Cardiac metaiodobenzylguanidine uptake in patients with moderate chronic heart failure: relationship with peak oxygen uptake and prognosis

AbstractOBJECTIVESThis prospective study was undertaken to correlate early and late metaiodobenzylguanidine (MIBG) cardiac uptake with cardiac hemodynamics and exercise capacity in patients with heart failure and to compare their prognostic values with that of peak oxygen uptake (VO2).BACKGROUNDThe cardiac fixation of MIBG reflects presynaptic uptake and is reduced in heart failure. Whether it is related to exercise capacity and has better prognostic value than peak VO2is unknown.METHODSNinety-three patients with heart failure (ejection fraction <45%) were studied with planar MIBG imaging, cardiopulmonary exercise tests and hemodynamics (n = 44). Early (20 min) and late (4 h) MIBG acquisition, as well as their ratio (washout, WO) were determined. Prognostic value was assessed by survival curves (Kaplan–Meier method) and uni- and multivariate Cox analyses.RESULTSLate cardiac MIBG uptake was reduced (131 ± 20%, normal values 192 ± 42%) and correlated with ejection fraction (r = 0.49), cardiac index (r = 0.40) and pulmonary wedge pressure (r = −0.35). There was a significant correlation between peak VO2and MIBG uptake (r = 0.41, p < 0.0001). With a mean follow-up of 10 ± 8 months, both late MIBG uptake (p = 0.04) and peak VO2(p < 0.0001) were predictive of death or heart transplantation, but only peak VO2emerged by multivariate analysis. Neither early MIBG uptake nor WO yielded significant insights beyond those provided by late MIBG uptake.CONCLUSIONSMetaiodobenzylguanidine uptake has prognostic value in patients with wide ranges of heart failure, but peak VO2remains the most powerful prognostic index

0307 : QSOX1 has a protective role in the myocardium face to acute stress

IntroductionQSOX1 was identified as a plasma biomarker of acute heart failure (AHF). QSOX1 being a sulfhydryl oxidase, our aim was to decipher the role of QSOX1 in the heart face to an AHF event.MethodsAHF was provoked by IP injections of Isoproterenol (ISO, 300mg/kg/12h) for 2 days in mice (C57Bl/6 J) whereas control (C) received NaCl 9‰. Mice were killed at day 3, after echocardiography. QSOX1 KO (C57Bl/6 J) mice were generated using a QSOX1tm1a embryonic stem cell clone (KOMP). The KO construct contains a promoter-less lacZ gene under the control of the QSOX1 regulatory sequences. The mRNA levels were analyzed by RT-qPCR. The cellular level of oxidative stress was detected by using DHE. Fibrosis was analysed by Sirius red and collagen mRNA.ResultsAt baseline QSOX1-/- adult mice did not display any cardiac or vascular phenotype. After ISO, lacZ expression dramatically increased in QSOX1+/- hearts with the strongest β-galactosidase staining in the atria. In mice receiving ISO, a pulmonary congestion, BNP (x2 p<0.001) and CD68 (x3, p<0.001) increases were observed only in QSOX1-/-, whereas Galectin 3 increased in both groups. After ISO, the severe cardiac dysfunction in QSOX1-/- mice was associated with signs of enhanced oxidative stress (DHE staining p<0.0001). An early fibrosis was observed by Sirius red analysis and associated with an increase of collagen 1 and 3 mRNAs without difference between WT and QSOX1-/- mice.ConclusionWe provided evidence that the absence of QSOX1 leads to a more serious cardiac dysfunction in response to acute cardiac stress by ISO than in WT counterparts. Hence, our data indicated that QSOX1 protects the heart in response to acute stress

Suivi immédiat au décours d'une hospitalisation pour insuffisance cardiaque aiguë (aperçu de la "vraie vie")

PARIS7-Xavier Bichat (751182101) / SudocSudocFranceF

Effets à long terme d'une réduction isolée de la fréquence cardiaque dans l'insuffisance cardiaque chronique

PARIS6-Bibl.Pitié-Salpêtrie (751132101) / SudocPARIS-BIUM (751062103) / SudocSudocFranceF

Épidémiologie et prise en charge pharmacologique des patients souffrant d insuffisance cardiaque dans les services de cardiologie et de médecine de l hôpital Lariboisière en 2004, 2008 et 2012

La prise en charge pharmacologique des patients insuffisants cardiaques (IC) reposant sur les inhibiteurs du système rénine angiotensine, les bétabloquants et les antagonistes des minéralocorticoides n est pas optimale. A partir du PMSI et du logiciel middle care nous avons étudié les traitements de sortie des patients hospitalisés pour insuffisance cardiaque en cardiologie et en médecine à l hôpital Lariboisière en 2004, 2008 et 2012. Dans le service de cardiologie la prescription des bétabloquants est en augmentation constante sur les trois années étudiées : 55% des patients sont traités par bétabloquants en 2004, 68% en 2008 et 76% en 2012. Celle des inhibiteurs du système rénine angiotensine augmente entre 2004 et 2008 passant de 68% à 79% en 2008 pour diminuer discrètement en 2012 avec 76% des patients traités. Celle des antagonistes des minéralocorticoides est en légère baisse sur les 3 années observées, elle passe de 35% en 2004 à 34% en 2008 et à 33% en 2012. La proportion des patients traités au sein du service de médecine est inférieure à celle observée au niveau du service de cardiologie pour toutes les classes thérapeutiques étudiées pour des FEVG et des âges compagnes. La prise en charge pharmacologique des patients insuffisants cardiaques au sein du service de cardiologie de l hôpital Lariboisière est plutôt bonne et s améliore avec le temps. Le constat est moins favorable en médecine où pour une même classe d âge ou de FEVG le pourcentage de patients traités est moindre qu en cardiologieThe pharmacological management of heart failure (HF) patients based on the inhibitors of the renin angiotensin system, beta blockers and mineralocorticoid antagonists is not optimal. Using the PMSI and the middle care software we have studied treatments output of patients hospitalized for heart failure at the department of cardiology and medicine at Lariboisière Hospital in 2004, 2008 and 2012. At the service of cardiology, the prescription of beta blockers is steadily increasing for the 3 years studied: 55% of patients were treated bu beta blockers in 2004, 68% in 2008 and 76% in 2012. As for the inhibitors of the rennin angiotensin system, their prescription increased between 2004 and 2008 from 68% to 79% in 2008 and decreased in 2012 with 76% of patients treated. That of mineralocorticoid antagonists has decreased slightly overt the 3 years studied, from 35% in 2004 to 34% in 2008 and to 33% in 2012. The proportion of patients treated within the department of medicine is less than that observed at the department of cardiology for all therapeutic classes studied for FEVG and comparables ages. The pharmalogical management of heart failure (HF) patients within the department of cardiology at Lariboisière Hospital is rather goof and is improving with time. The situation is less faborable in medicine where for the same age range of FEVG, the percentage of patients treated is less than in cardiologyST QUENTIN EN YVELINES-BU (782972101) / SudocSudocFranceF

Développement préclinique de la thérapie génique du myocarde (optimisation de la délivrance in vivo et application à la surexpression d' une Ca2+-ATPase du réticulum sarcosplasmique)

PARIS7-Bibliothèque centrale (751132105) / SudocSudocFranceF

Remodelage précoce du ventricule gauche après un accident coronarien aigu

Le remodelage ventriculaire survenant à la suite d’un syndrome coronarien aigu est complexe et multiforme. Il est le fait de la réponse du myocarde aux différentes agressions intervenant au cours de ces syndromes, principalement de l’ischémie et de la nécrose du territoire en aval de l’artère occluse. Il ne faut toutefois pas négliger la responsabilité des lésions liées à la reperfusion spontanée ou provoquée des tissus ou encore liées aux embolies dans la microcirculation coronaire de divers types de cellules et de débris responsables du phénomène d’absence de reperfusion (no-reflow). Le remodelage à la phase aiguë de l’infarctus est dominé par la dilatation précoce du ventricule qui conditionne largement le pronostic tardif, la détersion de la nécrose remplacée par une fibrose cicatricielle et l’hypertrophie compensatrice associée à la fibrose des zones non infarcies survenant parallèlement. Les mécanismes cellulaires et moléculaires de ces divers aspects du remodelage sont de mieux en mieux connus, permettant d’expliquer l’effet bénéfique de nombreuses molécules déjà disponibles et offrant aussi des cibles potentielles pour de nouvelles thérapeutiques. Une valorisation de ces connaissances associée à l’identification de facteurs de risque de remodelage et à une intervention thérapeutique toujours plus précoce devrait permettre de limiter encore plus les aspects délétères de ce processus, afin d’éviter ou retarder encore l’évolution vers l’insuffisance cardiaque.Ventricular remodelling following acute coronary syndromes is both complex and multiform. It is due to the response of the myocardium to the different agressions associated with these syndromes, in particular the ischemia and necrosis downstream of the occluded artery. We must not however neglect the role of the remodelling of the lesions resulting from spontaneous reperfusion or provoked by the cells and tissues associated with coronary microcirculation embolisms and the no-reflow phenomenon. Acute post-infarct remodelling is dominated by early ventricular dilatation which largely affects late prognosis, necrosis elimination and its replacement by a fibrotic scar in parallel with a compensatory hypertrophy of the non-infarcted myocardium. The diverse cellular and molecular components of this remodelling are increasingly well-known, allowing us to better explain the beneficial effects of the currently available medications and providing us with new potential therapeutic targets. A grading of this knowledge associated with the identification of new risk factors and early therapeutic interventions should help us to further limit the deleterious aspects of this remodelling in the goal of preventing, or at least delaying, the devolution towards heart failure

Hepatopulmonary syndrome-attributed extreme hypoxemia and polycythemia revealing liver cirrhosis

International audienc

The use of natriuretic peptides in the intensive care unit

PURPOSE OF REVIEW: B-type natriuretic peptides are quantitative markers of heart failure (and/or cardiac stress) that summarize the extent of systolic and diastolic left ventricular dysfunction, valvular dysfunction, and right ventricular dysfunction. Based on the observation that heart failure is common albeit difficult to diagnose in the ICU, several studies have begun to evaluate the potential use of B-type natriuretic peptides in various ICU settings. RECENT FINDINGS: Previous pilot studies have examined the use of B-type natriuretic peptide in the differential diagnosis of hypoxemic respiratory failure, to differentiate cardiogenic from noncardiogenic shocks or to predict fluid responsiveness, to assess myocardial dysfunction and prognosis in patients with severe sepsis, and to predict ventilatory weaning failure. SUMMARY: Although previous studies were small, they highlight the potential of using B-type natriuretic peptides as a noninvasive easily available tool to quantify cardiac stress