Background: Percutaneous mechanical circulatory support devices are increasingly used in acute myocardial infarction complicated by cardiogenic shock (AMI-CS), despite limited evidence for their effectiveness. The aim of this study was to evaluate outcomes associated with use of the Impella device compared with intra-aortic balloon pump (IABP) and medical treatment in patients with AMI-CS. Methods: Data of patients with AMI-CS treated with the Impella device at European tertiary care hospitals were collected retrospectively. All patients underwent early revascularization and received optimal medical treatment. Using IABP-SHOCK II (Intraaortic Balloon Pump in Cardiogenic Shock II) trial inclusion and exclusion criteria, 372 patients were identified and included in this analysis. These patients were matched to 600 patients from the IABP-SHOCK II trial. The following baseline criteria were used as matching parameters: age, sex, mechanical ventilation, ejection fraction, prior cardiopulmonary resuscitation, and lactate. Primary end point was 30-day all-cause mortality. Results: In total, 237 patients treated with an Impella could be matched to 237 patients from the IABP-SHOCK II trial. Baseline parameters were similarly distributed after matching. There was no significant difference in 30-day all-cause mortality (48.5% versus 46.4%, P =0.64). Severe or life-threatening bleeding (8.5% versus 3.0%, P <0.01) and peripheral vascular complications (9.8% versus 3.8%, P =0.01) occurred significantly more often in the Impella group. Limiting the analysis to IABP-treated patients as a control group did not change the results. Conclusions: In this retrospective analysis of patients with AMI-CS, the use of an Impella device was not associated with lower 30-day mortality compared with matched patients from the IABP-SHOCK II trial treated with an IABP or medical therapy. To further evaluate this, a large randomized trial is warranted to determine the effect of the Impella device on outcome in patients with AMI-CS. Clinical Trial Registration: URL: https://www.clinicaltrials.gov . Unique identifier: NCT03313687.

In spite of their common hypersaline environment, halophilic archaea are surprisingly different in their nutritional demands and metabolic pathways. The metabolic diversity of halophilic archaea was investigated at the genomic level through systematic metabolic reconstruction and comparative analysis of four completely sequenced species: Halobacterium salinarum, Haloarcula marismortui, Haloquadratum walsbyi, and the haloalkaliphile Natronomonas pharaonis. The comparative study reveals different sets of enzyme genes amongst halophilic archaea, e.g. in glycerol degradation, pentose metabolism, and folate synthesis. The carefully assessed metabolic data represent a reliable resource for future system biology approaches as it also links to current experimental data on (halo)archaea from the literature.

IntroductionThe key event in the pathogenesis of arteriosclerosis is believed to be a dysfunction of the endothelium with disruption of vascular homeostasis, predisposing blood vessels to vasoconstriction, inflammation, leukocyte adhesion, thrombosis, and proliferation of vascular smooth muscle cells. Red blood cells (RBCs) are typically considered as shuttles of respiratory gases and nutrients for tissues, less so compartments important to vascular integrity. Patients with coronary artery disease (CAD) and concomitant anemia have a poorer prognosis after myocardial infarction, percutaneous coronary intervention, and coronary artery bypass grafting, and are more prone to developing heart failure with fatal outcomes. [1][2][3] Surprisingly, erythropoietin treatment fails to improve diagnosis, indicating that a compromised gas exchange/nutrient transport capacity of blood is insufficient to explain this outcome.Nitric oxide (NO) is an essential short-lived signaling/ regulatory product of a healthy endothelium that is critically important for vascular health. Decreased production and/or bioactivity of NO are a hallmark of endothelial dysfunction and have been shown to contribute to accelerated atherogenesis. In the cardiovascular system, NO is continuously produced in endothelial cells (ECs) by the type III isoform of NO synthase (eNOS, NOS3; EC 1.14.13.39). 4 In addition to endothelial cells, some circulating blood cells also contain eNOS.It is an accepted dogma that RBCs take up and inactivate endothelium-derived NO via rapid reaction with oxyhemoglobin to form methemoglobin and nitrate, thereby limiting NO available for vasodilatation. Yet it has also been shown that RBCs not only act as "NO sinks" but synthesize, store, and transport NO metabolic products. Under hypoxic conditions in particular, it has been demonstrated that RBCs induce NO-dependent vasorelaxation. 5,6 Mechanisms of release and potential sources of NO in RBCs are still a matter of debate, but candidates include iron-nitrosylhemoglobin, 7 S-nitrosohemoglobin, [8][9][10] and nitrite. The latter may form NO either via deoxyhemoglobin 5,11 or xanthine oxidoreductase (XOR)-mediated reduction, 6,12 or via spontaneous 12 and carbonic anhydrase-facilitated disproportionation. 13 Most of these processes show a clear oxygen-dependence, and several are favored by low oxygen tensions. The relative contribution of either mechanism to NO formation varies with oxygen partial pressure along the vascular tree. In addition, RBCs release ATP when subjected to hypoxia, providing an alternative vasodilatory pathway. 14 The publication costs of this article were defrayed in part by page charge payment. Therefore, and solely to indicate this fact, this article is hereby marked ''advertisement'' in accordance with 18 USC section 1734. 16,19 and citrulline 15,18 in the supernatant. However, Kang et al failed to measure citrulline production in RBC lysates, 20 maybe because of loss of cellular structures or cofactors important for activity. 21 Another recent study fai...

The results show a higher oxygenation potential of HBOC than with autologous stored red cells because of a more pronounced oxygen extraction.

BackgroundWhile most patients recover from suspected acute myocarditis (sAMC) some develop progressive disease with 5-year mortality up to 20%. Recently, parametric Cardiovascular Magnetic Resonance (CMR) approaches, quantifying native T1 and T2 relaxation time, have demonstrated the ability to increase diagnostic accuracy. However, prognostic implications of T2 values in this cohort are unknown. The purpose of the study was to investigate the prognostic relevance of elevated CMR T2 values in patients with sAMC.Methods and ResultsWe carried out a prospective study in 46 patients with sAMC defined by current ESC recommendations. A combined endpoint was defined by the occurrence of at least one major adverse cardiac event (MACE) and hospitalisation for heart failure. Event rate was 24% (n = 11) for 1-year-MACE and hospitalisation. A follow-up after 11 ± 7 months was performed in 98% of the patients. Global T2 values were significantly increased at acute stage of disease compared to controls and decreased over time. During acute disease, elevated global T2 time (odds ratio 6.3, p < 0.02) as well as myocardial fraction with T2 time >80 ms (odds ratio 4.9, p < 0.04) predicted occurrence of the combined endpoint. Patients with clinical recovery revealed significantly decreased T2 relaxation times at follow-up examinations; however, T2 values were still elevated compared to healthy controls.ConclusionAssessment of myocardial T2 relaxation times at initial presentation facilitates CMR-based risk stratification in patients with acute myocarditis. T2 Mapping may emerge as a new tool to monitor inflammatory myocardial injuries during the course of disease.