Search

(1) Background: infective endocarditis (IE) is a significant health concern associated with important morbidity and mortality. Only limited, often monocentric, retrospective data on IE in Belgium are available. This prospective study sought to assess the clinical characteristics and outcomes of Belgian IE patients in the ESC EORP European endocarditis (EURO-ENDO) registry; (2) Methods: 132 IE patients were identified based on the ESC 2015 criteria and included in six tertiary hospitals in Belgium; (3) Results: The average Belgian IE patient was male and 62.8 ± 14.9 years old. The native valve was most affected (56.8%), but prosthetic/repaired valves (34.1%) and intracardiac device-related (5.3%) IE are increasing. The most frequently identified microorganisms were S. aureus (37.2%), enterococci (15.5%), and S. viridans (15.5%). The most frequent complications were acute renal failure (36.2%) and embolic events (23.6%). Cardiac surgery was effectively performed when indicated in 71.7% of the cases. In-hospital mortality occurred in 15.7% of patients. Predictors of mortality in the multivariate analysis were S. aureus (HR = 2.99 [1.07–8.33], p = 0.036) and unperformed cardiac surgery when indicated (HR = 19.54 [1.91–200.17], p = 0.012). (4) Conclusion: This prospective EURO-ENDO ancillary analysis provides valuable contemporary insights into the profile, treatment, and clinical outcomes of IE patients in Belgium. [ABSTRACT FROM AUTHOR]

Background Percutaneous transvenous mitral commissurotomy (PTMC) is the first-line therapy of clinically significant rheumatic mitral stenosis. While the procedure is generally safe, new onset or aggravation of mitral regurgitation (MR) may occur, mainly due to commissural splitting and, less frequently, to leaflet tear and chordal rupture. Papillary muscle rupture (PMR) is exceedingly rare in this setting. Case summary A 74-year-old woman with a history of aortic valve replacement and prior rheumatic mitral commissurotomy presented for worsening exercise intolerance and exertional dyspnoea. Transthoracic echocardiography showed a mean pressure gradient of 10 mmHg and a mitral valve area of 1.0 cm², consistent with clinically significant mitral stenosis. Subsequent PTMC was complicated by anterolateral PMR. However, the resulting MR was unexpectedly only of mild-to-moderate severity. Because of residual mitral stenosis and persisting symptoms, surgical mechanical mitral valve replacement and tricuspid annuloplasty were performed 6 weeks after PTMC. Papillary muscle rupture was confirmed during surgery. Discussion We herein describe the occurrence of PMR induced by PTMC; the resulting MR was unexpectedly of mild-to-moderate severity, as a result of extensive rheumatic lesions limiting valve mobility. This case challenges the dogma according to which PMR invariably leads to severe MR. This might not be necessarily the case when it occurs following PTMC. [ABSTRACT FROM AUTHOR]

Cardiac resynchronization therapy (CRT) decreases muscle sympathetic nerve activity (MSNA) in patients with severe congestive heart failure (CHF) and cardiac asynchrony. Whether this affects equally patients who clinically respond or not to CRT is unknown. We tested the hypothesis that the favorable effects of CRT on MSNA disappear on CRT interruption only in those who respond to CRT. Twenty-three consecutive CHF patients participated in the study, among whom 16 presented a symptomatic improvement by one or more New York Heart Association (NYHA) functional classes 15 [+ or -] 5 mo after CRT (responders), and seven had not improved after 12 [+ or -] 4 mo of CRT (nonresponders). MSNA and echocardiographic recordings were obtained in random order during atrio-right ventricular pacing (ARV), without stimulation in patients who were not pacemaker dependent (OFF, n = 17), and during atrio-biventricular pacing (BIV). Responders had a longer 6-min walking distance, a lower NYHA class and brain natriuretic peptide levels, and a better quality of life than did nonresponders (all P < 0.05). MSNA increased by 25 [+ or -] 7% in the responders, whereas it remained unchanged in the nonresponders, when shifting from the BIV mode to a nonsynchronous condition (ARV and OFF modes) (P < 0.01). Cardiac output decreased by 0.7 [+ or -] 0.2 l/min in the responders but did not change when shifting from the BIV mode to the nonsynchronous pacing mode in the nonresponders (P < 0.01). In conclusion, reversible sympathoinhibition is a marker of the clinical response to CRT. sympathetic nervous system; heart failure; muscle sympathetic nerve activity

Hypoxia has been reported to alter left ventricular (LV) diastolic function, but associated changes in right ventricular (RV) systolic and diastolic function remain incompletely documented. We used echocardiography and tissue Doppler imaging to investigate the effects on RV and LV function of 90 min of hypoxic breathing (fraction of inspired 02 of 0.12) compared with those of dobutamine to reproduce the same heart rate effects without change in pulmonary vascular tone in 25 healthy volunteers. Hypoxia and dobutamine increased cardiac output and tricuspid regurgitation velocity. Hypoxia and dobutamine increased LV ejection fraction, isovolumic contraction wave velocity (ICV), acceleration (ICA), and systolic ejection wave velocity (S) at the mitral annulus, indicating increased LV systolic function. Dobutamine had similar effects on RV indexes of systolic function. Hypoxia did not change RV area shortening fraction, tricuspid annular plane systolic excursion, ICV, ICA, and S at the tricuspid annulus. Regional longitudinal wall motion analysis revealed that S, systolic strain, and strain rate were not affected by hypoxia and increased by dobutamine on the RV free wall and interventricular septum but increased by both dobutamine and hypoxia on the LV lateral wall. Hypoxia increased the isovolumic relaxation time related to RR interval (IRT/RR) at both annuli, delayed the onset of the E wave at the tricuspid annulus, and decreased the mitral and tricuspid inflow and annuli E/A ratio. We conclude that hypoxia in normal subjects is associated with altered diastolic function of both ventricles, improved LV systolic function, and preserved RV systolic function. dobutamine; right ventricle; left ventricle; echocardiography

Byline: Guy Berkenboom, Vincent Crasset, Christophe Giot, Philippe Unger, Jean-Luc Vachiery, Jean-Louis LeClerc Abstract: The objective of this study was to examine the endothelial function of internal mammary artery in patients with coronary artery disease and in heart transplant recipients. Therefore the response of this artery to increasing concentrations of acetylcholine (1, 10, 20 [mu]g/min for 2.5 minutes each) was assessed in 6 patients in a control group, 16 patients with coronary artery disease (CAD group) matched for risk factors with 16 heart graft recipients (who underwent transplantation for nonischemic heart failure), and 12 patients with coronary artery disease and peripheral vascular disease (PVD group). Diameters of proximal and middle segments of internal mammary artery were measured by quantitative angiography. The responses to the first concentration of acetylcholine were attenuated in these three groups compared with the control group. At the highest concentration of acetylcholine the diameter increase was similar in the control and CAD groups, whereas the responses remained significantly impaired in the transplant and PVD groups. However, after selective infusion of l-arginine (30 mg/min for 11 minutes), the precursor of endothelium-derived nitric oxide, was performed, the responses to acetylcholine were restored in these two latter groups. Endothelin plasma levels were significantly enhanced in the PVD group, which exhibited the most severe impairment in acetylcholine-induced vasodilation. Thus some patients with CAD, mainly those with advanced atherosclerosis, and cardiac transplant recipients exhibit internal mammary artery endothelial dysfunction, and this abnormality seems reversible. (Am Heart J 1998;35:488-94.) Author Affiliation: Brussels, Belgium Article History: Received 10 September 1996; Accepted 8 May 1997 Article Note: (footnote) [star] From the Department of Cardiology, Erasme Hospital, Free University of Brussels., [star][star] Supported in part by research grants from the Bekales Foundation, Valduz, Liechtenstein and the 'Fondation pour la Chirurgie Cardiaque,' Brussels., a Reprint requests: G. Berkenboom, MD, Cardiology Department, Erasme Hospital, Route de Lennik 808, 1070, Brussels, Belgium., aa 0002-8703/98/$5.00 + 0 4/1/86057