Objectives: Patients with COVID-19 may be at high risk for thrombotic complications due to excess inflammatory response and stasis of blood flow. This study aims to assess the incidence of pulmonary embolism among hospitalized patients with COVID-19, risk factors, and the impact on survival. Methods: A retrospective case-control study was conducted at Al-Noor Specialist Hospital in Saudi Arabia between 15 March 2020 and 15 June 2020. Patients with confirmed COVID-19 diagnosis by a real-time polymerase chain reaction (PCR) and confirmed diagnosis of pulmonary embolism by Computed Tomography pulmonary angiogram (CTPA) formed the case group. Patients with confirmed COVID-19 diagnosis by a real-time polymerase chain reaction (PCR) and without confirmed diagnose of pulmonary embolism formed the control group. Logistic regression analysis was used to identify predictors of pulmonary embolism and survival. Results: A total of 159 patients participated were included in the study, of which 51 were the cases (patients with pulmonary embolism) and 108 patients formed the control group (patients without pulmonary embolism). The incidence of PE among those hospitalized was around 32%. Smoking history, low level of oxygen saturation, and higher D-dimer values were important risk factors that were associated with a higher risk of developing PE (p < 0.05). Higher respiratory rate was associated with higher odds of death, and decreased the possibility of survival among hospitalized patients with PE. Conclusions: Pulmonary embolism is common among hospitalized patients with COVID-19. Preventive measures should be considered for hospitalized patients with smoking history, low level of oxygen saturation, high D-dimer values, and high respiratory rate.

Background: Thrombotic consequences have been reported in COVID-19-infected patients, especially those who are critically ill. Multiple studies have tested antiphospholipid antibodies (aPLs) among COVID-19 patients, but to date, the actual frequency of aPLs is still uncharted. In this cohort study, we analyzed the outcomes of 173 consecutive patients with confirmed COVID-19 infection. Anti-phospholipid antibodies, which include anti-cardiolipin antibodies [aCL (IgM), aCL (IgG)], and B2-glycoprotein I antibodies [aβ2GPI (IgM), aβ2GPI (IgG)] were detected by using immunoassays. In contrast, lupus anti-coagulant (LAC) antibodies are identified through a coagulation-based assay. Results: The study demonstrated a high incidence of thrombotic consequences in severe COVID pneumonia cases and supported an increased risk of developing aPLs following COVID-19 infection. Pulmonary embolism had the most common prevalence of all thrombotic events. Among the various aPLs tested in thrombotic patients, lupus anti-coagulant (LAC) had the highest positivity (46.2%). Most patients with arterial thromboembolism (stroke, myocardial infarction, limb ischemia, bowel ischemia, and renal artery thrombosis) had triple positivity of anti-phospholipid antibodies. Testing aPLs antibodies after 12 weeks of recovery for survived patients only 2 out of 23 patients had aPLs positivity compared to 35 out of 65 tested during hospital admission. Furthermore, we found no significant changes in aPLs positivity between survived and non-survived patients with thrombotic event. Conclusions: aPLs increased transiently as an inflammatory-mediated condition. Individuals with aPLs triple positivity (positive LAC, aCL, and aB2GPI) had a considerable risk of arterial thromboembolism (ATE).