Hypoxic-ischemic brain injury can affect and disturb the autonomous nervous system (ANS), which regulates various visceral systems including the gastro-intestinal and emetic system. The present study aimed to analyze the predictive value of gastric regurgitation (GReg) for neurological outcome in out-of-hospital cardiac arrest (OHCA) survivors. In this prospective, single-center study, 79 OHCA survivors treated at a university-affiliated tertiary care centre were included and GReg was measured at the first day after successful cardiopulmonary resuscitation. Neurological outcome was assessed by the Cerebral Performance Categories score at discharge. Seventy-six percent of the study population had a poor neurological outcome. GReg was found to be associated with poor neurological outcome with an adjusted OR of 5.37 (95% CI 1.41-20.46; p = 0.01). The area under the ROC curve for GReg was 0.69 (95% CI, 0.56-0.81) for poor neurological outcome. GReg on the first day after OHCA is an early, strong and independent predictor for poor neurological outcome in comatose OHCA survivors. These results are particularly compelling because measurement of GReg is inexpensive and routinely performed in critical care units.

Background: Venoarterial-extracorporeal membrane oxygenation (VA-ECMO) is a life-saving method for patients with low-output failure after cardiac surgery. However, VA-ECMO therapy may increase left ventricular afterload due to retrograde blood flow in the aorta, which may lead to progression of pulmonary congestion. We examined the predictive value of pulmonary congestion in patients that need VA-ECMO support after cardiovascular surgery. Methods: We enrolled a total of 266 adult patients undergoing VA-ECMO support following cardiovascular surgery at a university-affiliated tertiary care centre into our single-center registry. Pulmonary edema was assessed on bedside chest X rays at day 0, 3, 5 after VA-ECMO implantation. Results: Median age was 65 (57-72) years, 69% of patients were male and 30-day survival was 63%. At ICUadmission 20% of patients had mild, 54% had moderate and 26% showed severe pulmonary congestion. Pulmonary congestion at day 0 was not associated with outcome (adjusted HR 1.31; 95%-CI 0.89-1.93;P = 0.18), whereas pulmonary congestion at day 3 (adj. HR 2.81; 95%-CI 1.76-4.46;P<0.001) and day 5 (adj. HR 3.01;95%-CI 1.84-4.93;P<0.001) was significantly associated with survival. Linear regression revealed that out of left ventricular function, cardiac output, central venous saturation, maximum dobutamine and norepinephrine dose as well as fluid balance solely ECMO rotation was associated with the evolution of pulmonary congestion (P = 0.007). Conclusions: Pulmonary edema three and five days after ECMO implantation are associated with poor survival. Interestingly, a high VA-ECMO output was the most important determinant of worsening pulmonary congestion within the first five days.

The generation of harmful reactive oxygen species (ROS), including hydrogen peroxide, in out-of-hospital cardiac arrest (OHCA) survivors causes systemic ischemia/reperfusion injury that may lead to multiple organ dysfunction and mortality. We hypothesized that the antioxidant enzyme catalase may attenuate these pathophysiological processes after cardiac arrest. Therefore, we aimed to analyze the predictive value of catalase levels for mortality in OHCA survivors. In a prospective, single-center study, catalase levels were determined in OHCA survivors 48 h after the return of spontaneous circulation. Thirty-day mortality was defined as the study end point. A total of 96 OHCA survivors were enrolled, of whom 26% (n = 25) died within the first 30 days after OHCA. The median plasma intensity levels (log2) of catalase were 8.25 (IQR 7.64–8.81). Plasma levels of catalase were found to be associated with mortality, with an adjusted HR of 2.13 (95% CI 1.07–4.23, p = 0.032). A Kaplan–Meier analysis showed a significant increase in 30-day mortality in patients with high catalase plasma levels compared to patients with low catalase levels (p = 0.012). High plasma levels of catalase are a strong and independent predictor for 30-day mortality in OHCA survivors. This indicates that ROS-dependent tissue damage is playing a crucial role in fatal outcomes of post-cardiac syndrome patients.

Background Treatment with monoclonal antibodies targeting circulating proprotein convertase subtilisin-kexin type 9 (PCSK9) was found to reduce all-cause mortality in addition to cardiovascular events, suggesting pleiotropic effects. Eicosanoids are bioactive metabolites involved in cardiovascular disease and have not yet been studied in the course of PCSK9 inhibition. Methods In this prospective translational single-center study, plasma samples were collected from 64 patients before and after initiation of PCSK9 inhibitor treatment. Metabolomic analyses were performed using liquid chromatography coupled to high-resolution mass spectrometry. Results A total of 62 bioactive eicosanoids were detected. Among the metabolites, four were significantly decreased by PCSK9 inhibition after one month and remained stable after 6 months (figure): arachidonic acid (p=0.003), 12,13-DiHOME (p&lt;0.001), 9-HpODE_9.91 (p=0.007) and HpODE_7.71 (p=0.011). Phospholipase A2 levels were reduced by 40% after 1 month (p=0.003) and by additional 50% after 6 months of treatment (p=0.015), but did not correlate with eicosanoids (p=0.057). The change in arachidonic acid levels resulted in a significant increase in the ratio of omega-3 to omega-6 polyunsaturated fatty acids (p=0.002). Conclusion PCSK9 inhibition leads to significant changes in the eicosanoid profile already after one month, in particular to a downregulation of arachidonic acid. This discovery complements the presumed pleiotropic effects of PCSK9 inhibition and may provide additional benefit in the treatment of atherosclerotic disease. Funding Acknowledgement Type of funding sources: None.

Funding Acknowledgements Type of funding sources: Public hospital(s). Main funding source(s): Medical University of Vienna. Background Intensive lipid lowering after acute coronary syndromes (ACS) reduces recurrent cardiovascular events, however recent studies have shown that LDL-cholesterol goal achievement is low in patients after myocardial infarction. We compared LDL-C goal achievement in patients after ACS that were discharged with statin monotherapy or with a combination lipid lowering therapy (LLT). Methods and Results We included 227 consecutive patients with a median age of 62 (IQR 52-72) years of which 67.8% of patients were male. 59.5% of patients underwent PCI because of ST-elevation myocardial infarction (STEMI) and 40.5% because of NSTEMI. 30.4% were on LLT at time of the ACS. Median LDL-C decreased from 104.8 (IQR 75.3-139.2) mg/dL before the acute event to 52.2 (IQR 37.8-74.6) mg/dL three to six months after the myocardial infarction, resulting in 55.1% of patients on LDL-C goal of 55 mg/dL. Only 5 (2.2 %) patients were discharged without LLT and 5 (2.2 %) patients were treated with PCSK9-inhibitors. 89.4% of patients were treated with high dose and 7.5% of patients with moderate or low dose statins. Patients that were discharged on statin monotherapy (n=160, 70.5%) reached a median LDL-C of 55.0 (IQR 41.0 to 78.8) mg/dL that was significantly higher as compared to patients on combination therapy with ezetimibe (n=62, 27.3%) that was 43.0 (IQR 32.3 to 62.5) mg/dL (p&lt;0.002). The proportion of patients with statin monotherapy that reached the LDL-C goal was only 50.6% as compared to 71.0% of patients with combination therapy (p&lt;0.001). Logistic regression analysis revealed that out of age, gender, type of myocardial infarction and statin-pretreatment only baseline LDL-C (p&lt;0.005) and combination therapy (HR 4.6; p&lt;0.001) were predictors for LDL-C goal achievement. Conclusions After acute myocardial infarction, only 50.6% of patients on statin monotherapy reach the recommended LDL-C goal of 55mg/dL. LLT combination therapy with ezetimibe significantly increased the proportion of patients reaching the treatment target and should be mandatory in most of the patients after acute myocardial infarction.