Characteristics and Outcomes of In-Hospital Cardiac Arrest Events During the COVID-19 Pandemic: A Single-Center Experience From a New York City Public Hospital.

BACKGROUND: Patients hospitalized for severe coronavirus disease 2019 (COVID-19) infection are at risk for in-hospital cardiac arrest (IHCA). It is unknown whether certain characteristics of cardiac arrest care and outcomes of IHCAs during the COVID-19 pandemic differed compared with a pre-COVID-19 period. METHODS: All patients who experienced an IHCA at our hospital from March 1, 2020 through May 15, 2020, during the peak of the COVID-19 pandemic, and those who had an IHCA from January 1, 2019 to December 31, 2019 were identified. All patient data were extracted from our hospital's Get With The Guidelines-Resuscitation registry, a prospective hospital-based archive of IHCA data. Baseline characteristics of patients, interventions, and overall outcomes of IHCAs during the COVID-19 pandemic were compared with IHCAs in 2019, before the COVID-19 pandemic. RESULTS: There were 125 IHCAs during a 2.5-month period at our hospital during the peak of the COVID-19 pandemic compared with 117 IHCAs in all of 2019. IHCAs during the COVID-19 pandemic occurred more often on general medicine wards than in intensive care units (46% versus 33%; 19% versus 60% in 2019; P<0.001), were overall shorter in duration (median time of 11 minutes [8.5-26.5] versus 15 minutes [7.0-20.0], P=0.001), led to fewer endotracheal intubations (52% versus 85%, P<0.001), and had overall worse survival rates (3% versus 13%; P=0.007) compared with IHCAs before the COVID-19 pandemic. CONCLUSIONS: Patients who experienced an IHCA during the COVID-19 pandemic had overall worse survival compared with those who had an IHCA before the COVID-19 pandemic. Our findings highlight important differences between these 2 time periods. Further study is needed on cardiac arrest care in patients with COVID-19.

Role of sphingomyelin synthesis in pulmonary endothelial cell cytoskeletal activation and endotoxin-induced lung injury.

Sphingomyelin (SM), a major sphingolipid in the lipid raft microdomains of the cell membrane, is synthesized by plasma membrane-bound sphingomyelin synthase 2 (SMS2). SMS2 is required for the maintenance of plasma membrane microdomain fluidity and receptor-mediated responses to inflammation in macrophages. However, the exact mechanism of SMS2 activation in endothelial barrier disruption and lung injury is not fully understood. To define the role of SMS activation in lung injury, we hypothesized that the inhibition of SM synthesis may provide protection against acute lung injury (ALI) by preserving endothelial barrier function. Using SMS2-silencing RNA (siRNA) treatment in human pulmonary endothelial cells (HPAECs) and tricyclodecan-9-yl-xanthogenate (D609), a competitive inhibitor of SMS, and phosphatidylcholine-specific phospholipase C in a murine model of bacterial LPS injury, we studied the role of sphingomyelin synthesis in ALI. Results show that pretreating mice with D609 significantly attenuated LPS-induced lung injury, as measured by a significant decrease in wet to dry ratio, bronchoalveolar lavage fluid cell and protein counts, and myeloperoxidase activity in lung tissue. Similarly, LPS-induced endothelial barrier disruption was significantly reduced in HPAECs pretreated with D609 or SMS2 siRNA, as demonstrated by an increase in paracellular integrity on an FITC-dextran assay, by the inhibition of LPS-induced stress fibers, and by the formation of cortical actin rings and lamellipodia at the periphery. These results indicate that D609 attenuates LPS-mediated endothelial barrier dysfunction and lung injury in mice through inhibition of SMS, suggesting a novel and essential role of SMS inhibition in modulating endothelial barrier integrity via actin cytoskeletal activation, with a potential therapeutic role in ALI.

Uric Acid as a potential biomarker of pulmonary arterial hypertension in patients with sickle cell disease.

Serum uric acid (UA) is emerging as a strong and independent marker for pulmonary arterial hypertension (PAH). PAH is well recognized as a life threatening complication of sickle cell disease (SCD). However, the association between UA and PAH in SCD is unknown. We reviewed electronic medical records (EMR) of 559 consecutive adult SCD patients from Kings County Hospital Center (KCHC) between January 2005 and February 2010. Patients (n = 96) with measurement of UA in close temporal proximity to the transthoracic echocardiography (TTE) were identified. PAH was defined as pulmonary artery systolic pressure (PASP) ≥30 mm Hg. Patients (n = 16) with other risk factors which may cause PAH and chronic renal insufficiency were excluded. In 18 patients, TTE could not measure PASP. Finally, 62 patients were selected. Statistical analysis was performed using Student t tests, Pearson correlation coefficient and multivariate regression analysis. Out of 62 patients, 30 had PAH. Patients with PAH had a higher UA level (8.67 ± 4.8 vs. 5.35 ± 2.1, P = 0.001). We found strong positive correlation between the UA level and PASP (r = 0.71; P < 0.0001). This correlation was independent of diuretic use. UA could be a potential marker for PAH in SCD. However, its' prognostic and pathophysiologic role in SCD patients with PAH needs to be further investigated.