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— Previously published evidence on ischemic mitral regurgitation (IMR) and its adverse prognosis after myocardial infarction has been based on the severity of IMR in the subacute or chronic period of myocardial infarction. However, the state of IMR can vary from the early stage to the chronic stage as a result of various responses of myocardium after primary percutaneous coronary intervention (PCI). Methods and Results— Standard echocardiography was serially performed in 546 consecutive patients with first-onset acute myocardial infarction (1) immediately after their arrival (pre-PCI), (2) before discharge (early post-PCI), and (3) 6 to 8 months after PCI (late post-PCI). The course of IMR after primary PCI and the prognostic impact of the IMR in each phase were investigated. IMR was found in 193/546 (35%) patients at the emergency room. In the acute phase after PCI, IMR improved in 63 patients. IMR worsened in 78 patients despite successful PCI. Shorter onset-to-reperfusion time and nontotal occlusion before PCI were the independent predictors of early improvement of IMR. In the chronic phase, IMR improved in 79 patients and worsened in 36 patients. Lower peak creatine kinase–myocardial band was an independent predictor of late improvement of IMR. IMR before PCI worsened 30-day prognosis ( P =0.02), and persistent IMR in the chronic phase worsened long-term prognosis ( P =0.04) after primary PCI. Conclusions— Degrees of IMR changed in the early and chronic phase after primary PCI for acute myocardial infarction. IMR on arrival and persistent IMR in the chronic phase worsened short-term and long-term prognosis after acute myocardial infarction, respectively.
Additional PAA might improve the WB and clinical outcomes (especially speed and extent of wound healing) in patients with CLI attributed to infrapopliteal and pedal artery disease.
Background: Mitral regurgitation is frequently complicated with atrial fibrillation without apparent organic changes in the leaflet, which occasionally improves after successful radiofrequency catheter ablation. We aimed to evaluate a possible geometric effect of radiofrequency catheter ablation on the mitral valve apparatus. Methods: Forty-three consecutive patients who underwent successful catheter ablation for persistent atrial fibrillation (maintaining sinus rhythm for 6 months after their procedure) were examined by serial real-time 3-dimensional transesophageal echocardiography before and 6 months after catheter ablation. Mitral valve complex geometry was measured using dedicated software for 3-dimensional transesophageal echocardiography. Results: Mitral valve apparatus showed significant reverse remodeling along with left atrial reverse remodeling 6 months after successful catheter ablation (50.5 [39.2–61.0] versus 36.4 [28.9–43.1] mL/m 2 ; P <0.001). The degree of mitral regurgitation decreased in a majority of patients (mitral regurgitation jet area; 1.83 [0.78–3.09] versus 0.77 [0.36–1.47] cm 2 ; P <0.001). Annular area significantly decreased (5.32±0.91 versus 4.73±0.76 cm 2 /m 2 ; P <0.001) in both anterior-posterior and medial-lateral directions. Mitral annular contraction significantly recovered after maintaining sinus rhythm for 6 months (7.51 [4.82–9.62]% versus 9.71 [6.27–13.85]%; P =0.008). There were no significant changes in tenting volume or tenting height (0.46 [0.27–0.89] versus 0.51 [0.32–0.72] mL/m 2 , P =0.744; 2.34 [1.75–3.48] versus 2.76 [1.99–3.08] mm/m 2 , P =0.717). The leaflet surface area also significantly decreased after catheter ablation (5.74 [5.01–6.33] versus 5.19 [4.63–5.64] cm 2 /m 2 ; P <0.001). Conclusions: Maintaining sinus rhythm after successful catheter ablation promotes reverse remodeling in the mitral valve apparatus and improves so-called atrial functional mitral regurgitation. The positive geometric effect of catheter ablation would be expected to be a possible contributor to better outcomes in patients with atrial fibrillation, in addition to the postprocedural freedom from rhythm disturbance.
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