BackgroundMetabolic dysfunction‐associated fatty liver disease (MAFLD) was recently recognized as an important risk factor for cardiovascular diseases.PurposeTo examine the effect of MAFLD on cardiac function in metabolic syndrome by MRI.Study TypeRetrospective.PopulationOne 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/Sequence3.0 T; balanced steady‐state free precession sequence.AssessmentLeft 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 TestsStudent's t test or Mann–Whitney U test; One‐way analysis of variance. A P value <0.05 was considered statistically significant.ResultsAmong 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 ConclusionMAFLD 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 Level3Technical Efficacy3

BackgroundMitral 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.PurposeTo explore how mitral regurgitation affects LA function in hypertension and to investigate atrioventricular interaction in hypertensive patients with mitral regurgitation.Study TypeRetrospective.PopulationA total of 193 hypertensive cases and 64 controls.Field Strength/SequenceA 3.0 T/balanced steady‐state free precession.AssessmentLA 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 TestsOne‐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.ResultsHypertensive 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 ConclusionMitral 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 Level4.Technical EfficacyStage 3.

The aim of this study was to evaluate left ventricular (LV) myocardial involvement in connective tissue disease (CTD) patients using multiparemetric imaging derived from cardiovascular magnetic resonance (CMR). CMR was performed on 146 CTD patients (comprising of 74 with idiopathic inflammatory myopathy (IIM) and 72 with non-IIM) and 72 healthy controls and included measures of LV global strains [including peak strain (PS), peak systolic (PSSR) and diastolic strain rate (PDSR)], myocardial perfusion [including upslope, max signal intensity (MaxSI), and time to maximum signal intensity (TTM)], and late gadolinium enhancement (LGE) parameters. Univariable and multivariable linear regression analyses were performed to determine the association between LV deformation and microvascular perfusion, as well as LGE. Our results indicated that CTD patients had decreased global longitudinal PS (GLPS), PSSR, PDSR, and myocardial perfusion (all p < 0.017) compared with normal controls. Non-IIM patients exhibited lower LV global strain and longer TTM than IIM patients. The presence of LGE was independently associated with global radial PS (GRPS: β = − 0.165, p = 0.011) and global circumferential PS (GCPS: β =  − 0.122, p = 0.022). TTM was independently correlated with GLPS (β = − 0.156, p = 0.027). GLPS was the best indicator for differentiating CTD patients from normal controls (area under curve of 0.78). This study indicated that CTD patients showed impaired LV global myocardial deformation and microvascular perfusion, and presence of LGE. Cardiac involvement might be more severe in non-IIM patients than in IIM patients. Impaired microvascular perfusion and the presence of LGE were independently associated with LV global deformation.