Faculty Bibliography

Aims/UNASSIGNED:To define outcomes of patients with COVID-19 compared to patients without COVID-19 suffering in-hospital cardiac arrest (IHCA). Materials and methods/UNASSIGNED:We performed a single-center retrospective study of IHCA cases. Patients with COVID-19 were compared to consecutive patients without COVID-19 from the prior year. Return of spontaneous circulation (ROSC), 30-day survival, and cerebral performance category (CPC) at 30-days were assessed. Results/UNASSIGNED:Fifty-five patients with COVID-19 suffering IHCA were identified and compared to 55 consecutive IHCA patients in 2019. The COVID-19 cohort was more likely to require vasoactive agents (67.3% v 32.7%, p = 0.001), invasive mechanical ventilation (76.4% v 23.6%, p < 0.001), renal replacement therapy (18.2% v 3.6%, p = 0.029) and intensive care unit care (83.6% v 50.9%, p = 0.001) prior to IHCA. Patients with COVID-19 had shorter CPR duration (10 min v 22 min, p = 0.002). ROSC (38.2% v 49.1%, p = 0.336) and 30-day survival (20% v 32.7%, p = 0.194) did not differ. A 30-day cerebral performance category of 1 or 2 was more common among non-COVID patients (27.3% v 9.1%, p = 0.048). Conclusions/UNASSIGNED:Return of spontaneous circulation and 30-day survival were similar between IHCA patients with and without COVID-19. Compared to previously published data, we report greater ROSC and 30-day survival after IHCA in COVID-19.

BACKGROUND:Thrombosis is a prominent feature of the novel Coronavirus disease 2019 (COVID-19). The incidence of thrombosis during hospitalization for non-COVID-19 viral respiratory infections is uncertain. We evaluated the incidence of thrombosis in patients hospitalized with non-COVID-19 acute viral respiratory illnesses compared to COVID-19. METHODS:Adults age >18 years hospitalized with a non-COVID-19 viral respiratory illness between 2002-2014 were identified. The primary study outcome was a composite of venous and arterial thrombotic events, including myocardial infarction (MI), acute ischemic stroke, and venous thromboembolism, as defined by ICD-9 codes. The incidence of thrombosis in non-COVID-19 viral respiratory illnesses was compared to the recently published incidence of thrombosis in COVID-19 from 3,334 patients hospitalized in New York in 2020. RESULTS:Among 954,521 hospitalizations with viral pneumonia from 2002 to 2014 (mean age 62.3 years, 57.1% female), the combined incidence of arterial and venous thrombosis was 5.0%. Acute MI occurred in 2.8% of hospitalizations, VTE in 1.6%, ischemic stroke in 0.7%, and other systemic embolism in 0.1%. Patients with thrombosis had higher in-hospital mortality (14.9% vs. 3.3%, p<0.001) than those without thrombosis. The proportion of hospitalizations complicated by thrombosis was lower in patients with viral respiratory illness in 2002-2014 than in COVID-19 (median age 64; 39.6% female) in 2020 (5% vs. 16%; p<0.001) CONCLUSION: In a nationwide analysis of hospitalizations for viral pneumonias, thrombosis risk was lower than that observed in patients with COVID-19. Investigations into mechanisms of thrombosis and risk reduction strategies in COVID-19 and other viral respiratory infections are necessary. SHORT ABSTRACT/UNASSIGNED:We evaluated the incidence of thrombosis in patients hospitalized with non-COVID-19 acute viral respiratory illnesses nationwide from 2012 to 2014 and compared this to the incidence among patients hospitalized with COVID-19 at a large health system in New York. Non-COVID-19 viral respiratory illness was complicated by acute MI in 2.8% of hospitalizations, VTE in 1.6%, ischemic stroke in 0.7%, and other systemic embolism in 0.1%. The proportion of hospitalizations complicated by thrombosis was lower in patients with viral respiratory illness in 2002-2014 than in COVID-19 (5% vs. 16%; p<0.001).

Background: Hyperoxia produces reactive oxygen species, apoptosis, and vasoconstriction, and is associated with adverse outcomes in patients with heart failure and cardiac arrest. Our aim was to evaluate the association between hyperoxia and mortality in patients (pts) receiving positive pressure ventilation (PPV) in the cardiac intensive care unit (CICU).
Method(s): Patients admitted to our medical center CICU who received any PPV (invasive or non-invasive) from 2001 through 2012 were included. Hyperoxia was defined as time-weighted mean of PaO2 >120mmHg and non-hyperoxia as PaO2 <=120mmHg during CICU admission. Primary outcome was in-hospital mortality. Multivariable logistic regression was used to assess the association between hyperoxia and in-hospital mortality adjusted for age, female sex, Oxford Acute Severity of Illness Score, creatinine, lactate, pH, PaO2/FiO2 ratio, PCO2, PEEP, and estimated time spent on PEEP.
Result(s): Among 1493 patients, hyperoxia (median PaO2 147mmHg) during the CICU admission was observed in 702 (47.0%) pts. In-hospital mortality was 29.7% in the non-hyperoxia group and 33.9% in the hyperoxia group ((log rank test, p=0.0282, see figure). Using multivariable logistic regression, hyperoxia was independently associated with in-hospital mortality (OR 1.507, 95% CI 1.311-2.001, p=0.00508). Post-hoc analysis with PaO2 as a continuous variable was consistent with the primary analysis (OR 1.053 per 10mmHg increase in PaO2, 95% CI 1.024-1.082, p=0.0002).
Conclusion(s): In a large CICU cohort, hyperoxia was associated with increased mortality. Trials of titration of supplemental oxygen across the full spectrum of critically ill cardiac patients are warranted

Background/Purpose: Patients with systemic lupus erythematosus (SLE) are at increased risk of premature atherosclerosis and thrombosis. Hydroxychloroquine (HCQ) is widely used in the treatment of SLE and has been considered of benefit for overall vascular health albeit studies to address this benefit at the cellular level have been limited. Accordingly, this study was initiated to investigate the relationship between HCQ use and dose with platelet activity, the platelet transcriptome, and vascular functional readouts.
Method(s): Patients fulfilling ACR or SLICC criteria for SLE were consecutively recruited for platelet evaluation with the only exclusion being on nonsteroidal anti-inflammatory medications, aspirin or anticoagulants. At enrollment, blood was collected for hematology analysis using the Sysmex XN-1000 analyzer, platelet aggregation via the Helena AggRAMTM system, and platelet RNA isolation and storage. Microvascular function was assessed via sublingual sidestream darkfield imaging. Brachial artery reactivity testing was used to evaluate large vessel function. Stored platelet RNA was isolated and analyzed by RNA sequencing (Illumina HiSeq4000 Sequencing).
Result(s): Among 132 SLE subjects, 108 were on HCQ. Mean age was 39.9 +/- 13.0 and 97% were female. Lupus disease activity at the time of blood draw assessed by the SELENA-SLEDAI activity index was 3.44 (range 0-20). Demographics and SLE disease activity did not differ between those on versus off HCQ (Table 1). Platelet count and size were not different between groups (Figure 1A). Platelet aggregation in response to submaximal ADP at multiple concentrations was lower in participants on HCQ (Figure 1B). Consistently, there was an inverse relationship between HCQ dosing and platelet aggregation in response to ADP (2uM: R=-0.213, P=0.037; 1uM: R=-0.310, P=0.0025; 0.4uM: R=-0.376, P=0.00018; Figure 1C). Since no subjects were on aspirin (or any other antiplatelet therapy at enrollment), aggregation in response to arachidonic acid (AA) was robust and similar between groups. However, after incubating platelets with aspirin (3mM) in vitro, platelet aggregation in response to AA was lower in the HCQ group compared to non-HCQ group (P=0.035, Figure 1B). To investigate the potential mechanisms of HCQ induced lower platelet aggregation, we evaluated platelet RNA sequencing in 49 subjects (8 no HCQ, 41 on HCQ). Positive regulation of pathways related to platelet activation (and in particular, P-selectin expression) was inversely related to HCQ, especially with higher doses (Figure 1E). In terms of vascular function, subjects on HCQ had improved microvascular function as noted by an increased proportion of sublingual capillaries filled with RBCs (P=0.011) and smaller perfused boundary region (PBR, P=0.010). HCQ dosing correlated with PBR (R=-0.599, P=0.002, Figure 1H) and RBC Filling (R=-0.592, P=0.002, Figure 1I). BART also trended positively with HCQ dose (R=0.385, P=0.094; Figure 1J).
Conclusion(s): These findings suggest that HCQ may provide benefit for vascular health in SLE as supported by ex vivo experiments demonstrating decreased platelet aggregation and downregulation of platelet functional pathways as well as improved vascular readouts