Emerging clinical data from COVID-19 cohorts

Latest evidences from literature suggest that SARS-CoV-2 disease 2019 (COVID-19) is commonly complicated with coagulopathy and that disseminated intravascular coagulation is present in the majority of deceased patients. Particularly, conventional coagulation parameters appear to be significantly altered in patients with poor prognosis. A wide-ranging crosstalk between coagulative haemostasis and inflammation, as well as the activation of coagulation cascade during viral infections, are well established. Another important evidence which may explain coagulation disorders in COVID-19 is the increase of thrombus formation under conditions of hypoxia. Despite the exact pathophysiological mechanism of coronavirus-induced thromboembolism needs to be further investigated, this finding suggests that it is good practice to assess the risk of thrombosis in COVID-19 patients to improve the clinical management in terms of anticoagulation therapy. Anticoagulants, mainly low-molecularweight heparin (LMWH), should be tailored in patients meeting sepsis induced coagulopathy (SIC) criteria or with markedly elevated D-dimer. In this context, further studies are needed to optimise the decision making in therapeutic approach. SARS-CoV-2 infection breakthrough Since December, 2019, the world is experiencing an outbreak of a novel beta-coronavirus known as Severe Acute Respiratory Syndrome Coronavirus 2 (SARSCoV-2). As of the 11th of March, 2020, WHO has declared 2019 novel coronavirus disease (COVID-19) a pandemic infection [1]. Italy has been the first country after China to identify a significant outbreak of COVID-19 disease, with 212,532 confirmed cases and 27,402 associated deaths in the last update (6th May 2020) [2]. COVID-19 patients who have died had a mean age of 79 years and an average of 3.3 co-morbidities, with cardiovascular diseases being the most common: 3.8% of deceased patients had no concomitant disease [3]. Growing evidence suggest that severe coronavirus disease 2019 is commonly complicated with coagulopathy and markedly elevated D-dimer was associated with poor prognosis of severe COVID-19 infection [4,5]. Recent prospective autoptic cohort study documented unpredictably elevated incidence of deep vein thrombosis (DVT) among deceased COVID-19 patients; massive pulmonary embolism (PE) was the direct cause of death in 33.3% of cases [6]. However, at this time comprehensive analysis of mechanisms underlying coagulative homeostasis unbalance are not fully depicted. We review the most recent evidences on interaction between pulmonary vascular endothelium and coagulative system implicated in pathogenetic mechanisms associated with SARS-CoV-2 infection. Emerging clinical data from COVID-19 cohorts Latest evidences from literature [7,8] suggest that COVID-19 is commonly complicated with coagulopathy and that disseminated intravascular coagulation (DIC) may exist in consistent number of deceased patients. DVT, PE or micro-thrombosis represent recurrent autoptic findings among COVID-19 patients [6,9]. In a recent clinical study, Han et al. [4] compared coagulation parameters including activated partial thromboplastin time (APTT), antithrombin (AT), fibrin/fibrinogen degradation products (FDP), fibrinogen (FIB), prothrombin time (PT), international normalized ratio (INR), prothrombin time activity (PT-act), and thrombin time (TT) between 94 patients with confirmed SARS-CoV-2 infection and 40 healthy controls. Compared with healthy controls, the AT values were found to be lower in COVID-19 patients (85% vs 99%; p<0.001). The PT-act was also found to be lower in patients than in controls (81% vs 97%; p<0.001), whereas the values of Ddimer (10.36 vs 0.26 ng/L; p<0.001), FDP (33.83 vs 1.55 mg/L; p<0.001) and FIB (5.02 vs 2.90 g/L; p<0.001) were higher in [Monaldi Archives for Chest Disease 2020; 90:1300] [page 271] Monaldi Archives for Chest Disease 2020; volume 90:1300 COVID-19 and coagulative axis: review of emerging aspects in a novel disease Matilde Boccia1, Luigi Aronne1, Benito Celia1, Grazia Mazzeo1, Maria Ceparano1, Vito D’Agnano1, Roberto Parrella2, Tullio Valente3, Andrea Bianco1, Fabio Perrotta4 1Department of Translational Medical Sciences, University of Campania "L. Vanvitelli", Naples; 2Department of Infectious Diseases, COVID Unit D, Cotugno Hospital, A.O.R.N. dei Colli, Naples; 3Department of Radiology, Monaldi Hospital, A.O.R.N. dei Colli, Naples; 4Department of Medicine and Health Sciences “V. Tiberio”, University of Molise, Campobasso, Italy Correspondence: Prof. Fabio Perrotta, Department of Medicine and Health Sciences “V. Tiberio”, University of Molise, 86100 Campobasso, Italy. E-mail: fabio.perrotta@unimol.it