Aims The EURO-ENDO registry aimed to study the management and outcomes of patients with infective endocarditis (IE). Methods and results Prospective cohort of 3116 adult patients (2470 from Europe, 646 from non-ESC countries), admitted to 156 hospitals in 40 countries between January 2016 and March 2018 with a diagnosis of IE based on ESC 2015 diagnostic criteria. Clinical, biological, microbiological, and imaging [echocardiography, computed tomography (CT) scan, 18F-fluorodeoxyglucose positron emission tomography/computed tomography (18F-FDG PET/CT)] data were collected. Infective endocarditis was native (NVE) in 1764 (56.6%) patients, prosthetic (PVIE) in 939 (30.1%), and device-related (CDRIE) in 308 (9.9%). Infective endocarditis was community-acquired in 2046 (65.66%) patients. Microorganisms involved were staphylococci in 1085 (44.1%) patients, oral streptococci in 304 (12.3%), enterococci in 390 (15.8%), and Streptococcus gallolyticus in 162 (6.6%). 18F-fluorodeoxyglucose positron emission tomography/computed tomography was performed in 518 (16.6%) patients and presented with cardiac uptake (major criterion) in 222 (42.9%) patients, with a better sensitivity in PVIE (66.8%) than in NVE (28.0%) and CDRIE (16.3%). Embolic events occurred in 20.6% of patients, and were significantly associated with tricuspid or pulmonary IE, presence of a vegetation and Staphylococcus aureus IE. According to ESC guidelines, cardiac surgery was indicated in 2160 (69.3%) patients, but finally performed in only 1596 (73.9%) of them. In-hospital death occurred in 532 (17.1%) patients and was more frequent in PVIE. Independent predictors of mortality were Charlson index, creatinine > 2 mg/dL, congestive heart failure, vegetation length > 10 mm, cerebral complications, abscess, and failure to undertake surgery when indicated. Conclusion Infective endocarditis is still a life-threatening disease with frequent lethal outcome despite profound changes in its clinical, microbiological, imaging, and therapeutic profiles.

Background-Studies of the effect of right ventricular ejection fraction (RVEF) on outcomes in heart failure (HF) are limited by small sample size and short follow-up. Methods and Results-We examined the effect of baseline RVEF on outcomes in 2008 Beta-Blocker Evaluation of Survival Trial (BEST) participants with HF and left ventricular ejection fraction Յ35% during 24 months of mean follow-up. RVEF, estimated by gated-equilibrium radionuclide ventriculography, was used to categorize patients into 4 RVEF groups: Ն40% (nϭ733), 30% to 39% (nϭ531), 20% to 29% (nϭ473), and Ͻ20% (nϭ271). Unadjusted rates for all-cause mortality in patients with RVEF Ն40%, 30% to 39%, 20% to 29%, and Ͻ20% were 27%, 32%, 35%, and 47%, respectively. When compared with patients with RVEF Ն40%, unadjusted hazard ratios and 95% confidence intervals for all-cause mortality for those with RVEF 30% to 39%, 20% to 29%, and Ͻ20% were 1.

Objectives We assessed myocardial damage in patients with chronic isolated mitral regurgitation (MR) and LV ejection fraction (EF) > 60%. Background MR patients typically have decreased LVEF after mitral valve (MV) repair despite normal pre-operative LVEF. Methods 27 patients with isolated MR had LV biopsies taken at time of MV repair. Magnetic resonance imaging with tissue tagging was performed in 40 normal subjects and in MR patients pre- and 6 months post-MV repair. Results LVEF (66 ± 1 to 54 ± 2% p<0.0001) and LV end-diastolic volume index (108 ± 5 to 78 ± 5 ml/m2 p<0.0001) decreased, while LV end-systolic volume index (ESVI) was 60% above normal pre- and post-MV repair (p<0.05). LV circumferential and longitudinal strain rates decreased below normal post-MV repair (6.38 ± 0.30 vs. 5.11 ± 0.25 p=0.0009, and 7.51 ± 0.50 vs. 5.31 ± 0.30, %RR, p<0.0001), as LVES stress (σ)/LVESVI ratio was depressed at baseline and post-MV repair vs. normals (0.25 ± 0.02 and 0.28 ± 0.01 vs. 0.33 ± 0.02, p < 0.01). LV biopsies demonstrated cardiomyocyte myofibrillar degeneration vs. normals (p=0.0016). Immunostaining and immunoblotting demonstrated increased xanthine oxidase (XO) in MR vs. normals (p<0.05). Lipofuscin deposition was increased in cardiomyocytes of MR vs. normals (0.62 ± 0.04 vs. 0.33 ± 0.04, % area, p <0.01). Conclusions Decreased LV strain rates and LVES σ/ESVI post-MV repair indicate contractile dysfunction, despite pre-surgical LVEF > 60%. Increased oxidative stress could cause myofibrillar degeneration and lipofuscin accumulation resulting in LV contractile dysfunction in MR.

Hyperuricaemia has a significant association with poor outcomes in HF patients without CKD but not in those with CKD, suggesting that hyperuricaemia may predict poor outcomes when it is primarily a marker of increased xanthine oxidase activity, but not when it is primarily due to impaired renal excretion of uric acid.