Objective. To identify factors associated with COVID-19 vaccine hesitancy and acceptance among the Mexican population. Methods. In a web-based nationwide survey in early December 2020, respondents were inquired about their sociodemographic characteristics and their willingness to accept a hypothetical COVID-19 vaccine given a 50% or 90% effectiveness. A logistic regression model was used to identify the factors associated with hesitancy and acceptance. Results. A total 3 768 responses were analyzed. A 90% effective vaccine was accepted by 85% of respondents, while only 46% would accept being vaccinated with a 50% effective vaccine. In univariate analysis, each age group (40–49, 50–59, and ≥60) was strongly associated with vaccine hesitancy for a 90% effective vaccine (OR 0.48, 95% CI 0.38, 0.63; OR 0.33, 95 CI 0.26, 0.41; and OR 0.28, 95 CI 0.21, 0.38, respectively) compared to the 18–39 age group. After multivariable adjustment, similar magnitudes of association were observed. Being female and higher socioeconomic status were also associated with higher vaccine hesitancy. Conclusions. Vaccine hesitancy represents a major public health problem in Mexico and is driven by multiple factors. Our study provides relevant insights for the development of effective policies and strategies to ensure widespread vaccination in Mexico.

Background High flow oxygen therapy (HFO) is a widely used intervention for pulmonary complications. Amid the coronavirus infectious disease 2019 (COVID-19) pandemic, HFO became a popular alternative to conventional oxygen supplementation therapies. Risk stratification tools have been repurposed –and new ones developed– to estimate outcome risks among COVID-19 patients. This study aims to provide a simple risk stratification system to predict invasive mechanical ventilation (IMV) or death among COVID-19 inpatients on HFO. Methods Among 529 adult inpatients with COVID-19 pneumonia, we selected unadjusted clinical risk factors for developing the composite endpoint of IMV or death. The risk for the primary outcome by each category was estimated using a Cox proportional hazards model. Bootstrapping was used to validate the results. Results Age above 62, eGFR under 60 ml/min, room air SpO2 ≤89 % upon admission, history of hypertension, history of diabetes, and any comorbidity (cancer, cardiovascular disease, COPD/ asthma, hypothyroidism, or autoimmune disease) were considered for the score. Each of the six criteria scored 1 point. The score was further simplified into 4 categories: 1) 0 criteria, 2) 1 criterion, 3) 2-3 criteria, and 4) ≥4 criteria. Taking the first category as the reference, risk estimates for the primary endpoint were HR; 2.94 [1.67 – 5.26], 4.08 [2.63 – 7.05], and 6.63 [3.74 – 11.77], respectively. In ROC analysis, the AUC for the model was 0.72. Conclusions Our score uses simple criteria to estimate the risk for IMV or death among COVID-19 inpatients with HFO. Higher category reflects consistent increases in risk for the endpoint.

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Background Heart failure (HF) and frailty are highly prevalent in late life and commonly co-exist, but the mechanisms underlying their bi-directional relationship are incompletely understood. This study aimed to identify shared molecular pathways associated with incident HF and frailty in late life. Methods Among participants in the Atherosclerosis Risk in Communities (ARIC) study, a communit-based cohort study in the United States, 4,877 plasma proteins were measured using an aptamer-affinity assay (Somascan v4) at study Visit 3 (V3; 1993–1994; n=10,368, age 60±6 years; 822 incident HF events) and at study Visit 5 (V5; 2011–2013; n=3,908, age 75±5 years; 336 incident HF events). Frailty was assessed at V5 using Fried criteria, which incorporates gait speed, grip strength, low energy expenditure, weight loss, and exhaustion. We examined the association of proteins at V3 with incident HF after V3 with Bonferroni corrected P<0.05 using multivariable Cox proportional hazard regression models. For HF-associated proteins at V3, we assessed the association of V5 protein levels with incident HF after V5. For the resulting HF-associated proteins, multivariable logistic regression was used to assess associations of V5 protein values with prevalent frailty at V5 (n=223 cases) and with incident frailty by study Visit 6 (2016–2018; n=152 incident cases). All models adjusted for age, sex, race, hypertension, diabetes, cardiovascular disease, BMI, atrial fibrillation, and stroke. The set of HF-related proteins that associated with incident frailty at FDR <0.05 using Benjamini-Hochberg correction was tested for pathway enrichment using the Reactome database. Results Of 289 proteins associated with incident HF post-V3 at p<1.0x10–5 (0.05/4,877), 84 were significantly associated with incident HF post-V5 at p<1.7x10–4 (0.05/289). Among 4,131 HF-free participants at V5, 48 of these 84 HF-associated proteins associated with prevalent frailty at p<5.9x10–4 (0.05/84). Among Visit 5 participants who completed a frailty assessment and were free of both prevalent HF and frailty (n=3,908), 31of 48 candidate proteins were also significantly associated with incident frailty at FDR 0.05, 18 of which were significantly associated with incident frailty at p<1.0x10–3 (0.05/48; Figure 1). The 31 proteins associated with incident frailty at FDR 0.05 enriched for collagen biosynthesis, formation, and trimerization (COL28A1, COL6A3, EFEMP1), and cytokine immune pathways and TNF receptor binding (TNFRSF1A and B, VEGFA, B2M, and HAVCR2) in pathway enrichment analysis. Conclusions Collagen metabolism and immune pathways may be shared biologic pathways between HF and frailty in late-life. Funding Acknowledgement Type of funding sources: Public Institution(s). Main funding source(s): The Atherosclerosis Risk in Communities study has been funded in whole or in part with Federal funds from the National Heart, Lung, and Blood Institute, National Institutes of Health, Department of Health and Human Services.

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At more than 10 months after the first case of COVID-19 was documented, the understanding of the pathogenesis of this viral illness is growing on a daily basis. A massive pro-inflammatory response on infected individuals involving several cytokines seems to play a key role on disease. As a result, therapeutic efforts have focused on anti-inflammatory strategies to ameliorate the disease, in sight of a lack of a truly effective anti-viral agent. Pentoxifylline (PTX) has been proposed by multiple authors as a potential therapeutic ally, targeting a variety of mechanisms as it has been shown to have antiviral, anti-inflammatory and hemodynamic effects. Importantly, anti-inflammatory effects center on down-regulation of cytokines such as interleukins and tumor necrosis factor. In pre-pandemic studies, PTX has demonstrated to change the clinical course of inflammatory diseases such as acute respiratory distress syndrome, which is a hallmark of severe COVID-19. Researchers agree it is pertinent to experimentally evaluate the effect this drug has on COVID-19 patients. The objective of this review is to summarize all the proposed mechanisms by which PTX may aid in the treatment of COVID-19, as well as prevent its deadly complications. Our interpretation of the literature is that the benefits PTX may bring to a patient with COVID-19 outweigh the risks this drug might pose on them. As a result, there is consensus regarding the evaluation of PTX in further experimental studies to better characterize its effects on COVID-19 patients.