Background The presence of myocardial fibrosis by cardiac MRI has prognostic value in cardiac sarcoidosis, and localisation may be equally relevant to clinical outcomes. Objective We aimed to analyse cardiac damage and function in detail and explore the relationship with clinical outcomes in patients with cardiac sarcoidosis using cardiac MRI. Methods We included 81 consecutive patients with cardiac sarcoidosis undergoing cardiac MR. Left ventricular mass and fibrosis mass were calculated, and localisation was analysed using a 17-segment model. Participants underwent follow-up through 2015, and the development of major adverse cardiac events including ventricular tachyarrhythmias was recorded. Results Increased left ventricular fibrosis mass was associated with increased prevalence of ventricular tachyarrhythmias (p< 0.001). When localisation was defined as the sum of late gadolinium enhancement in the left ventricular basal anterior and basal anteroseptal areas, or the right ventricular area, it was associated with ventricular tachyarrhythmias (p< 0.001). Kaplan-Meier analysis during a median follow-up of 22.1â €..months showed that both the mass and localisation groupings for fibrosis were significantly associated with major adverse cardiac events or ventricular tachyarrhythmias and that when combined, the risk stratification was better than for each variable alone (p< 0.001, respectively). By Cox-proportional hazard risk analysis, the localisation grouping was an independent predictor for the both. Conclusions In patients with cardiac sarcoidosis, both fibrosis mass and its localisation to the basal anterior/anteroseptal left ventricle, or right ventricle was associated with the development of major adverse cardiac events or ventricular tachyarrhythmias. Cardiac MR with late gadolinium enhancement may be useful for improving risk stratification in patients with cardiac sarcoidosis.

Myocardial fibrosis is frequently observed and may be associated with the prognosis in patients with hypertrophic cardiomyopathy (HCM); however, the clinical pathophysiological features, particularly in terms of fibrosis, of hypertrophic obstructive cardiomyopathy (HOCM) remain unclear. This study aimed to determine a role of local fibrosis in HOCM using cardiac magnetic resonance (CMR). 108 consecutive HCM patients underwent CMR. HOCM was defined as a left ventricular outflow tract (LVOT) pressure gradient a parts per thousand yen30 mmHg at rest. Myocardial mass and fibrosis mass by late gadolinium-enhancement CMR (LGE-CMR) were calculated and the distribution/pattern was analyzed using the AHA 17-segment model. LV ejection fraction (LVEF) was significantly higher in patients with HOCM (n = 19) than in those with nonobstructive HCM (n = 89) (P < 0.05). Both total myocardial and fibrosis masses in LV were similar in the two groups (P = 0.385 and P = 0.859, respectively). However, fibrosis in the basal septum was significantly less frequent in the HOCM group than in the nonobstructive HCM group (P < 0.01). The LVOT pressure gradient was significantly higher in the basal-septal non-fibrosis group than in the fibrosis group (23.6 +/- A 37.3 vs. 4.8 +/- A 11.4 mmHg, P < 0.01). Multivariate analysis revealed that basal-septal fibrosis was an independent negative predictor of LVOT obstruction in addition to the local wall thickness and LVEF as positive predictors in HCM patients. In conclusion, a significant association was observed between LVOT obstruction and basal septal fibrosis by LGE-CMR in HCM patients. In addition to negative impact of basal-septal fibrosis, basal-septal hypertrophy and preserved global LV contractility may be associated with the pathophysiological features of LVOT obstruction.

Background: Gliptins should have beneficial effects beyond glycemic control, potentially on the pathophysiology of cardiovascular (CV) diseases, with some basic studies demonstrating this possibility. However, we are yet to answer whether there are any direct CV effects in the clinical setting. We aimed to examine the beneficial effects of sitagliptin in Japanese patients with diabetes and high CV risk for 12 months. Methods: This was a prospective, multicenter, observational study of 205 patients with type 2 diabetes. All participants had more than one major CV risk factor and were treated with sitagliptin for 12 months. At 3 or 12 months, we examined the effects of treatment on glycemic control, CV function (by electrocardiography, echocardiography, and reactive hyperemia-peripheral arterial tonometry), and CV biomarkers. Results: Patients were predominantly elderly (68.8 +/- 9.9 years) and male (71.5 %) and typically had more than three CV risk factors (79.2 %). Treatment with sitagliptin significantly reduced the hemoglobin A1c (HbA1c) level from 7.09 % +/- 0.81 % at baseline to 6.67 % +/- 0.69 % at 3 months and 6.68 % +/- 0.73 % at 12 months (both P < 0.001). The reduction in HbA1c was also in tandem with the decrease in the level of high-sensitive C-reactive protein throughout the study. Independent of the change in HbA1c, sitagliptin reduced systolic (-7.0 +/- 18.9 mmHg) and diastolic blood pressure (-5.1 +/- 11.7 mmHg) at 12 months, and this was associated with a decrease in urinary albumin. In contrast, there were no beneficial effects on cardiac and endothelial function or on the levels of serum B-type natriuretic peptide, high-sensitive troponin T, and urinary 8-hydroxy-2'-deoxyguanosine. Conclusions: In Japanese patients with diabetes and multiple CV risk factors, sitagliptin showed a decrease in blood pressure associated with an improvement in albuminuria in addition to glycemic control.

Objective Increased left ventricular mass (LVM) and LV fibrosis mass (LVFM) are characteristics of hypertrophic cardiomyopathy (HCM). Additionally, a substantial increase in the plasma B-type natriuretic peptide (BNP) level is observed. Therefore, we investigated the interrelationship and clinical significances of these parameters in a HCM cohort that underwent cardiac MRI (CMR). Methods Patients with HCM (n=109) receiving regular outpatient treatment underwent CMR and follow-up through 2015 from CMR examinations. The clinical outcome measures were all-cause mortality, admission for worsening heart failure, and ventricular tachycardia/fibrillation. Results The baseline body mass index (BMI), LV outflow tract (LVOT) obstruction, New York Heart Association (NYHA) class, and increased left atrial dimension (LAD) index were associated with the plasma BNP level. In the CMR analysis, LVM and LVFM indices significantly correlated with the BNP level (r=0.422 and 0.368, respectively), which were independent determinants according to a multivariate analysis (p=0.009 and 0.023, respectively). A Kaplan-Meier analysis during a median follow-up of 19.4 months showed that the baseline LVM or LVFM index was not associated with the clinical outcomes. However, the baseline BNP level was significantly associated with them (p<0.001). In addition, a multivariate Cox proportional hazard analysis showed that plasma BNP was an independent predictor for the clinical outcomes after adjusting for age, sex, LVM, and LVFM. Conclusion The LVM and LVFM are determinants of the BNP level independent of the BMI, LVOT obstruction, LAD, and NYHA class in patients with HCM. However, plasma BNP may be a more sensitive integrated-marker for the clinical outcomes than LVM or LVFM.