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.