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Introduction: The presence of cerebral microbleeds (CMBs) has been described using MRI in patients with cardiovascular risk factors or prior stroke and could predict future cognitive dysfunction or cardiovascular mortality. CMBs are highly frequent (> 50%) in patients with infective endocarditis (IE). However, the association of CMBs and clinical factors in patients' valvular disease without IE remains unclear. Hypothesis: Valvular heart disease without IE confers a risk factor for microbleeds. Methods: We retrospectively examined data from the consecutive 96 patients ( 72 ± 9 years, 49 men) with severe valvular disease who underwent T2*-weighted brain MRI before cardiac surgery. The patients with neurological abnormalities or IE were excluded. Conventional echocardiography was performed to evaluate the left ventricular volume and valvular abnormalities. CMBs were coded by researchers blind to clinical details, who independently assessed the presence and location of CMBs using a standardized form. The study population consisted of 59 patients with severe aortic stenosis (AS) (group A) and 40 patients with severe aortic or mitral regurgitation (group B). Results: CMBs were found in 26 patients (27%), 14 (15%) had multiple CMBs. CMBs were most frequently seen in the lobar locations (69%), followed by deep or infratentorial locations (62%). No significant relationship was found between CMBs in dyslipidemia, diabetes mellitus, smoking status, anticoagulant, and antiplatelet therapy in both groups. In group A, the HAS-BLED score was higher in patients with CMBs, and the presence of CMBs was associated with hypertension (P2 vs 125 ± 32 g/m 2 , P < 0.01 ; 150 ± 39 ml vs 111 ± 38 ml, P Conclusion: CMBs were frequently observed in severe valvular heart disease without IE. The presence of CMBs was independent of antiplatelet or anticoagulant therapy. In aortic or mitral regurgitation patients, LV remodeling may contribute to the development of CMBs.

Introduction: Elevated right atrial pressure (RAP) exhibits residual congestion and poor clinical outcomes in patients with heart failure (HF). In HF patients, persistent high RAP causes liver damage, which leads to liver fibrosis. Recent advances in T1 mapping of the liver using MRI allow the quantification of liver fibrosis. Hypothesis: Hepatic T1 mapping value may predicts high RAP in patients with chronic HF. Methods: We examined the data from the consecutive 40 patients with DCM ( 60 ± 13 years, 27 men) who underwent 3 Tesla cardiac and liver MRI, which were conducted within seven days of right heart catheterization. RV end-diastolic volume (RVEDV), end-systolic volume (RVESV), RV ejection fraction (RVEF), right atrial (RA) and left atrial (LA) volume, left ventricular end-diastolic volume (LVEDV), end-systolic volume (LVESV), LV ejection fraction (LVEF) and LV mass index (LVMI) were calculated from cine cardiac MRI. Native T1 mapping image (T1 short modified look locker inversion recovery-ShMOLLI- sequence) was acquired the heart and the liver (Figure A). Patients were divided into two groups according to RAP; high ( ≥ 8 mmHg; n=10) and low ( Results: Ten patients had high RAP. There were no significant differences in LVEDV,LVESV, LVEF, LVMI, RVEDV, RVESV and RVEF between patients with high RAP group and those without ( 192 ± 54 ml vs 212 ± 57 ml; 136 ± 49 ml vs 154 ± 51 ml; 30 ± 9 % vs 28 ± 8 %; 79 ± 21 g/m 2 vs 81 ± 22 g/m 2 ; 45 ± 27 ml vs 46 ± 19 ml; 27 ± 18 ml vs 25 ± 15 ml; 42 ± 19% vs 46 ± 18%, respectively). The hepatic T1 mapping value was higher in the high RAP group ( 845 ± 47 ms vs 759 ± 90 ms, p < 0.01) and exhibited a positive correlation with RAP ( R = 0.34, P < 0.05). The hepatic T1 mapping value of ≥ 820ms was the optimal cutoff values for identifying high RAP ( T1: sensitivity, 89%; specificity, 72%; AUC, 0.80, Figure B). Conclusion: Increased native T1 mapping value of the liver may be helpful in non-invasively estimating elevated RAP.

Introduction: The prognosis of patients with idiopathic dilated cardiomyopathy (DCM) has improved in recent decades with guideline-directed medical therapy. There is an essential need for better biomarkers to predict left ventricular reverse remodeling (LVRR) in DCM. Native T1, T2 and left ventricular (LV) global strain by cardiac magnetic resonance (CMR) without contrast agents provides a novel quantitative method for myocardial tissue characterization. Hypothesis: CMR parameters predict LVRR in patients with DCM. Methods: A total 34 patients ( 58 ± 13 years, 25 male) with DCM underwent baseline CMR imaging (3T Philips), including cine, late gadolinium enhancement (LGE) CMR, and triple-slice T1 and T2 mapping (short modified look locker inversion recovery ShMOLLI sequence). The 6SD-LGE (% area), global circumferential strain (GCS), global radial strain (GRS), global longitudinal strain (GLS), global radial strain (GRS), LV mass index (LVMI), LV end-diastolic volume (EDV), end-systolic volume (ESV) and ejection fraction (EF) were calculated from multiple short-axis views. Echocardiography was conducted before and > 1 year after after optimal medical therapy. Results: The patients were divided into two groups, LVRR with LVEF increase of >10% and the final value of ≥40% for those without. There were no significant differences in LV mass index, LVEDV, LVESV, and LVEF between the two groups (80 ± 20 g/m 2 vs 78 ± 19 g/m 2 ; 174 ± 54 ml vs 165 ± 48 ml; 134 ± 51 ml vs 122 ± 46 ml; 24 ± 9% vs 28 ± 9%, respectively). The any LV global strain showed no significant difference between the two groups. The 6SD-LGE, native T1, and T2 values were significantly lower in LVRR+ group than in LVRR-group (15.3 ± 15.5 % vs 5.9 ± 6.8%;1376 ± 59 ms vs 1301 ± 42 ms;55 ± 3.5 ms vs 50 ± 2.5 ms,respectively). The LGE-6SD < 13%. native T1 value < 1330 ms and T2 values < 53ms were the best threshold values for predicting LVRR (The LGE-6SD: sensitivity, 82%; specificity, 41%; AUC 0.72, T1:sensitivity, 82%; specificity, 71%; AUC 0.87, and T2: sensitivity, 82%; specificity, 63%; AUC 0.88). Conclusions: Native T1 and T2 mapping values may be useful for assessing of the LVRR in patients with DCM even without contrast.