The study focused on COVID-19 positive patients who have been taking prescribed anticoagulant class rugs including warfarin, a direct oral anticoagulant or DOAC such as apixaban, rivaroxaban, dabigatran, edoxaban), and enoxaparin in the immediate 90 days prior to COVID-19 diagnosis.
The study involved a total of 6195 patients, 598 were immediately hospitalized and 5597 were treated as outpatients. The overall case-fatality rate was 2•8% (n = 175 deaths). Among the patients who were hospitalized, the inpatient mortality was 13%. Among the 5597 COVID-19 patients initially treated as outpatients, 160 (2.9%) were on anticoagulation and 331 were eventually hospitalized (5.9%).
In a multivariable analysis, outpatient anticoagulation use was associated with a 43% reduction in risk for hospital admission, HR (95% CI = 0.57, 0.38–0.86), p = 0.007, but was not associated with mortality, HR (95% CI=0.88, 0.50 – 1.52), p = 0.64. Inpatients who were not on anticoagulation (before or after hospitalization) had an increased risk for mortality, HR (95% CI = 2.26, 1.17–4.37), p = 0.015.
Failure to initiate anticoagulation upon hospitalization or maintaining outpatient anticoagulation in hospitalized COVID-19 patients was associated with increased mortality risk.
The study findings were published in the peer reviewed journal: EClinical Medicine by Lancet.
reference link : https://www.thelancet.com/journals/eclinm/article/PIIS2589-5370(21)00419-3/fulltext
going into the specifics of the research ….
The pathophysiology of hypercoagulability in COVID-19 is incompletely understood. However, the increased risk of thromboembolic events is likely related to traditional risk factors and mechanisms unique to COVID-19, such as increased inflammation, hypoxia, and endothelium inflammation [[9],[10]].
The binding of SARS-CoV-2 to the target host cell generates the release of inflammatory cytokines, promoting immune cell migration to the site of tissue damage [[11]]. These activated immune cells exacerbate endothelial damage through increased vascular leak and micro thrombus formation [[12],[13]].
The higher mortality rates observed among COVID-19 patients with elevated D-dimers may be related to these mechanisms [[7],[14],[15]].
Anticoagulants are indicated in patients with venous thromboembolism and atrial fibrillation with the shortest duration of three months for provoked venous thromboembolism [[16],[17]]. We decided to study the impact of persistent outpatient anticoagulation (OPAC) on the risk of adverse outcomes in the setting of COVID-19.
A retrospective Italian study involving seventy elderly patients found that outpatient anticoagulation was associated with reduced COVID-19 mortality [[18]]. In an uncontrolled study from the USA, one hundred patients on outpatient anticoagulation had lower thrombotic complications and less severe disease when they are diagnosed with COVID-19 [[19]].
While some studies have explored the role of outpatient anticoagulation, most have focused on inpatient anticoagulation strategies to reduce thrombotic events and mortality. For example, in a study of 4389 hospitalized COVID-19 patients from the USA, anticoagulation lowered in-hospital mortality and intubation, although there was no statistically significant difference in patients’ outcomes with prophylactic versus therapeutic anticoagulation strategies [[20]].
In another retrospective study of 395 COVID-19 inpatients in New York City requiring mechanical ventilation, in-hospital mortality was 29% for those treated with therapeutic anticoagulant versus 62% for those who did not receive any anticoagulation [[21]]. In a Chinese single-center study of hospitalized COVID-19 patients, 99 of 449 were treated with prophylactic dose low molecular weight heparin.
Heparin treatment was not associated with mortality overall; however, heparin treatment was associated with a lower risk of death among patients with elevated D-dimer or an elevated sepsis-induced coagulopathy score [[22]].
Few studies have examined the impact of risk-stratified initiation of anticoagulation based on illness severity using age, gender, comorbid conditions, vital signs, and D-dimer value among patients hospitalized with COVID-19 despite their widespread use [23, 24, 25, 26, 27, 28].
To that effect, the improved outcomes of hospitalized COVID-19 patients on anticoagulation negated prior concerns in the scientific community for disseminated intravascular coagulopathy (DIC) that were reported earlier in the pandemic [[29]]. This paper defined inpatient anticoagulation (IPAC) as the initiation of anticoagulation for prophylactic, escalated prophylactic or therapeutic dose, or continuation of outpatient anticoagulation.
To further explore the impact of anticoagulation on COVID-19 outcomes, we leveraged data from a large sample of adult COVID-19 patients from a single hospital system in the upper Midwest.
Based on the improved outcomes among hospitalized patients exposed to anticoagulation, we hypothesized that outpatient anticoagulation (OPAC) would be associated with decreased risk of hospital admission and mortality among patients on anticoagulation before COVID-19 diagnosis compared to patients who were not. We also hypothesized that IPAC would decrease the risk of mortality among inpatients compared to patients who are not on any anticoagulation.
