Temporal trends, outcomes, and predictors of mortality after pericardiocentesis in the United States.

BACKGROUND: Data regarding the temporal trends, outcomes, and predictors of in-hospital mortality after pericardiocentesis are limited. METHODS: The National Inpatient Sample database was used to extract hospitalizations of patients who underwent pericardiocentesis from January 2007 to September 2015. We examined the rates of in-hospital mortality, its predictors, and the temporal trends of pericardiocentesis utilization in the United States during the study period. We also examined trends and outcomes of pericardiocentesis associated with different cardiovascular procedures. RESULTS: A total of 96,377 hospitalizations with pericardiocentesis were examined. The number of pericardiocentesis procedures performed trended up significantly between 2007 and 2015 (p trend <.001), and this increase was observed predominantly in patients with unstable conditions. In-hospital mortality after pericardiocentesis decreased over time (14.6% in 2007 vs. 12.0% in 2015, p trend <.001), but remained higher than that after surgical pericardial intervention (13.1 vs. 8.9%, p value <.0001), predominantly attributable to a higher patient risk profile. Rates of in-hospital mortality were not statistically different between the procedural cohort and the nonprocedural cohort, 13.5 versus 13.0%, p value = .051. After multivariable adjustment, structural heart interventions (odds ratio [OR] 2.86; 95% confidence interval [CI] 2.35-3.49), bacterial and/or infective endocarditis (OR 2.09; 95% CI 1.72-2.54) and active neoplasms (OR 1.72; 95% CI 1.6-1.85) were independently associated with increased in-hospital mortality in pericardiocentesis patients. CONCLUSION: In this nationwide analysis, the number of pericardiocentesis procedures increased significantly over time. Structural interventions, endocarditis, and active neoplasms were associated with increased in-hospital mortality after pericardiocentesis.

Two Arabidopsis loci encode novel eukaryotic initiation factor 4E isoforms that are functionally distinct from the conserved plant eukaryotic initiation factor 4E.

Canonical translation initiation in eukaryotes begins with the Eukaryotic Initiation Factor 4F (eIF4F) complex, made up of eIF4E, which recognizes the 7-methylguanosine cap of messenger RNA, and eIF4G, which serves as a scaffold to recruit other translation initiation factors that ultimately assemble the 80S ribosome. Many eukaryotes have secondary EIF4E genes with divergent properties. The model plant Arabidopsis (Arabidopsis thaliana) encodes two such genes in tandem loci on chromosome 1, EIF4E1B (At1g29550) and EIF4E1C (At1g29590). This work identifies EIF4E1B/EIF4E1C-type genes as a Brassicaceae-specific diverged form of EIF4E. There is little evidence for EIF4E1C gene expression; however, the EIF4E1B gene appears to be expressed at low levels in most tissues, though microarray and RNA Sequencing data support enrichment in reproductive tissue. Purified recombinant eIF4E1b and eIF4E1c proteins retain cap-binding ability and form functional complexes in vitro with eIF4G. The eIF4E1b/eIF4E1c-type proteins support translation in yeast (Saccharomyces cerevisiae) but promote translation initiation in vitro at a lower rate compared with eIF4E. Findings from surface plasmon resonance studies indicate that eIF4E1b and eIF4E1c are unlikely to bind eIF4G in vivo when in competition with eIF4E. This study concludes that eIF4E1b/eIF4E1c-type proteins, although bona fide cap-binding proteins, have divergent properties and, based on apparent limited tissue distribution in Arabidopsis, should be considered functionally distinct from the canonical plant eIF4E involved in translation initiation.

Various Manifestations of 5-Fluorouracil Cardiotoxicity: A Multicenter Case Series and Review of Literature.

5-Fluorouracil is a key element to the treatment of colon cancer. But it is also one of the most cardiotoxic chemotherapies, and the management of those that experience cardiotoxicity can be challenging. We present three cases of 5-FU cardiac toxicity that manifested as myocardial infarction, cardiogenic shock, and ventricular fibrillation. Additionally, we discuss the current literature regarding 5-fluorouracil cardiotoxicity mechanisms as well as management.