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COVID-19, caused by severe acute respiratory syndrome coronavirus 2 (SARS CoV-2), has caused an international pandemic, with over 32 million cases and more than 500,000 deaths nationwide. With the significant health consequences seen secondary to COVID-19, healthcare disparities have been further exacerbated. Mechanisms that have been proposed to account for the increased disparity seen during the COVID-19 pandemic are multifactorial. This review of the literature outlines the unique barriers to health and disparities which are associated with vulnerable communities who have been most impacted by the COVID-19 pandemic in the United States.

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Background Existing evidence indicates Black patients have higher incidence of pulmonary embolism (PE) and PE‐related mortality compared with other races/ethnicities, yet disparities in presenting severity and treatment remain incompletely understood. Methods and Results We retrospectively queried a multihospital healthcare system for all hospitalizations for acute PE (2012–2019). Of 10 329 hospitalizations, 8743 met inclusion criteria. Black patients (14.3%) were significantly younger (54.6±17.8 versus 63.1±16.6 years; P <0.001) and more female (56.1% versus 51.6%; P =0.003) compared with White patients. Using ordinal regression, Black race was significantly associated with higher PE severity after matching 1:3 on age and sex (1210:3264; odds ratio [OR], 1.08; 95% CI, 1.03–1.14), adjusting for clinical (OR, 1.13; 95% CI, 1.01–1.27), and socioeconomic (OR, 1.05; 95% CI, 1.05–1.35) characteristics. Among intermediate and high‐severity PE, Black race was associated with a decreased risk of intervention controlling for the competing risk of mortality and censoring on hospital discharge. This effect was modified by PE severity ( P value <0.001), with a lower and higher risk of intervention for intermediate and high‐severity PE, respectively. Race was not associated with in‐hospital mortality (OR, 0.84; 95% CI, 0.69–1.02). Conclusions Black patients hospitalized with PE are younger with a higher severity of disease compared with White patients. Although Black patients are less likely to receive an intervention overall, this differed depending on PE severity with higher risk of intervention only for life‐threatening PE. This suggests nuanced racial disparities in management of PE and highlights the complexities of healthcare inequalities.

Summary Venous thromboembolism is a major cause of death during and immediately post-sepsis. Venous thrombosis (VT) is mediated by cell adhesion molecules and leukocytes, including neutrophil extracellular traps (NETs). Sepsis, or experimentally, endotoxaemia, shares similar characteristics and is modulated via toll like receptor 4 (TLR4). This study was undertaken to determine if endotoxaemia potentiates early stasis thrombogenesis, and secondarily to determine the role of VT TLR4, ICAM-1 and neutrophils (PMNs). Wild-type (WT), ICAM-1-/- and TLR4-/- mice underwent treatment with saline or LPS (10 mg/kg i. p.) alone, or followed by inferior vena cava (IVC) ligation to generate stasis VT. In vivo microscopy of leukocyte trafficking was performed in non-thrombosed mice, and tissue and plasma were harvested during early VT formation. Pre-thrombosis, circulating ICAM-1 was elevated and increased leukocyte adhesion and rolling occurred on the IVC of LPS-treated mice. Post-thrombosis, endotoxaemic mice formed larger, platelet-poor thrombi. Endotoxaemic TLR4-/- mice did not have an augmented thrombotic response and exhibited significantly decreased circulating ICAM-1 compared to endotoxaemic WT controls. Endotoxaemic ICAM-1-/- mice had significantly smaller thrombi compared to controls. Hypothesising that PMNs localised to the inflamed endothelium were promoting thrombosis, PMN depletion using anti-Ly6G antibody was performed. Paradoxically, VT formed without PMNs was amplified, potentially related to endotoxaemia induced elevation of PAI-1 and circulating FXIII, and decreased uPA. Endotoxaemia enhanced early VT occurs in a TLR-4 and ICAM-1 dependent fashion, and is potentiated by neutropenia. ICAM-1 and/or TLR-4 inhibition may be a unique strategy to prevent sepsis-associated V T.

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Since December 2020, four vaccines for severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) have been developed and three have been approved for immediate use in the United States. Two are mRNA vaccines, while one uses a viral vector mechanism. There are reports of thrombotic complications following vaccine administration, which are primarily cerebral sinus thromboses following administration of the viral vector vaccines. Here, we are the first to report venous thrombotic complications within days of administration of the mRNA-1273 (Moderna) vaccine. We present a series of three women who developed venous thromboembolism (VTE) following mRNA-1273 vaccination at a single healthcare system.

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