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Background: Patients with repaired tetralogy of Fallot (rTOF) continue to face a heightened risk of deteriorating cardiac function, and quantitative techniques of cardiac MRI‐derived cardiac structure and function provide an opportunity to explore the causes and mechanisms of cardiac deterioration. Purpose: To explore right–left ventricular interdependence in rTOF patients before and after the onset of right ventricular (RV) heart failure. Study Type: Retrospective. Population: One hundred eighteen rTOF patients (21.85 [16.74, 29.20] years, 58 females) and 34 controls (23.5 [21, 26.5] years, 17 females) that underwent cardiac MRI were analyzed, with rTOF patients being further subdivided into those with preserved RV function (N = 54) and those that experienced RV heart failure (N = 64). Field Strength/Sequence: 3.0 T/balanced steady‐state free precession sequence. Assessment: RV, left ventricular (LV), and septal strain; RV and LV volume. Statistical Tests: Chi‐squared tests or Fisher's exact test, One‐way ANOVAs with Bonferroni's post hoc test, Pearson/Spearman correlation, and multivariate backward linear regression analysis. A two‐tailed P < 0.05 was deemed as the significance threshold. Results: The MRI‐derived RV, LV, and septal strain decreased sequentially in controls, patients with preserved RV function, and patients with RV heart failure, with a good intra‐observer (0.909–0.964) and inter‐observer (0.879–0.937) agreement. Correlations between LV and RV strain were found to change sequentially with RV function and were the closest in rTOF patients with RV heart failure (r = −0.270 to 0.506). Correlations between RV volume and septal strain was variable in controls (r = 0.483 to −0.604), patients with preserved RV function (r = −0.034 to −0.295), and patients with RV heart failure (r = −0.026 to 0.500). Multivariate analyses revealed that the RV longitudinal strain was independently correlated with LV strain in three directions in rTOF patients with RV heart failure (Radial −0.70 [−1.33, −0.06]; Circumferential 0.44 [0.17, 0.72]; Longitudinal 0.54 [0.26, 0.81]). Data Conclusion: In rTOF patients, the coupling between RV volume and septal strain was broken during RV function compensation, and the adverse effect of RV on LV deformation was highest in patients with RV heart failure. Evidence Level: 4 Technical Efficacy: Stage 5 [ABSTRACT FROM AUTHOR]

Background: Understanding the impact of aortic regurgitation (AR) on hypertensive patients' hearts is important. Purpose: To assess left ventricular (LV) strain and structure in hypertensive patients and investigate the relationship with AR severity. Study Type: Retrospective. Population: 263 hypertensive patients (99 with AR) and 62 controls, with cardiac MRI data. Field Strength/Sequence: Balanced steady‐state free precession (bSSFP) sequence at 3.0T. Assessment: AR was classified as mild, moderate, or severe based on echocardiographic findings. LV geometry was classified as normal, concentric remodeling, eccentric hypertrophy, or concentric hypertrophy based on MRI assessment of LV mass/volume ratio and LV Mass index (LVMI). LV global radial peak strain (GRPS), global circumferential peak strain (GCPS), and global longitudinal peak strain (GLPS) were obtained by post‐processing bSSFP cine datasets using commercial software. Statistical Tests: ANOVA, Kruskal–Wallis test, Spearman's correlation coefficients (r), chi‐square test, and multivariable linear regression analysis. A P value <0.05 was considered statistically significant. Results: Hypertensive patients with AR had significantly lower LV myocardial strain and higher LVMI than the group without AR (GRPS 26.25 ± 12.23 vs. 34.53 ± 9.85, GCPS −17.4 ± 5.84 vs. −20.57 ± 3.57, GLPS −9.86 ± 4.08 vs. −12.95 ± 2.94, LVMI 90.56 ± 38.56 vs.58.84 ± 17.55). Of the 99 patients with AR, 56 had mild AR, 26 had moderate AR and 17 had severe AR. The degree of AR was significantly negatively correlated to the absolute values of LV GRPS, GCPS and GLPS (r = −0.284 – −0.416). LV eccentric hypertrophy increased significantly with AR severity (no AR 21.3%, mild AR 42.9%, moderate AR 73.1%, severe AR 82.4%). In multivariable analysis, the degree of AR was an independent factor affecting LV global strain and LVMI even after considering confounding factors (β values for global myocardial strain were −0.431 to −0.484, for LVMI was 0.646). Data Conclusion: Increasing AR severity leads to decreased cardiac function and worse ventricular geometric phenotypes in hypertensive patients. Level of Evidence: 4 Technical Efficacy: Stage 3 [ABSTRACT FROM AUTHOR]

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 [ABSTRACT FROM AUTHOR]

Background: Cardiac MRI feature‐tracking (FT) with breath‐holding (BH) cine balanced steady state free precession (bSSFP) imaging is well established. It is unclear whether FT‐strain measurements can be reliably derived from free‐breathing (FB) compressed sensing (CS) bSSFP imaging. Purpose: To compare left ventricular (LV) strain analysis and image quality of an FB CS bSSFP cine sequence with that of a conventional BH bSSFP sequence in children. Study Type: Prospective. Subjects: 40 children able to perform BHs (cohort 1 [12.1 ± 2.2 years]) and 17 children unable to perform BHs (cohort 2 [5.2 ± 1.8 years]). Field Strength/Sequence: 3T, bSSFP sequence with and without CS. Assessment: Acquisition times and image quality were assessed. LV myocardial deformation parameters were compared between BH cine and FB CS cine studies in cohort 1. Strain indices and image quality of FB CS cine studies were also assessed in cohort 2. Intraobserver and interobserver variability of strain parameters was determined. Statistical Tests: Paired t‐test, Wilcoxon signed‐rank test, intraclass correlation coefficient (ICC), and Bland–Altman analysis. A P‐value <0.05 was considered statistically significant. Results: In cohort 1, the mean acquisition time of the FB CS cine study was significantly lower than for conventional BH cine study (15.6 s vs. 209.4 s). No significant difference were found in global circumferential strain rate (P = 0.089), global longitudinal strain rate (P = 0.366) and EuroCMR image quality scores (P = 0.128) between BH and FB sequences in cohort 1. The overall image quality score of FB CS cine in cohort 2 was 3.5 ± 0.5 with acquisition time of 14.7 ± 2.1 s. Interobserver and intraobserver variabilities were good to excellent (ICC = 0.810 to 0.943). Data Conclusion: FB CS cine imaging may be a promising alternative technique for strain assessment in pediatric patients with poor BH ability. Level of Evidence: 1 Technical Efficacy: Stage 1 [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 dysfunction‐associated fatty liver disease (MAFLD) was recently recognized as an important risk factor for cardiovascular diseases. Purpose: To examine the effect of MAFLD on cardiac function in metabolic syndrome by MRI. Study Type: Retrospective. Population: One hundred seventy‐nine patients with metabolic syndrome (MetS), 101 with MAFLD (MAFLD [+]) and 78 without (MAFLD [−]). Eighty‐one adults without any of the components of MetS or cardiac abnormalities were included as control group. Field Strength/Sequence: 3.0 T; balanced steady‐state free precession sequence. Assessment: Left atrial (LA) strain was assessed during three phases: reservoir strain (LA‐RS), conduit strain (LA‐CS), and booster strain (LA‐BS). Left ventricular (LV) global longitudinal (LV‐GLS) strain was also derived. The left atrioventricular coupling index (LACI) was calculated as the ratio of LA end‐diastolic volume (LA‐EDV) and LV‐EDV. Statistical Tests: Student's t test or Mann–Whitney U test; One‐way analysis of variance. A P value <0.05 was considered statistically significant. Results: Among MetS patients, individuals with MAFLD had significantly lower magnitude LV‐GLS (−11.6% ± 3.3% vs. −13.8% ± 2.7%) than those without MAFLD. For LA strains, LA‐RS (36.9% ± 13.7% vs. 42.9% ± 13.5%) and LA‐CS (20.0% ± 10.6% vs. 24.1% ± 9.2%) were also significantly reduced in MAFLD (+) compared to MAFLD (−). The LACIs (17.2% [12.9–21.2] % vs. 15.8% [12.2–19.7] %) were significantly higher in patients with MAFLD compared to those without MAFLD. After adjustment for other clinical factors, MAFLD was found to be independently correlated with LV‐GLS (β = −0.270) and LACI (β = 0.260). Data Conclusion: MAFLD had an unfavorable effect on LV myocardial strain in MetS. Moreover, LA strain and atrioventricular coupling were further impaired in patients with concomitant MAFLD compared to those without MAFLD. Last, MAFLD was independently associated with subclinical LV dysfunction and atrioventricular coupling after adjustment for other clinical factors. Evidence Level: 3 Technical Efficacy: 3 [ABSTRACT FROM AUTHOR]

Background: Hypertension (HTN) is highly prevalent in non‐ischemic dilated cardiomyopathy (NIDCM) patients, but little is known about its impact on left ventricular (LV) function and remodeling. Purpose: To evaluate the effect of hypertension on LV function and remodeling in NIDCM patients. Study Type: Retrospective. Population: Two‐hundred and twelve NIDCM (HTN−) patients, 91 NIDCM (HTN+) patients, and 74 normal controls. Field Strength/Sequence: 3.0 T/bSSFP and phase‐sensitive inversion recovery sequence. Assessment: The LV geometry, myocardial strain, remodeling index (calculated as LVM/LVEDV), and LGE were measured and compared between groups. Determinants of LV strain and remodeling in NIDCM were investigated. Statistical Tests: Student's t‐test, Mann–Whitney U test, one‐way analysis of variance, Kruskal–Wallis test, univariable and multivariable linear regression. A P value <0.05 was considered statistically significant. Results: Compared with normal controls, NIDCM patients had significantly higher LVEDV and significantly impaired LV strains, including LV global peak strain (PS) and peak systolic and diastolic strain rates in the radial, circumferential, and longitudinal directions. The NIDCM (HTN+) group had significantly decreased LV global longitudinal PS and peak diastolic strain rate (PDSR), and significantly increased LV mass index and remodeling index compared to the NIDCM (HTN−) group, despite there being no significant difference in ejection fraction (P = 0.241). The prevalence of LV LGE was significantly higher in the NIDCM (HTN+) group than in the NIDCM (HTN−) group. In multivariable regression models adjusted for potential confounders, hypertension was independently associated with LV global longitudinal PS and PDSR. Male sex, resting heart rate, and log(NT‐proBNP) level were independent determinants of LV strains. Moreover, male sex, systolic and diastolic blood pressure, and presence of LGE were independent determinants of LV remodeling index. Data Conclusion: These findings suggest that coexistence of hypertension may further exacerbate the reduction in LV global strain and the aggravation of LV remodeling in NIDCM patients. Level of Evidence: 3 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: Obesity is highly prevalent in patients with hypertrophic cardiomyopathy (HCM) and believed to influence its phenotype. Purpose: To explore the effects of obesity on left ventricular (LV) remodeling and long‐term clinical course in Chinese patients with HCM. Study Type: Longitudinal. Population: A total of 247 patients with HCM classified according to body mass index (BMI) (normal weight: BMI = 18.0–22.9 kg/m2 [N = 90]; overweight: BMI = 23.0–24.9 kg/m2 [N = 58]; and obese: BMI ≥ 25 kg/m2 [N = 99]). Field Strength/Sequence: 3.0 T/Balanced steady‐state free precession sequence and phase‐sensitive inversion recovery late gadolinium enhancement (LGE) sequence. Assessment: LV function and geometry were measured. LV peak strain analysis was performed. The presence and percentage of LGE in the LV were recorded. The endpoints including heart failure, sudden cardiac death, and overall composite outcome were assessed during a median follow‐up of 4.1 years (interquartile range, 3.0–6.2 years). Statistical Tests: One‐way analysis of variance, Kruskal–Wallis test, or chi‐square test; Pearson correlation coefficient (r); multivariable linear regression analysis; Kaplan–Meier survival analysis; and Cox proportional hazards model analysis were conducted. A two‐tailed P‐value < 0.05 was considered statistically significant. Results: Obese patients exhibited a significant progressive increase in LV mass compared with normal‐weight patients. The magnitude of all LV strain indices gradually and significantly decreased as BMI increased, whereas LV ejection fraction was not significantly different among BMI groups (P = 0.364). Multivariable linear regression analysis showed that obesity had a significant association with impaired strain indices as well as with indexed LV mass. Multivariable Cox model analysis retained obesity as an independent marker for future endpoints, and conveyed a > 3‐fold increase in risk compared with patients with normal weight (hazard ratio, 3.04; 95% confidence interval, 1.07–6.57). Data Conclusion: Obesity is an important environmental modifier that is associated with adverse LV remodeling and is independently associated with future clinical outcomes in Chinese patients with HCM. Level of Evidence: 3 Technical Efficacy: Stage 2 [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: The majority of heart failure (HF) in hypertrophic cardiomyopathy (HCM) manifests as a phenotype with preserved left ventricular (LV) ejection fraction; however, the exact contribution of left atrial (LA) phasic function to HF with preserved ejection fraction (HFpEF) in HCM remains unresolved. Purpose: To define the association between LA function and HFpEF in HCM patients using cardiac magnetic resonance imaging (MRI) feature tracking. Study Type: Retrospective. Population: One hundred and fifty‐four HCM patients (HFpEF vs. non‐HF: 55 [34 females] vs. 99 [43 females]). Field Strength/Sequence: 3.0 T/balanced steady‐state free precession. Assessment: LA reservoir function (reservoir strain [εs], total ejection fraction [EF]), conduit function (conduit strain [εe], passive EF), booster‐pump function (booster strain [εa] and active EF), LA volume index, and LV global longitudinal strain (LV GLS) were evaluated in HCM patients. Statistical Tests: Chi‐square test, Student's t‐test, Mann–Whitney U test, multivariate linear regression, logistic regression, and net reclassification analysis were used. Two‐sided P < 0.05 was considered statistically significant. Results: No significant difference was found in LV GLS between the non‐HF and HFpEF group (−10.67 ± 3.14% vs. −10.14 ± 4.01%, P = 0.397), whereas the HFpEF group had more severely impaired LA phasic strain (εs: 27.40 [22.60, 35.80] vs. 18.15 [11.98, 25.90]; εe: 13.80 [9.20, 18.90] vs. 7.95 [4.30, 14.35]; εa: 13.50 [9.90, 17.10] vs. 7.90 [5.40, 14.15]). LA total EF (37.91 [29.54, 47.94] vs. 47.49 [39.18, 55.01]), passive EF (14.70 [7.41, 21.49] vs. 18.07 [9.32, 24.78]), and active EF (27.19 [17.79, 36.60] vs. 36.64 [26.63, 42.71]) were all significantly decreased in HFpEF patients compared with non‐HF patients. LA reservoir (β = 0.90 [0.85, 0.96]), conduit (β = 0.93 [0.87, 0.99]), and booster (β = 0.86 [0.78, 0.95]) strain were independently associated with HFpEF in HCM patients. The model including reservoir strain (Net Reclassification Index [NRI]: 0.260) or booster strain (NRI: 0.325) improved the reclassification of HFpEF based on LV GLS and minimum left atrial volume index (LAVImin). Data Conclusion: LA phasic function was severely impaired in HCM patients with HFpEF, whereas LV function was not further impaired compared with non‐HF patients. Level of Evidence: 4 Technical Efficacy: Stage 3 [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]

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]

Background: Both acute and chronic myocardial infarction (AMI and CMI, respectively) exhibit delayed enhancement; however, clinical decision-making processes frequently require the differentiation of these two types of myocardial injury.Purpose: To investigate the reliability of AMI and CMI characterization using native T1 mapping and its feasibility for discriminating AMI from CMI.Study Type: Case-control.Animal Model: The study cohort comprised 12 AMI (mean post-MI, 3.75 ± 1.29 days) and 15 CMI (mean post-MI, 39.53 ± 6.10 days) Bama mini-pigs.Field Strength/sequence: Balanced steady-state free precession (bSSFP), segmented-turbo-FLASH-PSIR, and modified Look-Locker inversion recovery (MOLLI) sequences at 3.0T.Assessment: The infarct sizes were compared on matching short-axis slices of late-gadolinium-enhanced (LGE) images and T1 maps by two experienced radiologists.Statistical Tests: The infarct sizes were compared on matching short-axis slices of LGE images and T1 maps, and agreement was determined using linear regression and Bland-Altman analyses. The native T1 values were compared between AMI and CMI models (independent sample t-test). The intraclass correlation coefficient was used to assess inter- and intraobserver variability.Results: Measured infarct sizes did not differ between native T1 mapping and LGE images (AMI: P = 0.913; CMI: P = 0.233), and good agreement was observed between the two techniques (AMI: bias, -3.38 ± 19.38%; R2  = 0.96; CMI: bias, -10.55 ± 10.90%; R2  = 0.90). However, the native infarction myocardium T1 values and the T1 signal intensity ratio of infarct and remote myocardium (T1 SI ratio) did not differ significantly between AMI and CMI (P = 0.173).Data Conclusion: Noncontrast native T1 mapping can accurately determine acute and chronic infarct areas as well as conventional LGE imaging; however, it cannot distinguish acute from chronic MI.Level Of Evidence: 1 Technical Efficacy: Stage 2 J. Magn. Reson. Imaging 2018;47:1406-1414. [ABSTRACT FROM AUTHOR]