Table of contentsP001 - Sepsis impairs the capillary response within hypoxic capillaries and decreases erythrocyte oxygen-dependent ATP effluxR. M. Bateman, M. D. Sharpe, J. E. Jagger, C. G. EllisP002 - Lower serum immunoglobulin G2 level does not predispose to severe flu.J. Solé-Violán, M. López-Rodríguez, E. Herrera-Ramos, J. Ruíz-Hernández, L. Borderías, J. Horcajada, N. González-Quevedo, O. Rajas, M. Briones, F. Rodríguez de Castro, C. Rodríguez GallegoP003 - Brain protective effects of intravenous immunoglobulin through inhibition of complement activation and apoptosis in a rat model of sepsisF. Esen, G. Orhun, P. Ergin Ozcan, E. Senturk, C. Ugur Yilmaz, N. Orhan, N. Arican, M. Kaya, M. Kucukerden, M. Giris, U. Akcan, S. Bilgic Gazioglu, E. TuzunP004 - Adenosine a1 receptor dysfunction is associated with leukopenia: A possible mechanism for sepsis-induced leukopeniaR. Riff, O. Naamani, A. DouvdevaniP005 - Analysis of neutrophil by hyper spectral imaging - A preliminary reportR. Takegawa, H. Yoshida, T. Hirose, N. Yamamoto, H. Hagiya, M. Ojima, Y. Akeda, O. Tasaki, K. Tomono, T. ShimazuP006 - Chemiluminescent intensity assessed by eaa predicts the incidence of postoperative infectious complications following gastrointestinal surgeryS. Ono, T. Kubo, S. Suda, T. Ueno, T. IkedaP007 - Serial change of c1 inhibitor in patients with sepsis – A prospective observational studyT. Hirose, H. Ogura, H. Takahashi, M. Ojima, J. Kang, Y. Nakamura, T. Kojima, T. ShimazuP008 - Comparison of bacteremia and sepsis on sepsis related biomarkersT. Ikeda, S. Suda, Y. Izutani, T. Ueno, S. OnoP009 - The changes of procalcitonin levels in critical patients with abdominal septic shock during blood purificationT. Taniguchi, M. OP010 - Validation of a new sensitive point of care device for rapid measurement of procalcitoninC. Dinter, J. Lotz, B. Eilers, C. Wissmann, R. LottP011 - Infection biomarkers in primary care patients with acute respiratory tract infections – Comparison of procalcitonin and C-reactive proteinM. M. Meili, P. S. SchuetzP012 - Do we need a lower procalcitonin cut off?H. Hawa, M. Sharshir, M. Aburageila, N. SalahuddinP013 - The predictive role of C-reactive protein and procalcitonin biomarkers in central nervous system infections with extensively drug resistant bacteriaV. Chantziara, S. Georgiou, A. Tsimogianni, P. Alexandropoulos, A. Vassi, F. Lagiou, M. Valta, G. Micha, E. Chinou, G. MichaloudisP014 - Changes in endotoxin activity assay and procalcitonin levels after direct hemoperfusion with polymyxin-b immobilized fiberA. Kodaira, T. Ikeda, S. Ono, T. Ueno, S. Suda, Y. Izutani, H. ImaizumiP015 - Diagnostic usefullness of combination biomarkers on ICU admissionM. V. De la Torre-Prados, A. Garcia-De la Torre, A. Enguix-Armada, A. Puerto-Morlan, V. Perez-Valero, A. Garcia-AlcantaraP016 - Platelet function analysis utilising the PFA-100 does not predict infection, bacteraemia, sepsis or outcome in critically ill patientsN. Bolton, J. Dudziak, S. Bonney, A. Tridente, P. NeeP017 - Extracellular histone H3 levels are in...

Aims We investigated the association between left ventricular (LV) torsional deformation and vascular dysfunction, fibrosis, neurohumoral activation, and exercise capacity in patients with normal ejection fraction Methods and results In 320 newly‐diagnosed untreated hypertensive patients and 160 controls, we measured: pulse wave velocity (PWV); coronary flow reserve (CFR) by Doppler echocardiography; global longitudinal strain and strain rate, peak twisting, the percentage changes between peak twisting, and untwisting at mitral valve opening (%dpTw – UtwMVO), at peak (%dpTw – UtwPEF), and the end of early LV diastolic filling (%dpTw – UtwEDF) by speckle tracking imaging; transforming growth factor (TGFb‐1), metalloproteinase‐9 (MMP‐9), tissue inhibitor of matrix metalloptoteinase‐1(TIMP‐1), markers of collagen synthesis, and N‐terminal pro‐brain natriuretic peptide (NT‐proBNP). Oxygen consumption (VO2), measured by means of cardiopulmonary exercise test, was assessed in a subset of 80 patients. The PWV, CFR, longitudinal strain and strain rate, %dpTw‐UtwMVO, %dpTw‐UtwPEF, and %dpTw‐UtwEDF were impaired in hypertensive patients compared with controls. In multivariable analysis, CFR, PWV, LV mass, and systolic blood pressure were independent determinants of longitudinal strain, strain rate, and untwisting markers (P < 0.05). Increased TGFb‐1 was related with increased collagen synthesis markers, TIMP‐1 and MMP‐9 and these biomarkers were associated with impaired longitudinal systolic strain rate, untwisting markers, CFR and PWV (P < 0.05). Delayed untwisting as assessed by reduced %dpTw – UtwEDF was related with increased NT‐proBNP and reduced VO2 (P < 0.05). Conclusions Impaired LV untwisting is associated with increased arterial stiffness and coronary microcirculatory dysfunction, and is linked to reduced exercise capacity and neurohumoral activation in hypertensive heart disease. A fibrotic process may be the common link between vascular dysfunction and abnormal myocardial deformation.

Background-Interleukin-6 (IL-6) and macrophage colony stimulating factor plasma levels are elevated in acute coronary syndromes. IL-6 has an inherent negative inotropic action and, with tissue factor (TF), mediates the ischemiareperfusion myocardial injury. We hypothesized that inducible ischemia leads to cytokine production, TF expression, and consequently persistent left ventricular dysfunction after dobutamine stress echocardiography (DSE) in coronary artery disease patients. Methods and Results-DSE was performed in 103 patients with angiographically documented coronary artery disease.Blood samples were obtained at rest, at peak stress, and 30 minutes after cessation of dobutamine infusion for measurement of macrophage colony stimulating factor, IL-6, and TF. New or worsening wall motion abnormalities at peak stress and their duration into recovery were noted. Median IL-6 and TF levels were increased at peak stress and at 30 minutes into recovery compared with rest (2.7 and 2.4 versus 2.1 pg/mL for IL-6, 310 and 385 versus 266 pg/mL for TF [PϽ0.01] in patients with an ischemic response; nϭ55). Compared with rest, a greater release of IL-6 at peak stress and recovery was observed in patients with increasing number of ischemic segments at peak DSE (2 versus 3 to 4 versus 5 to 6 versus 7 to 8 segments; Pϭ0.03). The time to recovery of wall motion abnormalities was also associated with IL-6 levels at peak stress and recovery (rϭ0. 51 and rϭ0.39, PϽ0.05). Macrophage colony stimulating factor levels remained unchanged throughout DSE. Conclusions-Reversible ischemia induced during DSE increases IL-6 and TF plasma levels. IL-6 is related to the extent of left ventricular dysfunction at peak stress and to persistent LV dysfunction during recovery. (Circulation. 2005;112: 3272-3279.)

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Popov S, Venetsanou K, Chedrese PJ, Pinto V, Takemori H, Franco-Cereceda A, Eriksson P, Mochizuki N, Soares-da-Silva P, Bertorello AM. Increases in intracellular sodium activate transcription and gene expression via the salt-inducible kinase 1 network in an atrial myocyte cell line. Am J Physiol Heart Circ Physiol 303: H57-H65, 2012. First published March 30, 2012 doi:10.1152/ajpheart.00512.2011.-Cardiac hypertrophy (CH) generally occurs as the result of the sustained mechanical stress caused by elevated systemic arterial blood pressure (BP). However, in animal models, elevated salt intake is associated with CH even in the absence of significant increases in BP. We hypothesize that CH is not exclusively the consequence of mechanical stress but also of other factors associated with elevated BP such as abnormal cell sodium homeostasis. We examined the effect of small increases in intracellular sodium concentration ([Na ϩ ]i) on transcription factors and genes associated with CH in a cardiac cell line. Increases in [Na ϩ ]i led to a timedependent increase in the expression levels of mRNA for natriuretic peptide and myosin heavy chain genes and also increased myocyte enhancer factor (MEF)2/nuclear factor of activated T cell (NFAT) transcriptional activity. Increases in [Na ϩ ]i are associated with activation of salt-inducible kinase 1 (snflk-1, SIK1), a kinase known to be critical for cardiac development. Moreover, increases in [Na ϩ ]i resulted in increased SIK1 expression. Sodium did not increase MEF2/ NFAT activity or gene expression in cells expressing a SIK1 that lacked kinase activity. The mechanism by which SIK1 activated MEF2 involved phosphorylation of HDAC5. Increases in [Na ϩ ]i activate SIK1 and MEF2 via a parallel increase in intracellular calcium through the reverse mode of Na ϩ /Ca 2ϩ -exchanger and activation of CaMK1. These data obtained in a cardiac cell line suggest that increases in intracellular sodium could influence myocardial growth by controlling transcriptional activation and gene expression throughout the activation of the SIK1 network.hypertension; cardiac hypertrophy; Na ϩ ,K ϩ -ATPase; ion gradients CARDIAC HYPERTROPHY IS CONSIDERED to be the heart's response to sustained mechanical stress caused by either obstruction of cardiac outflow (valve stenosis) or elevated systemic arterial blood pressure. At the molecular level, its development involves the activation of numerous genes and transcription factors (9, 18, 30) that ultimately lead to abnormal myocardial growth. Hypertension is presently one of the major causes of cardiac hypertrophy. Although systemic hypertension has multiple causes, it ultimately results from the kidney's inability to maintain sodium homeostasis after normal or excessive sodium intake (1, 16). Whereas a sustained increase in systemic blood pressure is likely to influence the development of cardiac hypertrophy, it has also been demonstrated that high salt intake is associated with left ventricle hypertrophy even without significant increases in systemic blood pr...

Objective: A number of different hormone changes have been described during the acute myocardial infarction (AMI), including those of the non-thyroidal illness syndrome (NTIS). Design and methods:We assessed the alterations of serum thyroid hormones, cytokines and cortisol levels in 30 patients with a first episode of AMI 4, 24, 48 h and 10 days (240 h) after the onset of the chest pain and we investigated the possible relationship of these alterations with the severity of AMI. Results: Fifteen patients had left ventricular ejection fraction (LVEF) Յ 50% (group I) and 15 patients had LVEF > 50% (group II). A transient decrease of total tri-iodothyronine (T 3 ), more prominent in group I (P < 0.05, t-test) with a concomitant rise of reverse T 3 (rT 3 ) occurred at 24 h. Total thyroxine (T 4 ), free T 4 (FT 4 ) and free T 4 index did not change significantly, but tended to be higher in group I patients, whereas TSH significantly increased in group II at 48 h. Interleukin-6 (IL-6) increased significantly at 24 h only in group I and declined thereafter (24 vs 240 h, P < 0.001) and this temporal change of IL-6 was associated with similar changes of creatine phosphokinase and creatine kinase isoenzyme MB (CK-MB). Tumor necrosis factor-a and IL-1b remained low in both groups. Cortisol was higher at 4 h and in 12 patients was above the normal values. Negative correlation was found between LVEF and IL-6 (P < 0.001), whereas T 3 , T 4 or cortisol levels were not correlated with the LVEF. Conclusions: Our data indicate that NTIS, in association with increase of IL-6, occurs in the early postinfarction period. In the NTIS following AMI the high level of IL-6 is the best predictor, among several parameters, of the severity of AMI as assessed by the LVEF and the rise of CK-MB.