19.2%, p = 0.008). The LV radial and longitudinal PS (radial: 36.60 ± 7.24% vs. 33.57 ± 7.30% vs. 30.72 ± 8.68%; longitudinal: − 15.03 ± 2.52% vs. − 13.39 ± 2.48% vs. − 11.89 ± 3.02%), as well as longitudinal PDSR [0.89 (0.76, 1.05) 1/s vs. 0.80 (0.71, 0.93) 1/s vs. 0.77 (0.63, 0.87) 1/s] were decreased significantly from controls through T2DM patients without DPN to patients with DPN (all p < 0.001). LV radial and circumferential PDSR, as well as circumferential PS were reduced in both patient groups (all p < 0.05), but were not different between the two groups (all p > 0.05). Radial and longitudinal PSSR were decreased in patients with DPN (p = 0.006 and 0.003, respectively) but preserved in those without DPN (all p > 0.05). Multivariable linear regression analyses adjusting for confounders demonstrated that DPN was independently associated with LV radial and longitudinal PS (β = − 3.025 and 1.187, p = 0.014 and 0.003, respectively) and PDSR (β = 0.283 and − 0.086, p = 0.016 and 0.001, respectively), as well as radial PSSR (β = − 0.266, p = 0.007). Conclusions: There was more severe subclinical LV dysfunction in T2DM patients complicated with DPN than those without DPN, suggesting further prospective study with more active intervention in this cohort of patients. [ABSTRACT FROM AUTHOR]

Background: Stress hyperglycemia occurs frequently in patients following acute myocardial infarction (AMI) and may aggravate myocardial stiffness, but relevant evidence is still lacking. Accordingly, this study aimed to examine the impact of admission stress hyperglycemia on left ventricular (LV) myocardial deformation in patients following AMI. Methods: A total of 171 patients with first AMI (96 with normoglycemia and 75 with hyperglycemia) underwent cardiac magnetic resonance (CMR) examination were included. AMI patients were classified according to admission blood glucose level (aBGL): < 7.8 mmol/L (n = 96), 7.8–11.1 mmol/L (n = 41) and ≥ 11.1 mmol/L (n = 34). LV strains, including global radial/circumferential/longitudinal peak strain (PS)/peak systolic strain rate (PSSR)/peak diastolic strain rate (PDSR), were measured and compared between groups. Further, subgroup analyses were separately conducted for AMI patients with and without diabetes. Multivariate analysis was employed to assess the independent association between aBGL and LV global PS in AMI patients. Results: LV global PS, PSSR and PDSR were decreased in radial, circumferential and longitudinal directions in hyperglycemic AMI patients compared with normoglycemic AMI patients (all P < 0.05). These differences were more obvious in patients with diabetes than those without diabetes. AMI patients with aBGL between 7.8 and 11.1 mmol/L demonstrated significant decreased radial and longitudinal PS, radial PSSR, and radial and longitudinal PDSR than those with aBGL < 7.8 mmol/L (all P < 0.05). AMI patients with aBGL ≥ 11.1 mmol/L showed significantly decreased PS, PSSR and PDSR in all three directions than those with aBGL < 7.8 mmol/L, and decreased longitudinal PSSR than those with aBGL between 7.8 and 11.1 (all P < 0.05). Further, aBGL was significantly and independently associated with radial (β = − 0.166, P = 0.003) and longitudinal (β = 0.143, P = 0.008) PS. Conclusions: Hyperglycemia may exacerbate LV myocardial stiffness in patients experienced first AMI, leading to reduction in LV strains. aBGL was an independent indicator of impaired LV global PS in AMI patients. Blood glucose monitoring is more valuable for AMI patients with diabetes. [ABSTRACT FROM AUTHOR]

Background: Due to the heterogeneity of anatomic anomalies in Ebstein's anomaly (EA), particularly in the subset of patients with atrial septal defect (ASD), hemodynamic changes, which ultimately cause left ventricular (LV) deterioration remain unclear. The current study aimed to investigate the effect of concomitant ASD on LV function using cardiovascular magnetic resonance (CMR) imaging in patients with EA. Methods: This study included 31 EA patients with ASD, 76 EA patients without ASD, 35 patients with simple ASD and 40 healthy controls. Left/right ventricular (RV, the RV was defined as a summation of the functional RV and atrialized RV in EA patients) volumes and functional parameters, LV strain parameters, and echocardiogram indices were compared among the four groups. Associations between variables were evaluated via Spearman or Pearson correlation analyses. The association between risk factors and LV ejection fraction (EF) was determined via multivariate linear regression analysis. Results: Both EA patients and ASD patients had a higher RV/LV end-diastolic volume (RVEDV/LVEDV) as well as lower LV and RV ejection fractions (LVEF/RVEF) compared to healthy controls (all p < 0.05). Moreover, the EA patients with ASD had a significantly higher RVEDV/LVEDV and a lower LVEF and RVEF than those without ASD (all p < 0.05). Multivariate linear regression analysis revealed that the presence of ASD was independently associated with LVEF (β = − 0.337, p < 0.001). The RVEDV/LVEDV index was associated with LVEF (r = − 0.361, p < 0.001). Furthermore, the LV longitudinal peak diastolic strain rate (PDSR) was lower in EA patients with ASD than those without ASD, patients with simple ASD, and healthy controls (p < 0.05). Conclusion: Concomitant ASD is an important risk factor of LV dysfunction in patients with EA, and diastolic dysfunction is likely the predominate mechanism related to LV dysfunction. [ABSTRACT FROM AUTHOR]

Background: Mitral regurgitation may occur when hypertension causes left ventricular (LV) and left atrial (LA) remodeling. However, its role in LA function in hypertensive patients remains unclear. Purpose: To explore how mitral regurgitation affects LA function in hypertension and to investigate atrioventricular interaction in hypertensive patients with mitral regurgitation. Study Type: Retrospective. Population: A total of 193 hypertensive cases and 64 controls. Field Strength/Sequence: A 3.0 T/balanced steady‐state free precession. Assessment: LA volume (LAV), LA strain (reservoir, conduit, and active), LA ejection fraction, and LV strain (global peak longitudinal [GLS], circumferential [GCS], and radial strain [GRS]) were evaluated and compared among groups. Regurgitant fraction (RF) was evaluated in regurgitation patients and used to subdivide patients into mild (RF: 0%–30%), moderate (RF: 30%–50%), and severe (RF: >50%) regurgitation categories. Statistical Tests: One‐way analysis of variance, Spearman and Pearson's correlation coefficients (r), and multivariable linear regression analysis. A P value <0.05 was considered statistically significant. Results: Hypertensive patients without mitral regurgitation showed significantly impaired LA reservoir and conduit functions and significantly decreased LV GLS but preserved pump function and LAV compared to controls (P = 0.193–1.0). Hypertensive cases with mild regurgitation (N = 22) had significantly enlarged LAV and further reduced LA reservoir function, while the group with moderate regurgitation (N = 20) showed significantly reduced LA pump function, further impaired conduit function, and significantly reduced LV strain. The severe regurgitation (N = 13) group demonstrated significantly more severely impaired LA and LV functions and LAV enlargement. Multivariable linear regression showed that regurgitation degree, GRS, GCS, and GLS were independently correlated with the LA reservoir, conduit, and active strain in hypertensive patients with mitral regurgitation. Data Conclusion: Mitral regurgitation may exacerbate LA and LV impairment in hypertension. Regurgitation degree, LV GRS, GCS, and GLS were independent determinants of the LA strain in hypertensive patients with mitral regurgitation, which demonstrated atrioventricular interaction. Evidence Level: 4. Technical Efficacy: Stage 3. [ABSTRACT FROM AUTHOR]

Background: Metabolic and hemodynamic alterations in metabolic syndrome (MetS) can cause a reduced myocardial energetic efficiency (MEE). Indexed MEE (MEEi), as a simple estimate of MEE, is emerging as a novel and useful imaging parameter. Purpose: To investigate the impact of MetS on MEE and systolic myocardial strain and to assess any sex difference. Study type: Retrospective. Population: A total of 161 patients with MetS (female: n = 82, 52.2 ± 11.7 years; male: n = 79, 51.8 ± 10.6 years) and 77 healthy subjects (female: n = 46, 52.7 ± 8.2 years; male: n = 31, 54.1 ± 11.2 years). Patients with left ventricular (LV) ejection fraction <50% were excluded. Field Strength/Sequence: A 3.0 T; balanced steady‐state free precession sequence. Assessment: LV volumes and mass (LVM) and global longitudinal strain (GLS) were obtained by MRI. Stroke volume (SV) divided by HR was used as a surrogate measure of MEE and normalized to LVM (MEEi). Statistical Tests: Student's t‐test or Mann–Whitney U‐test; Multivariable linear regression (coefficient of determination, R2). P < 0.05 was considered statistically significant. Results: For both males and females, MEEi and GLS were lower in MetS patients than in the normal controls. Among MetS patients, men had significantly higher LVM (59.7 ± 13.4 g/m2 vs. 48.8 ± 11.3 g/m2) and significantly lower MEEi (0.68 ± 0.23 mL/g/s vs. 0.84 ± 0.23 mL/g/s) and GLS (−11.7% ± 2.8% vs. −13.9% ± 2.7%) than women. After adjustment for clinical variables, male gender (β = −0.291) was found to be inversely correlated with MEEi. Multivariable analysis showed that MEEi (β = 0.454) were independently associated with GLS (adjusted R2 = 0.454) after adjustment for clinical and other MRI parameters. Data Conclusion: MEEi was significantly impaired in MetS without overt systolic dysfunction. There was a sex difference regarding the cardiac alterations in MetS, with men having significantly lower MEEi and GLS and significantly higher LVM than women. Further, MEEi was independently associated with GLS. Evidence Level: 3 Technical Efficacy: Stage 3 [ABSTRACT FROM AUTHOR]

Background: The relationship of left atrial (LA) strain to high‐risk heart failure (HF) events in patients with left ventricular myocardial noncompaction (LVNC) remains to be thoroughly investigated. Purpose: To evaluate the LA performance in patients with LVNC, and to investigate the prognostic value of LA phasic strain on high‐risk HF events, and its influencing factors. Study Type: Retrospective. Population: A total of 95 LVNC patients (74 with LA enlargement [LAE] and 21 without LAE) and 50 healthy controls. Field Strength/sequence: A 3.0 T, balanced steady‐state free‐precession cine imaging. Assessment: LA longitudinal strains were measured by cardiac MRI feature tracking technique. LA volume index (LAVI) and LA ejection fraction (LAEF) were calculated. Their intraobserver and interobserver reproducibility were evaluated. The primary outcome was high‐risk HF events, a composite of first HF hospitalization, hospitalization for worsening HF and death from HF. Statistical Tests: Student's t/Mann–Whitney U, one‐way analysis of variance/Kruskal–Wallis, Chi‐squared, receiver operating characteristic, Kaplan–Meier, log‐rank, Cox regression, Pearson and Spearman correlation and linear regression analyses were performed. The significance threshold was set at P < 0.05. Results: LAEF and LA longitudinal strains decreased in LVNC patients irrespective of the presence of LAE. During a median follow‐up of 32.17 months, high‐risk HF occurred in 13 (13.68%) patients. Patients with increased LAVI, decreased LAEF and decreased LA longitudinal strain had significantly higher risks of high‐risk HF events. In patients with LVNC, LA reservoir strain (εs) was independently associated with high‐risk HF (hazard ratio = 23.208 [95% CI: 2.993–179.967]). LV global longitudinal strain (LV GLS) (β = −1.783 [95% CI: −2.493 to −1.073]) was significantly and independently associated with εs. Intraobserver and interobserver reproducibility was excellent for LAVI, LAEF, and LA strain. Conclusion: In patients with LVNC, εs was an independent predictor for high‐risk HF events. LV GLS was an independent determinant of εs in LVNC. Evidence Level: 4 Technical Efficacy: Stage 4 [ABSTRACT FROM AUTHOR]

Background: Previous researches on large animal models of diabetic cardiomyopathy were insufficient. The aim of this study was to evaluate early changes in left ventricular (LV) function and morphology in diabetic pigs using a cardiac magnetic resonance (CMR) time-volume curve and feature tracking technique. Methods: Streptozotocin (STZ) was used to induce diabetic in sixteen pigs. 3.0T MRI scanned the pig's heart before and 2, 6, 10 and 16 months after modelling. CMR biomarkers, including time-volume curve and myocardial strain, were compared to analyse the longitudinal changes in LV function and morphology. Pearson correlation was used to evaluate the relationship between LV strain and remodelling. Cardiac specimens were obtained at 6, 10, and 16 months after modelling to observe the myocardial ultrastructural and microstructure at different courses of diabetes. Results: Twelve pigs developed diabetes. The 80% diastolic volume recovery rate (DVR) at 6 months after modelling was significantly higher than that before modelling (0.78 ± 0.08vs. 0.67 ± 0.15). The LV global longitudinal peak strain (GLPS) (− 10.21 ± 3.15 vs. − 9.74 ± 2.78 vs. − 9.38 ± 3.71 vs. − 8.71 ± 2.68 vs. − 6.59 ± 2.90%) altered gradually from the baseline data to 2, 6, 10 and 16 months after modelling. After 16 months of modelling, the LV remodelling index (LVRI) of pigs increased compared with that before modelling (2.19 ± 0.97 vs. 1.36 ± 0.45 g/ml). The LVRI and myocardial peak strain were correlated in diabetic pigs (r= − 0.40 to − 0.54), with GLPS being the most significant. Electron microscopy and Masson staining showed that myocardial damage and fibrosis gradually increased with the progression of the disease. Conclusion: Intravenous injection of STZ can induce a porcine diabetic cardiomyopathy model, mainly characterized by decreased LV diastolic function and strain changes accompanied by myocardial remodelling. The changes in CMR biomarkers could reflect the early myocardial injury of diabetic cardiomyopathy. [ABSTRACT FROM AUTHOR]

Objectives: We aimed to evaluate myocardial fibrosis using cardiac magnetic resonance (CMR) T1 mapping in type 2 diabetes mellitus (T2DM) patients and investigate the association between left ventricular (LV) subclinical myocardial dysfunction and myocardial fibrosis.Methods: The study included 37 short-term (≤ 5 years) and 44 longer-term (> 5 years) T2DM patients and 41 healthy controls. The LV global strain parameters and T1 mapping parameters were compared between the abovementioned three groups. The association of T1 mapping parameters with diabetes duration, in addition to other risk factors, was determined using multivariate linear regression analysis. The correlation between LV strain parameters and T1 mapping parameters was evaluated using Pearson's correlation.Results: The peak diastolic strain rates (PDSRs) were significantly lower in longer-term T2DM patients compared to those in healthy subjects and short-term T2DM patients (p < 0.05). The longitudinal peak systolic strain rate and peak strain were significantly lower in the longer-term T2DM compared with the short-term T2DM group (p < 0.05). The extracellular volumes (ECVs) were higher in both subgroups of T2DM patients compared with control subjects (all p < 0.05). Multivariate linear regression analysis showed that diabetes duration was independently associated with ECV (β = 0.413, p < 0.001) by taking covariates into account. Pearson's analysis showed that ECV was associated with longitudinal PDSR (r = - 0.441, p < 0.001).Conclusion: T1 mapping could detect abnormal myocardial fibrosis early in patients with T2DM, which can cause a decline in the LV diastolic function.Key Points: • CMR T1 mapping could detect abnormal myocardial fibrosis early in patients with T2DM. • The diabetes duration was independently associated with ECV. • Myocardial fibrosis can cause a decline in the LV diastolic function in T2DM patients. [ABSTRACT FROM AUTHOR]

Background: Type 2 diabetes mellitus (T2DM) and obesity often coexist and together contribute to left atrial (LA) functional abnormalities. However, little is known about the impact of body mass index (BMI) on LA strains measured using cardiac magnetic resonance feature tracking (MR‐FT). Purpose: To investigate the additive effect of BMI on LA functional remodeling using MR‐FT as well as to explore abnormal atrioventricular interaction in T2DM patients. Study Type: Retrospective. Population: One hundred and fifty‐nine T2DM patients (53, 34, and 72 normal‐weight, overweight, and obese individuals) and 105 non‐diabetic controls (46, 32, and 27 normal‐weight, overweight, and obese individuals). Field Strength/Sequence: 3.0 T/balanced steady‐state free precession. Assessment: LA reservoir strain (εs), conduit strain (εe), and active strain (εa) and their corresponding strain rates (SRs, SRe, SRa) were measured together with left ventricular (LV) radial, circumferential, and longitudinal peak strain, peak systolic strain rate, and peak diastolic strain rate. Statistical Tests: Student's t‐test or Mann–Whitney U test, one‐way ANOVA, univariate and multivariate linear regression. A P value <0.05 was considered statistically significant. Results: Compared to controls in the same BMI category, T2DM patients had significantly decreased reservoir and conduit function, while pump function was not significantly different (εa and SRa: P = 0.757 and 0.583 for normal‐weight, P = 0.171 and 0.426 for overweight, P = 0.067 and 0.330 for obese). LA strains were significantly correlated with BMI (r = −0.346 for εs, −0.345 for εe) in T2DM patients. Multivariable linear regression analysis indicated that BMI was independently associated with LA εs and εe, LV global longitudinal strain was independently associated with LA εs and εa, and LV circumferential peak diastolic strain rate was independently associated with LA εe. Data Conclusion: These findings suggest that the coexistence of increased body weight and T2DM patients can exacerbate the impairment of LA strains and indicate abnormal atrioventricular interactions. Level of Evidence: 3 Technical Efficacy: Stage 3 [ABSTRACT FROM AUTHOR]

Background: The pathophysiological changes in the remote myocardium after acute myocardial infarction (MI) remains less understood. Purpose To assess the inflammation in the remote myocardium post‐MI and its association with left ventricular (LV) remodeling using T2 mapping. Study type: Prospective. Animal Model and Subjects: Twelve pigs at 3‐day post‐MI, 6 pigs at 3‐month post‐MI, 6 healthy pigs; 54 patients at 3‐day and 3‐month post‐MI, 31 healthy volunteers; Field Strength/Sequence: A 3 T MRI/ steady‐state free‐precession sequence for T2 mapping (animals: 0, 30, and 55 msec; human: 0, 25, and 55 msec), phase‐sensitive inversion recovery gradient echo for late gadolinium enhancement (LGE), balanced steady free‐precession sequence for cine. Assessment Infarcted myocardium was defined on LGE, remote T2 was measured on T2 maps. LV remodeling was evaluated as LV end‐diastolic volume change index between two scans using cine. CD68 staining was conducted to detect monocyte/macrophage. Statistical Tests: Student‐t test and one‐way ANOVA were used to compare remote T2 with normal controls. The association of remote T2 with LV remodeling was assessed using linear regression. P values of <0.05 were used to denote statistical significance. Results: Compared with healthy pigs, remote T2 significantly increased from 3 days to 3 months post‐MI (31.43 ± 0.67 vs. 33.53 ± 1.15 vs. 36.43 ± 1.07 msec). CD68 staining demonstrated the inflammation in remote myocardium post‐MI but not in healthy pigs. Significant remote myocardial alterations in T2 were also observed in human group (40.51 ± 1.79 vs. 41.94 ± 1.14 vs. 42.52 ± 1.71 msec). In patients, the 3‐month remote T2 (β = 0.432) and remote T2 variation between two scans (β = 0.554) were both independently associated with LV remodeling. Conclusion: T2 mapping could characterize the abnormalities in the remote myocardium post‐MI, which was potentially caused by the inflammatory response. Moreover, variations in remote T2 were associated with LV remodeling. Evidence Level 1 Technical Efficacy: Stage 3 [ABSTRACT FROM AUTHOR]

Background: Progressive cardiomyopathy accounts for almost all mortality among Duchenne muscular dystrophy (DMD) patients.‍ Thus, our aim was to comprehensively characterize myocardial involvement by investigating the heterogeneity of native T1 mapping in DMD patients using global and regional (including segmental and layer-specific) analysis across a large cohort. Methods: We prospectively enrolled 99 DMD patients (8.8 ± 2.5 years) and 25 matched male healthy controls (9.5 ± 2.5 years). All subjects underwent cardiovascular magnetic resonance (CMR) with cine, T1 mapping and late gadolinium enhancement (LGE) sequences. Native T1 values based on the global and regional myocardium were measured, and LGE was defined. Results: LGE was present in 49 (49%) DMD patients. Global native T1 values were significantly longer in LGE-positive (LGE +) patients than in healthy controls, both in basal slices (1304 ± 55 vs. 1246 ± 27 ms, p < 0.001) and in mid-level slices (1305 ± 57 vs. 1245 ± 37 ms, p < 0.001). No significant difference in global native T1 was found between healthy controls and LGE-negative (LGE−) patients. In segmental analysis, LGE + patients had significantly increased native T1 in all analyzed segments compared to the healthy control group. Meanwhile, the comparison between LGE− patients and healthy controls showed significantly elevated values only in the basal anterolateral segment (1273 ± 62 vs. 1234 ± 40 ms, p = 0.034). Interestingly, the epicardial layer had a significantly higher native T1 in LGE− patients than in healthy controls (p < 0.05), whereas no such pattern was noticed in the global myocardium. Epicardial layer native T1 resulted in the highest diagnostic performance for distinguishing between healthy controls and DMD patients in receiver operating curve analyses (area under the curve [AUC] 0.84 for basal level and 0.85 for middle level) when compared to global native T1 and endocardial layer native T1. Conclusions: Myocardial regional native T1, particularly epicardial native T1, seems to have potential as a novel robust marker of very early cardiac involvement in DMD patients. Trial registration: Chinese Clinical Trial Registry (http://www.chictr.org.cn/index.aspx) ChiCTR1800018340, 09/12/2018, Retrospectively registered. [ABSTRACT FROM AUTHOR]

The safety profiles when performing stress oxygenation‐sensitive magnetic resonance imaging (OS‐MRI) have raised concerns in clinical practice. Adenosine infusion can cause side effects such as chest pain, dyspnea, arrhythmia, and even cardiac death. The aim of this study was to investigate the feasibility of breathing maneuvers‐induced OS‐MRI in acute myocardial infarction (MI). This was a prospective study, which included 14 healthy rabbits and nine MI rabbit models. This study used 3 T MRI/modified Look‐Locker inversion recovery sequence for native T1 mapping, balanced steady‐state free precession sequence for OS imaging, and phase‐sensitive inversion recovery sequence for late gadolinium enhancement. The changes in myocardial oxygenation (ΔSI) were assessed under two breathing maneuvers protocols in healthy rabbits: a series of extended breath‐holding (BH), and a combined maneuver of hyperventilation followed by the extended BH (HVBH). Subsequently, OS‐MRI with HVBH in acute MI rabbits was performed, and the ΔSI was compared with that of adenosine stress protocol. Student's t‐test, Wilcoxon rank test, and Friedman test were used to compare ΔSI in different subgroups. Pearson and Spearman correlation was used to obtain the association of ΔSI between breathing maneuvers and adenosine stress. Bland–Altman analysis was used to assess the bias of ΔSI between HVBH and adenosine stress. In healthy rabbits, BH maneuvers from 30 to 50 s induced significant increase in SI compared with the baseline (all p < 0.05). By contrast, hyperventilation for 60 s followed by 10 s‐BH (HVBH 10 s) exhibited a comparable ΔSI to that of stress test (p = 0.07). In acute MI rabbits, HVBH 10 s‐induced ΔSIs among infarcted, salvaged, and the remote myocardial area were no less effectiveness than adenosine stress when performing OS‐MRI (r = 0.84; p < 0.05). Combined breathing maneuvers with OS‐MRI have the potential to be used as a nonpharmacological alternative for assessing myocardial oxygenation in patients with acute MI. Level of Evidence: 2 Technical Efficacy Stage: 2 [ABSTRACT FROM AUTHOR]