ABSTRACT
ObjectivesTo compare risk factors for COVID-19 mortality among hospitalized Hispanic, Non-Hispanic Black, and White patients. DesignRetrospecitve cohort study SettingFive hosptials within a single academic health system Participants3,086 adult patients with self-reported race/ethnicity information presenting to the emergency department and hospitalized with COVID-19 up to April 13, 2020. Main outcome measuresIn-hospital mortality ResultsWhile older age (multivariable OR 1.06, 95% CI 1.05-1.07) and baseline hypoxia (multivariable OR 2.71, 95% CI 2.17-3.36) were associated with increased mortality overall and across all races/ethnicities, Non-Hispanic Black (median age 67, IQR 58-76) and Hispanic (median age 63, IQR 50-74) patients were younger and had different comorbidity profiles compared to Non-Hispanic White patients (median age 73, IQR 62-84; p<0.05 for both comparisons). Among inflammatory markers associated with COVID-19 mortality, there was a significant interaction between the Non-Hispanic Black population and interleukin-1-beta (interaction p-value 0.04). ConclusionsThis analysis of a multi-ethnic cohort highlights the need for inclusion and consideration of diverse popualtions in ongoing COVID-19 trials targeting inflammatory cytokines.
ABSTRACT
In a population with ongoing vaccination, the trajectory of a pandemic is determined by how the virus spreads in unvaccinated and vaccinated individuals that exhibit distinct transmission dynamics based on different levels of natural and vaccine-induced immunity. We developed a mathematical model that considers both subpopulations and immunity parameters including vaccination rates, vaccine effectiveness, and a gradual loss of protection. The model forecasted the spread of the SARS-CoV-2 delta variant in the US under varied transmission and vaccination rates. We further obtained the control reproduction number and conducted sensitivity analyses to determine how each parameter may affect virus transmission. Our results show that a combination of strengthening vaccine-induced immunity and preventative behavioral measures will likely be required to deaccelerate the rise of infectious SARS-CoV-2 variants. One-Sentence SummaryMathematical models considering vaccinated and unvaccinated individuals help forecast and manage the spread of new SARS-CoV-2 variants.
ABSTRACT
Background: Little is known about risk factors for COVID-19 outcomes, particularly across diverse racial and ethnic populations in the United States. Methods: In this prospective cohort study, we followed 3,086 COVID-19 patients hospitalized on or before April 13, 2020 within an academic health system in New York (The Mount Sinai Health System) until June 2, 2020. Multivariable logistic regression was used to evaluate demographic, clinical, and laboratory factors as independent predictors of in-hospital mortality. The analysis was stratified by self-reported race and ethnicity. Findings: A total of 3,086 COVID-19 patients were hospitalized, of whom 680 were excluded (78 due to missing race or ethnicity data, 144 were Asian, and 458 were of other unspecified race/ethnicity). Of the 2,406 patients included, 892 (37.1%) were Hispanic, 825 (34.3%) were black, and 689 (28.6%) were white. Black and Hispanic patients were younger than White patients (median age 67 and 63 vs. 73, p<0.001 for both), and they had different comorbidity profiles. Older age and baseline hypoxia were associated with increased mortality across all races. There were suggestive but non-significant interactions between Black race and diabetes (p=0.09), and obesity (p=0.10). Among inflammatory markers associated with COVID-19 mortality, there was a significant interaction between Black race and interleukin-1-beta (p=0.04), and a suggestive interactions between Hispanic ethnicity and procalcitonin (p=0.07) and interleukin-8 (p=0.09). Interpretation: In this large, racially and ethnically diverse cohort of COVID-19 patients in New York City, we identified similarities and important differences across racial and ethnic groups in risk factors for in-hospital mortality.
ABSTRACT
ObjectiveTo identify sex-specific effects of risk factors for in-hospital mortality among COVID-19 patients admitted to a hospital system in New York City. DesignProspective observational cohort study with in-hospital mortality as the primary outcome. SettingFive acute care hospitals within a single academic medical system in New York City. Participants3,086 hospital inpatients with COVID-19 admitted on or before April 13, 2020 and followed through June 2, 2020. Follow-up till discharge or death was complete for 99.3% of the cohort. ResultsThe majority of the cohort was male (59.6%). Men were younger (median 64 vs. 70, p<0.001) and less likely to have comorbidities such as hypertension (32.5% vs. 39.9%, p<0.001), diabetes (22.6% vs. 26%, p=0.03), and obesity (6.9% vs. 9.8%, p=0.004) compared to women. Women had lower median values of laboratory markers associated with inflammation compared to men: white blood cells (5.95 vs. 6.8 K/uL, p<0.001), procalcitonin (0.14 vs 0.21 ng/mL, p<0.001), lactate dehydrogenase (375 vs. 428 U/L, p<0.001), C-reactive protein (87.7 vs. 123.2 mg/L, p<0.001). Unadjusted mortality was similar between men and women (28.8% vs. 28.5%, p=0.84), but more men required intensive care than women (25.2% vs. 19%, p<0.001). Male sex was an independent risk factor for mortality (OR 1.26, 95% 1.04-1.51) after adjustment for demographics, comorbidities, and baseline hypoxia. There were significant interactions between sex and coronary artery disease (p=0.038), obesity (p=0.01), baseline hypoxia (p<0.001), ferritin (p=0.002), lactate dehydrogenase (p=0.003), and procalcitonin (p=0.03). Except for procalcitonin, which had the opposite association, each of these factors was associated with disproportionately higher mortality among women. ConclusionsMale sex was an independent predictor of mortality, consistent with prior studies. Notably, there were significant sex-specific interactions which indicated a disproportionate increase in mortality among women with coronary artery disease, obesity, and hypoxia. These new findings highlight patient subgroups for further study and help explain the recognized sex differences in COVID-19 outcomes.
