BACKGROUND
In late 2019 a novel form of coronavirus (SARS-CoV-2) was considered as the cause of a cluster of respiratory diseases in Wuhan, China. In late february 2020, after a rapid spread worldwide, the coronavirus disease (COVID-19) outbreak began in Italy, resulting up to now in more than 150000 infected individuals and more than 20000 deaths[1]. Despite the fact that viral acute pneumonitis is the major cause of morbidity and mortality, there is increasing evidence that patients with COVID-19 along with respiratory symptoms show a variable degree of systemic disease involvement[2]. Among those involving the cardiovascular system[3] there is evidence regarding a possible pathological hypercoagulability status, leading to higher reported embolic complications such as DIC or pulmonary embolism[4]. This prothrombotic state could be caused by the combined and synergic action of different factors related to covid-19: massive elevation of d-dimer[5], elevation of fibrinogen and inflammatory markers (the so called “cytokine storm”[6]), along with reported major thrombocytopenia[7] and indirect signs of endothelial disfunction (such as alterations in IL-6 and CRP levels[8]. Furthermore, COVID-19 positive patients could have also an intrinsic increased risk VTE due to prolonged immobilization following social distancing measures. This increased risk of potentially lethal thromboembolic complications, not only in the elderly with comorbidities but also in the younger age groups, led the major clinical societies (e.g. International Society of Thrombosis and Haemostasis) to suggest pharmacologic thromboprophylaxis to all hospitalized covid-19 patients, unless contraindicated[9]. However currently there are no recommendations for the outpatient setting, which involves a large number of patients (between 40-50%[1]), and also data are lacking regarding arterial thrombotic risk in these patients.