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Introduction: Severe acute respiratory syndrome-coronavirus-2 (SARS-CoV-2) exhibits 25-30% mortality in hospitalized patients with heart failure (HF). Cardiovascular disease is the most significant comorbidity associated with increased mortality in COVID-19 patients with data suggesting local and systemic inflammation play a critical role in cardiac functional abnormalities. SARS-CoV-2 vaccination reportedly reduces severity of infection. We sought to characterize if vaccination had any protective effect on patients with HF hospitalized for acute COVID-19. Hypothesis: Baseline cardiac biomarkers including CRP, ferritin, high sensitivity cardiac troponin I (hs-cTnI), and pro-brain natriuretic peptide (pBNP) may be lower in vaccinated COVID-19 HF patients revealing the impact of vaccination on reducing inflammation by SARS-CoV-2 infection. Method(s): Electronic health records underwent IRB exempted extraction of demographics, anthropometrics, vital signs, laboratory tests, and ICD-10-CM-based Elixhauser comorbidity categories. Continuous data summarized with median [IQR] were compared using Kruskal-Wallis test and discrete data with chi-squared test. Result(s): Among HF patients with a recorded vaccine status admitted between July 3, 2021 and March 17, 2022, 206 underwent acute COVID-19 hospitalization. Vaccinated (n=91, 44%) and unvaccinated (115, 56%) patients exhibited statistically similar distribution of males (56%), aged 78[69-86] years with comorbidities 5[4-7] distributed across Whites (88%), Blacks (8%), and other races (4%). There were no intergroup differences with most prevalent comorbidities at admission including hypertension (99%), diabetes (41%), chronic pulmonary disease (37%), obesity (36%), deficiency anemia (31%), and renal failure (25%). There were no intergroup differences in initiation of COVID-19 directed treatments. Baseline biomarkers in vaccinated versus unvaccinated were CRP 6.0[1.3-9.5] vs. 6.9[2.7-11.3] mg/dL (p=.25), ferritin 171[76-552] vs. 432[79-876] ng/mL (p=.13), LDH 245[192-317] vs. 338[260-439] U/L (p=.003), D-dimer 0.89[0.53-1.73] vs. 1.36[0.95-2.80] mg/L FEU (p=.06), hs-cTnI 27[14-67] vs. 28[16-81] ng/L (p=.39), and pro-BNP 3487[1516-7162] vs. 3278[1549 vs. 9001] pg/mL (p=.90). Clinical visit criteria respectively were hospital LOS 4.9[2.9-10.3] vs. 5.4[3.4-10.3] days (p=.27), ICU admission 10% vs. 17% (p=.15), and discharge disposition expired or Hospice 15% vs. 16% (p=.48). Rehospitalization occurred similarly between groups and was not significant. Conclusion(s): Acute and chronic inflammation are pathogenic drivers of HF. Inflammatory biomarkers lower among vaccinated patients with HF included CRP, ferritin, D-dimer, and hs-cTnI, although not significant. LDH, however, was significantly lower suggesting improved host widespread tissue perfusion as one mechanism of reduced severity in patients with HF undergoing SARS-CoV-2 vaccine breakthrough infection. One study caveat is that despite inclusion of all patients, these preliminary findings are likely not sufficiently powered to validate our hypothesis.Copyright © 2022
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Background: The impact of SARS-CoV-2 infection on intrinsic myocardial conduction continues to be an area of focus amongst the medical community. Our objective was to investigate if specific myocardial conduction abnormalities were independently associated with mortality in patients hospitalized with COVID 19. Method(s): Under IRB exemption, the electronic medical records of COVID-19 patients (N=3840) undergoing index hospitalization were reviewed to extract presentation ECG conduction data, demographics, and laboratory results (within 8h). This patient cohort was then separated into two groups based on mortality vs. no mortality (N=520). Logistical regression was used to test association of ECG conduction intervals with mortality. A subgroup analysis of 651 patients who underwent at least 1 ECG in the 12 months prior to their COVID hospitalization were analyzed to detect statistically significant differences in conduction intervals pre and post SARS-CoV-2 infection. Result(s): According to our nominal logistic fit for hospital mortality, Heart Rate (HR) >100 (p=0.0007;LW 4.14), QRS duration > 120 ms (p=0.0053;LW 2.27), and QTc prolongation (defined as QTc > 450ms in males;QTc > 460ms in females) (p=0.0089;LW 2.04) were independently associated with higher risk of mortality. LogWorth (LW) calculations were included in an effort to estimate the proportional effect each variable has on overall mortality. LW > 2 were shown to be statistically significant with p< 0.05 with HR > 100 (LW 4.14) having the highest proportional effect on mortality followed by QRSd (LW 2.27) then QTc prolongation (LW 2.04). PR interval> 200ms (p=0.30) and QRS axis (p=0.15) were not associated with higher risk of mortality. Our subgroup analysis of the 651 patients mentioned above yielded no statistically significant differences in conduction intervals pre & post SARS-CoV-2 infection. Conclusion(s): : Amongst our patient cohort, HR > 100, QRSd > 120ms, and QTc prolongation (QTc > 450 in males;QTc > 460 in females) were each independently associated with higher risk of mortality in patients hospitalized with COVID 19. Subgroup analysis of 651 patients showed no statistically significant differences in conduction intervals pre and post SARS-CoV-2 infection. These findings support the use of objective ECG data in risk stratifying patients hospitalized with COVID 19.Copyright © 2022
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INTRODUCTION: Serum albumin (ALB) is inversely associated with COVID-19 severity through an unclear mechanism. We addressed this gap using machine learning to identify traits exhibiting explanatory variance (EV%) in mortality risk within 12h of admission versus near end of hospitalization in the context of hypoalbuminemia. METHOD(S): Data were extracted under IRB exemption from medical records of COVID-19 patients at least 18 years old in the ICU with at least two ALB measures from March 2020 through September 2021. ALB, COVID-19 inflammation and injury traits were characterized across hospitalization. Hypoalbuminemia present on admission (POA) was defined as ALB < 3.2 g/dL. Traits associated with mortality were controlled for age, sex, COVID-19 directed treatment and the four COVID surges. Bootstrap Forest (BF) evaluated EV% of traits in mortality. Continuous data were compared using KruskalWallis. Discrete data were compared with chi-squared test. RESULT(S): Among 878 patients, 631 (72%) vs. 247 (28%) POA respectively with ALB < 3.2g/dL vs. >3.2g/ dL. Median age 68(57,77) years distributed across 64% males with 75% Whites, 10% Blacks and 15% other races exhibiting hypertension (53%), coagulopathy (28%), chronic pulmonary disease (22%) and heart failure (22%). Excess comorbidity associated with hypoalbuminemia included obesity (48% vs. 38%, p=.004), anemias (42% vs. 28%, p<.0001), and diabetes (39% vs. 32%, p=.03). Respective hypoalbuminemia near end of hospitalization increased to 97% (p<.0001) and 84% (p<.0001) with hospital mortality of 51% vs. 31% (p=<.0001). Associated ALB declines were 0.5(0.1, 1.0) vs. 1.0 (0.6, 1.0) g/dL. BF modeling (RSquared=0.69) identified POA traits EV% including CRP (21%), AST/SGOT (11%), proBNP (9%), WBC (9%), and ferritin (9%) among others. BF modeling (RSquared=0.84) identified near end visit traits EV% including WBC (31%), CRP (13%), platelet (12%), and ANC (11%) among others. CONCLUSION(S): The EV% of CRP at presentation corroborates an inverse relationship with ALB suggesting acute phase signaling may evoke hypoalbuminemia. Specifically, increased endothelial permeability allowing ALB extravasation as evidenced by proBNP EV%. Secondary etiology may derive from inhibited albumin synthesis secondary to liver injury as suggested by AST/SGOT at presentation and visit end.
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SESSION TITLE: ECMO and ARDS in COVID-19 Infections SESSION TYPE: Rapid Fire Original Inv PRESENTED ON: 10/17/2022 12:15 pm - 1:15 pm PURPOSE: Inhaled nitric oxide (iNO) is a potent vasodilator of pulmonary vasculature improving perfusion to ventilated alveoli in ARDS and other lung pathologies. During the pandemic, intensivists turned to iNO as “salvage” therapy in COVID-19 patients. Rationale was driven by vasodilatory effect and antiviral properties despite lack of evidence of clear benefit even in patients without COVID. We hypothesized that iNO would provide reduced increases in pulmonary perfusion and subsequent gas exchange improvement in COVID-19 patients due to extensive endothelial damage and coagulopathy throughout the pulmonary vasculature. METHODS: Our IRB exempt analysis examined patients hospitalized with and without COVID-19 from January 2020 to September 2021 who received at least 24h of invasive mechanical ventilation with iNO (15-20ppm). Effectiveness outcomes were PaO2/FIO2 ratio(PFR), PEEP/CPAP level, and PaCO2 serially measured and observed up to 24 hours prior to initiation of iNO and for up to 120h post iNO administration. Data were statistically controlled for age, sex, race, time to initiation of therapy and COVID-19 directed treatment. RESULTS: From January 2020 and September 2021, 42 patients were admitted to the ICU and received invasive mechanical ventilation and iNO. Results are sequenced as ARDS COVID-negative, ARDS COVID-positive, viral pneumonia COVID-negative, viral-pneumonia COVID-positive. Patient n = 8/14/6/14. Median age was 56/55/63/62 years. Demographics split 64-62% male vs 36-38% female in ARDS without/with COVID, 50%/83% male vs 50%/17% female in viral pneumonia without/with COVID. Racial distribution resulted 75%/93%/86%/83% White vs 25%/0%/17%/14% Black. Other races constituted less than 7% of patient total in any category. PFR delta from -24h to +120h post-iNO = +35/+35/+41/+22. PEEP/CPAP delta from -24h to +120h = -4/-1/-3/-2. PaCO2 delta mmHg from -24h to +120h = -21/-23/-9/-13. Median Hospital LOS = 26/26.5/17/19 days. Median ICU LOS = 15.8/19.0/13.8/17.6 days. Hospital mortality = 100% across all 4 subgroups. CONCLUSIONS: ARDS patients with or without COVID showed similar rates of PFR response to iNO, however viral pneumonia patients with COVID exhibited a blunted PFR response vs those without COVID. No statistically significant difference was observed with respect to PEEP/CPAP levels, PaCO2 mmHg, hospital or ICU LOS, or mortality. CLINICAL IMPLICATIONS: Our findings suggest that the presence of COVID-19 did not significantly inhibit response to iNO in ARDS or other viral pneumonia patients. Further evaluation of other indirect markers of gas exchange could provide further evidence of responsiveness. DISCLOSURES: No relevant relationships by Katherine Burns No relevant relationships by Karen Hamad No relevant relationships by Bobby Malik No relevant relationships by Richard Walo Jr No relevant relationships by Wilhelmine Wiese-Rometsch No relevant relationships by Stephanie Williams
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SESSION TITLE: Critical Care Management of COVID-19 SESSION TYPE: Original Investigations PRESENTED ON: 10/17/2022 01:30 pm - 02:30 pm PURPOSE: We hypothesized that supplementation of NIH recommended remdesivir (REM) and dexamethasone (DEX) combination treatment with tocilizumab (TOCI) or baricitinib (BARI) initiated inside 48h of index hospitalization would enhance reduction of inflammatory markers and discharges to home in adults over 18 years old who received intensive care. METHODS: Electronic medical record data were extracted under IRB exemption. Treatment responsiveness was estimated using delta in C-reactive protein (CRP), ferritin, lactate dehydrogenase (LDH) and D-dimer levels from assays respectfully respectively first within 24h and last between 25-72h of initiating REM/DEX with vs without TOCI or BARI. Confounder balanced multigroup contrasts were significant when p<.017. RESULTS: Between March 10, 2020 and January 31, 2022, 891 COVID-19 patients were admitted to the ICU with 459 receiving REM/DEX (n=326) or supplemented with BARI (n=85) or TOCI (n=41). Results are sequenced as REM/DEX, REM/DEX/BARI, REM/DEX/TOCI. Age was 67[57,77] (p<.0001) vs. 61[51,69] and 62[48,68] among statistically similar sex (male, 65%;female, 35%) and race (White, 76%;Black, 8%;Other, 16%) distributions and BMI (32[27,38] kg/m2). Hypertension (70%), obesity (59%), diabetes (38%), deficiency anemia (36%), coagulopathy (29%) chronic pulmonary disease (22%), and renal failure (17%) were similarly distributed. Initial CRP, ferritin, LDH and D-dimer levels -24h to +24h of REM/DEX first dose respectively were 12.1[7.1,18.2], 11.4[7.5,15.7], 14.0[11.2,21.0] mg/dL;811[441,1390], 1178[529,1956], 1110[653,1810] ng/mL (REM/DEX, p=.013);437[321,576], 516[403,695], 518[397,692] U/L (REM/DEX, p=.0001);and 1.02[0.67,2.28], 0.97[0.72,1.88], 1.47[0.86,2.19] ug/mL. Responsiveness quantified using last levels 25h-72h post REM/DEX first dose respectively included -3.4[-7.2,-0.6], -4.3[-7.7,-1.9], -7.2[-10.1,-3.6] mg/dL (REM/DEX/TOCI, p=.014);7[-125,202], -94[-329,69], -29[-181, 535] U/L;-3[-74,80], 85[-58,273], -33[-188,-3] U/L (p=.051);and 0.00[-0.50,1.05], 0.88[-0.45,10.52], -0.01[-0.38,0.50] ug/mL. ICU length of stay (LOS) was 6[3,13], 6[3,12], 8[5,15] days (p<.00001) with hospital LOS of 16[10,24], 20[12,33], 17[11,23] days (REM/DEX/BARI, p<.021). Hospital mortality was 51%, 71%, 43%, with REM/DEX/BARI exhibiting increase (p=.0019), but REM/DEX/TOCI numerically lowest (p>.017). Discharge to home was 24%, 18%, 43%, with REM/DEX/TOCI demonstrating increase (p=.0038). CONCLUSIONS: REM/DEX/TOCI combination therapy provided largest reduction of inflammatory markers and mortality while substantially increasing percentage of discharges to home. REM/DEX treatment responsiveness was adversely impacted by addition of baricitinib, while augmented by tocilizumab. CLINICAL IMPLICATIONS: Our findings highlight need to refine early longitudinal biomarker-tracking to identify patient-centric COVID-19 treatment responsiveness to COVID-19 directed treatments. DISCLOSURES: No relevant relationships by Qassem Abdelal No relevant relationships by Kevin Dawkins No relevant relationships by Karen Hamad No relevant relationships by Natalia Lattanzio No relevant relationships by Richard Walo Jr No relevant relationships by Wilhelmine Wiese-Rometsch No relevant relationships by Stephanie Williams
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BACKGROUND: COVID-19 patients at hospitalization exhibit heterogeneous risk factors putatively associated with hospital mortality. However, stability of risk stratification across readmission (ReAdm) remains unclear. We evaluated longitudinal patterns in presentation clinical traits at index COVID-19 hospitalization and subsequent ReAdm(s). METHODS: Under IRB exemption, discharge electronic medical records underwent extraction of presentation demographics, anthropometrics, laboratory results, and ICD-10 codes. Univariate logistic regression was used to test association (p<.05) of putative clinical traits with COVID-19 hospitalization mortality. Continuous data summarized with median [IQR] were compared using Kruskal-Wallis K statistic. Discrete data summarized as counts or proportions were compared with chi-squared test. Confounders statistically balanced included age, sex, race, comorbidities, and attendant local 4-surges of pandemic. Statistical significance was Bonferroni corrected for multiple contrasts at .017. RESULTS: Among patients discharged alive not to hospice between March 18, 2020 and September 30, 2021, 4430 underwent index COVID-19 hospitalization. Incident with at least one subsequent ReAdm was experienced respectively by 630 and 166 patients. There was no difference in median age 76 [62,85] years among 45% woman distributed across Whites (82%), Blacks (9%) and other races (9%). Time to incident and first subsequent ReAdm respectively was 14 [4,59] vs 21 [6,54] days. Prominent comorbidity prevalence sustained included hypertension (54%), diabetes (34%), chronic pulmonary disease (29%), obesity (24%), and coagulopathy (15%). Significant differential comorbidity prevalence manifested sequentially with deficiency anemias (26%, 32%, 49%) and heart failure (23%, 28%, 38%). Notable at two or more ReAdms and consistent with some comorbidity patterns, is significantly worsening hypoalbuminemia, anemia, neutropenia with increasing creatinine, pBNP and D-dimer. CONCLUSIONS: Patients undergoing ReAdm demonstrated that characterizing trends in SARS-CoV-2 evoked clinical traits may reveal mitigable features of post-acute COVID-19 syndrome. Evaluating linkage between biomarkers and comorbidities across ReAdm patterns can identify those of value for estimating a given outcome.
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BACKGROUND: The impact of SARS-CoV-2 infection on intrinsic myocardial conduction continues to be an area of focus amongst the medical community. Our objective was to investigate if specific myocardial conduction abnormalities were independently associated with mortality in patients hospitalized with COVID 19. METHODS: Under IRB exemption, the electronic medical records of COVID-19 patients (N=3840) undergoing index hospitalization were reviewed to extract presentation ECG conduction data, demographics, and laboratory results (within 8h). This patient cohort was then separated into two groups based on mortality vs. not (N=520). Logistical regression was used to test association of ECG conduction intervals with mortality. RESULTS: According to our nominal logistic fit for hospital mortality, Heart Rate (HR) >100 (p=0.0007;LW 4.14), QRS duration > 120 ms (p=0.0053;LW 2.27), and QTc prolongation (defined as QTc > 450ms in males;QTc > 460ms in females) (p=0.0089;LW 2.04) were independently associated with higher risk of mortality. LogWorth (LW) calculations were included in an effort to estimate the proportional effect each variable has on overall mortality. LW > 2 were shown to be statistically significant with p< 0.05 with HR > 100 (LW 4.14) having the highest proportional effect on mortality followed by QRSd (LW 2.27) then QTc prolongation (LW 2.04). PR interval> 200ms (p=0.30) and QRS axis (p=0.15) were not associated with higher risk of mortality. CONCLUSIONS: Amongst our patient cohort, HR > 100, QRSd > 120ms, and QTc prolongation (QTc > 450 in males;QTc > 460 in females) were each independently associated with higher risk of mortality in patients hospitalized with COVID 19. These findings support the use of objective ECG data in risk stratifying patients hospitalized with COVID 19.
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BACKGROUND: Severe acute respiratory syndrome-coronavirus-2 (SARSCoV- 2) has substantial morbidity and mortality in patients with heart failure (HF). Hospital mortality exceeds 30% in the American Heart Association's COVID-19 Cardiovascular Disease registry. We characterized clinical traits associated with progression to critical illness (PCI, ICU admission or hospital death) during index and subsequent hospitalizations in SARS-CoV-2 infected patients with extant HF. METHODS: Electronic health records underwent extraction of demographics, anthropometrics, vital signs, laboratory tests, and ICD-10-CM-based Elixhauser comorbidity categories. Univariate logistic regression was used to identify features associated with PCI. Continuous data summarized with median [IQR] were compared using Kruskal-Wallis test and discrete data with chi-squared test. Confounders statistically balanced included age, sex, race, COVID-19 directed treatment, and 4-waves of pandemic. RESULTS: Among HF patients admitted between March 14, 2020 and September 30, 2021, 530 underwent index COVID-19 hospitalization. Among those, 111 were readmitted once, and 43 readmitted at least twice. Index admission median age was 75 [65-84] years, body mass index (BMI) 29.5 [24.9-35.3], and time to readmission 247.7 [44.7-784.1] days. Subsequent time to readmission was 34.7 [5.7-92] days. Most common admission comorbidities were hypertension (81%), diabetes (43%), renal failure (42%), obesity (38%), chronic pulmonary disease (36%), and deficiency anemia (32%). The most common comorbidities at second readmission were renal failure (60%), deficiency anemia (53%), diabetes (40%), and chronic pulmonary disease (40%). PCI occurred in 32% of index admissions, 21% of first readmissions, and 14% of second readmissions. Hospital death or discharge to hospice occurred in 28%, 18%, and 23% of readmissions respectively. CONCLUSIONS: Days to readmission declined revealing impact of inflammation and immunomodulation caused by SARS-CoV-2. Although hypertension was the most common comorbidity at index admission it was the least common at subsequent readmissions. This may represent improved control or death of those poorly controlled. Renal failure being the most common comorbidity at second readmission may represent worsening function due to SARS-CoV-2 infection and injury or worsening HF syndrome. Progressively worsening pBNP and hsTnI likely reflect direct myocyte injury by heightened entry of SARS-CoV-2 viral particle due to expression of angiotensinconverting enzyme 2. HF patients should be urged to undergo SARS-CoV-2 vaccination with apropos boost.
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Introduction: The SARS-CoV-2 pandemic highlighted the need for a way to predict progression to critical illness and ICU admission amongst infected patients. Previous liver disease is a known risk for progression to critical illness. Attempts to identify biomarkers for progression to critical illness suggest inflammatory markers and coagulation markers as useful. We used a machine learning approach to compare the admission liver panel and inflammatory biomarker assays in hospitalized COVID-19 patients with extant mild or severe hepatic disease who progressed to critical illness (ICU admission) versus those who were progression-free. Methods: We included data ed under IRB exemption from electronic medical records (EMR) for SARS-CoV-2 patients admitted to the hospital with chronic liver disease ICD-10-CM codes. Demographics, laboratory results and administrative data were archived and analyzed (SAS, Cary, NC). Generalized regression identified inflammatory and liver panel biomarkers assayed within 8h of hospital admission associated (p<.05) with progression to critical illness. Retained biomarkers underwent bootstrap forest analysis forming a receiver operating characteristic (ROC) that optimized area under ROC (AUROC) estimating model accuracy (precision). Continuous data summarized with median [IQR] were compared using Kruskal-Wallis Test. Discrete data summarized as counts or proportions were compared with chi-squared test. Two-tailed p<.05 was significant. Results: Out of the 4411 COVID-19 patients who were discharged between March 14, 2020 and September 30, 2021, 333 with a previous diagnosis chronic liver disease were included in this study. Demographics for this population are presented in Table 1. Statistical values for biomarkers and progression to critical illness are seen in table 1. Statistically significant markers are compared via explained variance and ROC curve in Figure 1. Although AST and D-dimer were statistically significant markers of progression to critical illness, when modelled as a predictive biomarker, they were not informative in the aggregated ensemble. Therefore, they were not included in the modeling analysis. Conclusion: Hypoalbuminemia, inflammatory markers, D-dimer, and AST were significantly associated with progression to critical illness. Indexing liver specific synthetic function (albumin) to CoV-2 evoked inflammatory markers improves explained variance for progression to critical illness. Alternative liver synthetic function biomarker (INR), ALT, and ALP were not a significant prognostic indicator for progression to severe illness. To our knowledge, this is debut of modeling hypoalbuminemia indexed with multiple routinely assayed inflammatory biomarkers for baseline risk assessment in COVID-19 patients with liver disease. (Table Presented) (Figure Presented)
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Introduction: SARS-CoV-2 evoked immunodysregulation drives inflammation, morbidity, and mortality across COVID-19 presentation spectrum. We sought to identify baseline cell counts and proportions reported with a complete blood count (CBC) that contribute independent information to a model predicting mortality in hospitalized patients with laboratory confirmed SARS-CoV-2 infection. Such a model may complement or improve presentation risk stratification informed by putative inflammatory markers. Methods: Our retrospective design, analyses and interpretations followed constructs detailed in the Strengthening the Reporting of Observational Studies in Epidemiology reporting guideline. Under IRB exemption, discharge medical electronic health records underwent extraction of administrative and clinical data. Demographics, anthropometrics, vital signs, laboratory test and ICD-10-CM-based Elixhauser comorbidity categories were included. Univariate logistic regression was used to identify CBC parameters and attendant ratios associated (p<.05) with hospital mortality. Generalized regression with adaptive LASSO modeling was used to evaluate explanatory probability while eliminating collinearities in identified CBC parameters (individual and ratio) associated with mortality while controlling age, sex, race, baseline vital signs, Elixhauser comorbidities and COVID-19 epoch quarters / treatment. Additional analysis with Bootstrap Forest (BF) was employed to evaluate aggregated synergies and retain parameters that optimized generalized RSquared representing multivariate prediction accuracy and explained variance proportion (EV%) in mortality provided by each variable. Further BF analysis was used to examine relative magnitude of EV% versus putative COVID-19 inflammatory markers. CBC variables included in final BF model were temporally parsed in 24h intervals then pooled when measured after 120h since first vital sign at hospitalization. Results were averaged when a patient underwent multiple assays within an interval. A two-way ANOVA was employed to compare survival vs. non-survival pathways. Results: Among patients consecutively discharged between March 14, 2020 through May 31, 2021, 208 (10 %) of 2153 died. Survivor vs. non-survivor patient and clinical characteristics are summarized in Table 1. CBC parameters identified as independently associated with hospital mortality included WBC, lymphocytes, bands, segmented neutrophils, monocytes, and RDW-CV. (Table 2) Ratios of CBC parameters associated with mortality included AMC/ALC and APC/ALC (Table 2). Results of BF EF% modeling including CBC parameters respectively without (Rsquare = 0.65) and with (Rsquare = 0.70) inclusion of putative inflammatory markers are illustrated in Figure 1a and 1b. Inflammatory markers alone exhibited lowest Rsquare (0.52) (Figure 1c). Figure 2 illustrates temporal kinetics of modeled CBC parameters across hospitalization. Intergroup differences at baseline were sustained, save for RDW-CV after 5-days. Conclusions: Machine learning approaches identified several CBC parameters measured at presentation that when modeled with putative COVID-19 inflammatory markers, enhanced early prediction of hospital mortality. CBC parameters are usually more often measured compared to other inflammatory markers that show COVID-19 severity and serve as an easily obtainable source of information to determine which patients may require a higher level of care before clinical symptoms follow. This includes progression to critical illness and hospital mortality. We recommend that CBC parameters, especially bands, APC/ALC ratio and AMC/ALC ratio be considered for baseline risk stratification of COVID-19 severity, as these trends are sustained at least 5-days after hospitalization. [Formula presented] Disclosures: No relevant conflicts of interest to declare.
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INTRODUCTION: Approximately 20% of COVID-19 patients require hospitalization including 5% needing intensive care. We compared outcomes among patients admitted to an academic community hospital undergoing ICU admission for COVID either directly from emergency department or from general medical units. METHODS: Data were collected after IRB exemption from APACHE IV database and electronic medical records including demographics;administrative data;baseline inflammatory, metabolic and coagulation biomarkers significantly associated with primary outcome;ICU day 1 APACHE IV score and Acute Physiology Score (APS);length of stay (LOS);ICU readmission within same hospital visit;and ICU and hospital mortality. Primary outcome was hospital mortality. Continuous data were summarized with mean [?SD] or median [IQR] respectively compared using t-test or Kruskal-Wallis Test. Discrete data were summarized as counts (proportions) compared with chi-square. Two-tailed p<.05 was significant. RESULTS: Of 244 COVID patients discharged between March 23 and July 28, 2020, respectively 26 and 40 underwent direct (2.6 [1.0-3.4] hrs), or indirect admission (49.8 [19.2 - 136.3] hrs) to ICU. Intergroup similar baseline data were pooled (63±2 years, 58% male, 61% White, 14% Black, 25% Other);temperature 99.0±1.2 °F;SpO2 95±3%;C-reactive protein 14.7±8.5 mg/dL;ferritin 1292±1741 ng/mL;lactate dehydrogenase 455±195 U/L;D-dimer 3.9±6.9 mg/L;prothrombin time 13.4±5.1 seconds;hemoglobin 13.0±2.3 gm/dL;APACHE IV score (66±29);APS (52±27);mechanical ventilation days 14.7±10.9 days;ICU LOS 11.6±10.7 days;and hospital LOS 20.9±14.6 days. There was no difference in number of comorbidities (3.6±1.6) or Elixhauser comorbidity score (9.9±9.8) across ICU admission pathways. Chronic condition prevalence included hypertension (56%), diabetes (28%), obesity (28%) and hypothyroidism (16%). COVID directed drug class treatment was similar. Six patients readmitted to ICU were indirect admissions. ICU (39.4%) and hospital (42.4%) mortality were independent of ICU trajectory. CONCLUSIONS: Outcomes were similar in patients admitted to the ICU directly versus those who decompensated and required transfer from medical floors. Given equivalent biomarker risk at presentation, this finding evinces care quality depth of our safety net.