Low Incidence of Symptomatic Thrombotic Events in Adult Patients Hospitalized with Coronavirus 19: A Retrospective Cohort Study.

BACKGROUND: Since the beginning of the severe acute respiratory syndrome coronavirus 2 (SARS-CoV2) pandemic, there have been many reports of increased incidence of venous thromboembolism and arterial events as a complication. OBJECTIVE: To determine the incidence of symptomatic thrombotic events (TEs) in patients hospitalized for SARS-CoV2 disease (coronavirus 19 [Covid-19]). METHODS: A retrospective single-center cohort study with adult patients with a positive reverse transcriptase-polymerase chain reaction (rt-PCR) for SARS-CoV2, included from the date of diagnosis of Covid-19 and followed for 90 days or until death. RESULTS: A total of 1621 patients were included in this study. The median age was 73 years (interquartile range25th-75th [IQR] 53-87 years) and 57% (913) were female. Overall mortality was 21.6% (348). The overall incidence of symptomatic TEs within 90 days of diagnosis was 1.8% (30 of 1621) occurring in 28 patients, including an incidence of pulmonary embolism of 0.9% (15, 95% confidence interval [CI] 0.60%-1.6%), deep venous thrombosis of 0.61% (10, 95% CI 0.2%-1%), ischemic stroke of 0.25% (4, 95% CI 0.09%-0.65%), and ischemic arterial events of 0.06% (1, 95% CI 0.008%-0.43%). No acute coronary syndrome events were recorded. The incidence of symptomatic TEs was significantly lower in the general ward than in intensive care units (1.2% vs 5.7%; p < .001). The median time since positive rt-PCR for SARS-CoV2 to symptomatic TE was 22.5 days (IQR 19-43 days). There was no significant difference in the proportion of patients receiving (53.6%) and not receiving thromboprophylaxis (66.5%) and the development of TEs. CONCLUSION: The overall incidence of symptomatic TEs among these patients was lower than the incidence previously reported.

Arterial Thrombosis in Coronavirus Disease 2019 Patients: A Rapid Systematic Review.

BACKGROUND: Emerging evidence suggests that severe form of coronavirus disease 2019 (COVID-19) is mediated, in part, by a hypercoagulable state characterized by micro- and macro-vascular thrombotic angiopathy. Although venous thrombotic events in COVID-19 patients have been well described, data on arterial thrombosis (AT) in these patients is still limited. We, therefore, conducted a rapid systematic review of current scientific literature to identify and consolidate evidence of AT in COVID-19 patients. METHODS: A systematic search of literature was conducted between November 1, 2019, and June 9, 2020, on PubMed and China National Knowledge Infrastructure to identify potentially eligible studies. RESULTS: A total of 27 studies (5 cohort, 5 case series, and 17 case reports) describing arterial thrombotic events in 90 COVID-19 patients were included. The pooled incidence of AT in severe/critically ill intensive care unit-admitted COVID-19 patients across the 5 cohort studies was 4.4% (95% confidence interval 2.8-6.4). Most of the patients were male, elderly, and had comorbidities. AT was symptomatic in >95% of these patients and involved multiple arteries in approximately 18% of patients. The anatomical distribution of arterial thrombotic events was wide, occurring in limb arteries (39%), cerebral arteries (24%), great vessels (aorta, common iliac, common carotid, and brachiocephalic trunk; 19%), coronary arteries (9%), and superior mesenteric artery (8%). The mortality rate in these patients is approximately 20%. CONCLUSIONS: AT occurs in approximately 4% of critically ill COVID-19 patients. It often presents symptomatically and can affect multiple arteries. Further investigation of the underlying mechanism of AT in COVID-19 would be needed to clarify possible therapeutic targets.

COVID-19: Coagulopathy, Risk of Thrombosis, and the Rationale for Anticoagulation.

The novel coronavirus infection (COVID-19) is caused by the new coronavirus SARS-CoV-2 and is characterized by an exaggerated inflammatory response that can lead to severe manifestations such as adult respiratory syndrome, sepsis, coagulopathy, and death in a proportion of patients. Among other factors and direct viral effects, the increase in the vasoconstrictor angiotensin II, the decrease in the vasodilator angiotensin, and the sepsis-induced release of cytokines can trigger a coagulopathy in COVID-19. A coagulopathy has been reported in up to 50% of patients with severe COVID-19 manifestations. An increase in d-dimer is the most significant change in coagulation parameters in severe COVID-19 patients, and progressively increasing values can be used as a prognostic parameter indicating a worse outcome. Limited data suggest a high incidence of deep vein thrombosis and pulmonary embolism in up to 40% of patients, despite the use of a standard dose of low-molecular-weight heparin (LMWH) in most cases. In addition, pulmonary microvascular thrombosis has been reported and may play a role in progressive lung failure. Prophylactic LMWH has been recommended by the International Society on Thrombosis and Haemostasis (ISTH) and the American Society of Hematology (ASH), but the best effective dosage is uncertain. Adapted to the individual risk of thrombosis and the d-dimer value, higher doses can be considered, especially since bleeding events in COVID-19 are rare. Besides the anticoagulant effect of LMWH, nonanticoagulant properties such as the reduction in interleukin 6 release have been shown to improve the complex picture of coagulopathy in patients with COVID-19.