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.

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Background: The early diagnosis and treatment of heart failure in β-thalassaemic patients is related to survival. Iron alone or in combination with other factors causes diastolic dysfunction, which usually precedes systolic dysfunction. NT-proBNP is a sensitive biomarker of ventricular dysfunction. Aim: To evaluate NT-proBNP in non heart failure β-thalassaemic patients. Methods: Fifty-two β-thalassaemia major patients (mean age: 27.2 ± 12.5 years) with normal LV systolic function, underwent NT-proBNP measurement and a thorough Doppler-echocardiographic and pulsed tissue-Doppler study, 4 days following blood transfusion. Fifty-two age matched healthy controls were also studied. Results: NT-proBNP and E/E′ ratio were increased in thalassaemic patients compared with controls [(469 ± 171 vs 262 ± 51 pmol/l, p < 0.001) and (10.8 ± 4.0 vs 6.6 ± 1.1, p < 0.001)] and were well correlated (r: 0.54, p < 0.01). Although NT-proBNP levels were increased in patients with higher E/E′ ratios (E/E′ < 8: 354 ± 119, 8-15: 516 ± 177, > 15: 565 ± 114 pmol/l, ANOVA p: 0.002) this increase only became statistically significant in the 3rd decade of life, while E/E′ ratio increased in the 4th decade. Conclusion: NT-proBNP increases in β-thalassaemia major patients and is related to age and LV diastolic dysfunction. NT-proBNP appears to be an early biomarker of LV diastolic dysfunction, compared with the conventional Echo-Doppler indexes.

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Inadvertent implantation of a pacemaker lead in the left ventricle is an uncommon complication. We report a case of a permanent pacemaker lead inadvertently placed through the left subclavian artery, across the aortic valve into the left ventricle. A chest X-ray one month after the procedure showed an unusual course of the lead and a 12-lead ECG and a transthoracic echocardiogram confirmed the diagnosis. The patient refused surgical removal and remained on full anticoagulation. No clinical events were recorded during a 3-year follow-up. In such cases we propose life-long full anticoagulation as an alternative to surgical lead extraction.

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Deposition of amyloid in the atria (isolated atrial/cardiac amyloid) is fairly common in the aging heart. It consists of amyloid fibrils, formed both by atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) and the precursor molecule of ANP, proANP. This study examines whether amyloidogenic determinants (short peptides/amyloid forming favoring regions) exist in the sequence of NT-proBNP, the N-terminal part of proBNP, and if these determinants form amyloid-like fibrils in vitro. We have predicted a possible amyloidogenic determinant in the sequence of the NT-proBNP, and we conclusively show, after its synthesis, that it forms amyloid-like fibrils in vitro, utilizing transmission electron microscopy, X-ray diffraction, attenuated total reflectance Fourier-transform infrared spectroscopy, and polarizing microscopy. Thus, for the first time, in this study, a possible biological role is attributed to a certain, specific part of this important cardiac prohormone/natriuretic peptide, which acts as an important biomarker indicative of heart failure. Its possible direct involvement in isolated cardiac amyloidosis, atrial fibrillation, and other types of cardiac amyloidoses is indicated and discussed. Since these cardiac hormones and their prohormones play key roles in cardiovascular homeostasis through natriuresis, diuresis, vasorelaxation, and inhibition of renin and aldosterone secretion (pathophysiology of hypertension and cardiovascular regulation), we also try to suggest these specific, short peptides as possible future structural targets of efforts toward inhibiting formation of natriuretic peptide(s) amyloid.

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