Background: Nearly 70,000 people die of a drug overdose every year. Yet, how drug induced cardiac arrests differ from presumed cardiac etiology cardiac arrests is not well described. In animal models, asphyxial arrests resemble drug induced arrests, demonstrating better hemodynamic profiles yet worse neurologic recovery. Theoretically, this is caused by hypoxemic but preserved perfusion prior to ultimate arrest. But, this has not been studied in humans. We hypothesize that drug induced cardiac arrests will have higher incidence of return of spontaneous circulation (ROSC) in all comers, yet worse neurologic recovery among hospitalized patients. Methods: From a large institutional dataset capturing all patients with out-of-hospital cardiac arrests admitted from 2011 to 2019, we assess the prevalence and outcomes of cardiac arrests, by drug-use status. Patients were excluded if the arrest was trauma induced, occurred in an extended care facility/nursing home, or if treatment was initiated at another medical center. The primary outcome was ROSC in all comers, and the secondary outcome was favorable neurologic function among those surviving to admission. Multivariable logistic regression was used to assess factors associated with differences in outcomes, accounting for traditional cardiac risk factors and arrest characteristics. Results: In total, 436 patients (57±10 years, 31.7% female, 58.5% non-white, 49.3% hypertensive, 28.4% diabetics, and 21.1% preceding coronary disease) were identified, including 94 (21.6%) with drug induced cardiac arrest. Of that total group 101 (23.2%) survived, to admission, 26.6% of the drug induced group and 22.2% of the presumed cardiac cohort, demonstrating no difference in ROSC (P=0.32). Among those that survived to admission, 8% (2/25) of the drug induced group had a favorable neurologic outcome, compared to 29.0% (22/76) of the cardiac induced group (P= 0.03). Following adjustment, the presence of presenting drug induced cardiac arrest remained associated with lower rates of neurologic recovery [OR 7.3 (1.03-51.6) P= 0.04]. There was no difference in survival to discharge. Conclusion: Drug induced cardiac arrest is associated with worse neurologic outcomes than presumed cardiac etiology cardiac arrests.

71 Background: Esophageal adenocarcinoma (EAC) is the sixth most common cause of cancer-related deaths worldwide. It commonly arises in the setting of reflux disease and Barett’s esophagus. It remains incurable and holds a poor prognosis. Dissecting the genetic signature of EAC can pave new therapeutic avenues. Methods: We employed our Search Tag Analyze Resource (STARGEO) platform to conduct meta-analysis using the National Center for Biotechnology’s (NCBI) Gene Expression Omnibus (GEO). We tagged 151 tumor samples from EAC patients and 62 normal esophageal samples as a control. We then analyzed the signature in Ingenuity Pathway Analysis, restricting genes that showed statistical significance (p < 0.05) and an absolute experimental log ratio greater than 0.15 between tumor and control. Results: Our analysis revealed granulocyte adhesion and diapedesis and FXR/RXR signaling as top canonical pathways. TGFB1, TNF, and beta-estradiol were top upstream regulators with predicted activation. TGFB1 and TNF expression have been correlated with poor prognosis in EAC. Also, beta-estradiol has tumorigenic activity in several cancers but has not been investigated in EAC. Among the top upregulated genes were oncogenic genes such as tetraspanin 8, the antiapoptotic factor OLFM4, and the protease cathepsin E (CTSE). SPINK1, a trypsin inhibitor with recently suggested role in cancer, and the choline transporter SLC44A4, a drug target for pancreatic cancer, were also upregulated. The most downregulated genes included alcohol dehydrogenase 7, associated with EAC in alcohol-drinkers, and the pro-apoptotic gene CRCT1. We also found downregulation of the serine peptidase inhibitor SPINK7. SPINK7 is involved in maintaining epithelial-barrier integrity and is implicated in eosinophilic esophagitis pathogenesis. Lastly, there was downregulation of the candidate tumor suppressor gene transglutaminase 3. Conclusions: Despite screening efforts, EAC incidence and mortality continues to increase as does the need for better treatment. This meta-analysis defines the significant gene expression changes within causal disease processes to provide markers for detection, prognostic insight, and therapeutic value for EAC.