JDP2 overexpression provokes cardiac dysfunction in mice

The transcriptional regulator JDP2 (Jun dimerization protein 2) has been identified as a prognostic marker for patients to develop heart failure after myocardial infarction. We now performed in vivo studies on JDP2-overexpressing mice, to clarify the impact of JDP2 on heart failure progression. Therefore, during birth up to the age of 4 weeks cardiac-specific JDP2 overexpression was prevented by doxycycline feeding in transgenic mice. Then, JDP2 overexpression was started. Already after 1 week, cardiac function, determined by echocardiography, decreased which was also resembled on the cardiomyocyte level. After 5 weeks blood pressure declined, ejection fraction and cardiac output was reduced and left ventricular dilatation developed. Heart weight/body weight, and mRNA expression of ANP, inflammatory marker genes, collagen and fibronectin increased. Collagen 1 protein expression increased, and fibrosis developed. As an additional sign of elevated extracellular matrix remodeling, matrix metalloproteinase 2 activity increased in JDP2 mice. Thus, JDP2 overexpression is deleterious to heart function in vivo. It can be concluded that JDP2 overexpression provokes cardiac dysfunction in adult mice that is accompanied by hypertrophy and fibrosis. Thus, induction of JDP2 is a maladaptive response contributing to heart failure development

A922 Sequential measurement of 1 hour creatinine clearance (1-CRCL) in critically ill patients at risk of acute kidney injury (AKI)

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International recommendations for glucose control in adult non diabetic critically ill patients

The purpose of this research is to provide recommendations for the management of glycemic control in critically ill patients.Comparative StudyJournal ArticleResearch Support, Non-U.S. Gov'tSCOPUS: ar.jinfo:eu-repo/semantics/publishedPour la Société Française d'Anesthésie-Réanimation (SFAR); Société de Réanimation de langue Française (SRLF) and the Experts grou

Risk of pocket hematoma in patients on chronic anticoagulation with warfarin undergoing electrophysiological device implantation: a comparison of different peri-operative management strategies

OBJECTIVE: Periprocedural management of warfarin remains challenging in patients requiring electrophysiological device surgery. For patients at high risk of thromboembolic events, guidelines recommend bridging therapy with heparin; however, this strategy is associated with a high risk of pocket hematoma. This paper systematically reviews studies appraising the risk of pocket hematoma with different perioperative anticoagulation strategies. METHODS: All relevant studies identified in MEDLINE/PubMed, The Cochrane Collaboration CENTRAL, clinicaltrials.org and in bibliographies of key articles. Estimates were combined using a fixed effects model. Heterogeneity was assessed by p values of chi(2) statistics and I-2. Publication bias was assessed by visual examination of funnel plots and by Egger test. Fifteen studies enrolling 5911 patients met all inclusion criteria and were included in this review. RESULTS: Heparin bridging compared with no heparin was associated with increased risk of pocket hematoma (OR = 4.47, 95% CI 3.21-6.23, p < 0.00001), and prolonged hospital stay (9.13 +/- 1.9 days vs. 5.11 +/- 1.39 days, p < 0.00001). Warfarin continuation was not associated with increased pocket hematoma compared to warfarin discontinuation (p = 0.38), but was associated with reduced risk of pocket hematoma compared with heparin bridging (OR = 0.37, 95% CI 0.2-0.69, p = 0.002). Thromboembolic complications were reduced with heparin bridging vs. no heparin (0.50% vs.1.07%, p = 0.02), and no significant differences were reported between heparin bridging vs. warfarin continuation (p = 0.83). CONCLUSIONS: Heparin bridging is associated with a higher risk of pocket hematoma and a prolonged hospital stay. Perioperative continuation of warfarin reduces the occurence of pocket hematoma compared with heparin bridging without any significant differences in thromboembolic complications