SummaryIntroduction. Thrombocytopenia is frequently encountered in intensive care unit (ICU) patients. The cause of thrombocytopenia is multifactorial, it develops as a result of infection, inflammation and depletion of coagulation factors. Therefore, thrombocytopenia could potentially serve as an indicator of severity of the illness and an outcome predictor in patients with severe community-acquired pneumonia (CAP).Aim of the study. To determine incidence and predictive value of thrombocytopenia in ICU patients with severe CAP.Material and methods. We carried out a retrospective study based on clinical records from patients admitted to the Pauls Stradins Clinical University Hospital Intensive Care and Reanimation Unit from 2011 to 2014. Thrombocytopenia was defined as platelet count ≤150×109/L.Results. A total of 98 patients were included in this study, 58 (59%) men and 40 (41%) women. The mean (±SD) age of patients was 61±17.9 years, 54% died and 46% survived. 57 patients (58%) developed thrombocytopenia, in 58% it was present at the admission to ICU, and 42% developed thrombocytopenia during their stay in ICU. The lowest platelet count, in survivors was on fifth day in ICU, while in non-survivors on fourth day in ICU. Platelet count on admission to ICU (ROC AUC: 0.610, p=0.095) had lower discriminative power for ICU mortality than SOFA score (ROC AUC: 0.729, p=0.001) and CURB-65 score (ROC AUC: 0.680, p=0.006). Patients with thrombocytopenia at any point of ICU stay had higher hospital mortality in comparison to patients without thrombocytopenia. (36 (63.1%) vs 17 (41.1%), p=0.041). In thrombocytopenic patients non-resolution of thrombocytopenia during the ICU stay was associated with higher mortality (OR 5.5; 95% CI, 1.6-18.7, p=0.006). After adjusting for age, gender and SOFA score, non-resolution of thrombocytopenia remained to be an independent mortality predictor (OR 8, 95% CI 1.7-37, p=0.008)Conclusions. Thrombocytopenia is frequently encountered in patients with severe CAP. Thrombocytopenia at any point of ICU stay is associated with higher hospital mortality. Resolution of thrombocytopenia is associated with better clinical outcome.

Background: Ivabradine lowers heart rate (HR) without affecting contractility or vascular tone. It is licensed for HR control in chronic heart diseases. We performed a systematic review and meta-analyses to examine whether ivabradine could decrease major adverse cardiovascular events (MACE) and mortality in critically ill patients. Methods: We searched Medline, Embase, Cochrane Library, and Web of Science for RCTs. Trial quality was assessed using the Cochrane risk of bias tool. Random-effects meta-analyses were performed if at least three trials or 100 patients were available. Results are reported as weighted mean difference (WMD), odds ratio (OR), and 95% confidence intervals (CIs). Trial sequential analyses were performed to estimate the sample size needed to reach definitive conclusions of efficacy or futility. Results: We included 13 RCTs (n¼1497 patients). We found no evidence of an impact of ivabradine on MACE (three RCTs, 819 patients; OR¼0.77; 95% CI, 0.53e1.11) or mortality (10 RCTs, 1356 patients; OR¼1.07; 95% CI, 0.63e1.82), but sample sizes were not reached to allow definitive conclusions. Compared with placebo or standard care, ivabradine reduced HR (eight RCTs, 464 patients; WMD, e9.5 beats min À1 ; 95% CI, e13.3 to e5.8). Risk of bradycardia was not different between ivabradine and control (five RCTs, 434 patients; OR¼1.2; 95% CI, 0.60e2.38). Risk of bias was overall high or unclear. Conclusions: Ivabradine reduces HR compared with placebo or standard care. The effect on MACE or mortality in acute care remains unclear. Further RCTs powered to detect changes in clinically relevant outcomes are warranted. Clinical trial registration: Prospero CRD42018086109.

M onodentate, Semicarbazone, Thiosem icarbazone, But-2-yne, Tungsten(II) Reaction of [W I(C O )(N C M e)(dppm )(772 -M eC2M e)][BF4] {dppm = Ph2 P(C H 2 )PPh2} with an equim olar quantity of L {L = R R 'C N N H C O N H 2 (R = R ' = Me; R = H, R ' = Ph)} or L {L = R R 'C N N H C S N H 2 (R = R ' = Me, Et; R = Me, R ' = E t, Pr", Bu', Ph; R = H, R ' = Ph)} gives the m onodentately coordinated sem icarbazone or thiosem icarbazone products [W I(CO)L(dppm)(?7 2 -M eC2M e)][BF4] (1 -9 ) . 13C N M R spectroscopy suggests that the but-2 -yne ligand is donating four electrons to the tungsten in [W I(CO){H(Ph)CNN H CSN H 2 }(dppm)(?7 2 -M eC2M e)][BF4].