Reasoned therapeutic protocol in outpatients with COVID-19.

BACKGROUND: Seventy percent of patients affected by SARS-COV-2 disease are asymptomatic or with symptoms that not required Hospitalization. A prodromal period lasting about 5 days can be identified. In this phase a patient with a positive swab for viral RNA may or may not evolve towards the phase of symptomatic disease. METHODS: In this paper we reviewed the literature related to COVID-19 therapy we propose a reasoned treatment protocols in outpatients according to the age and the comorbidity. RESULTS: The aim of this study was to reduce the impact of the virus by reducing its ability to attack cells and the inflammatory burden and the prothrombotic effects proposing two therapeutic schemes of proven efficacy according to the age of the patients and the comorbidities. CONCLUSIONS: We aimed to reduce worsening of clinical status and hospitalization while protecting patients at home.

The vascular side of COVID-19 disease. Position paper of the International Union of Angiology.

The SARS-CoV-2 infection (COVID-19) is causing an ongoing pandemic and potentially fatal disease. Development of coagulopathy with thrombotic complications such as deep vein thrombosis and pulmonary embolism are emerging as factors for progression to severe disease and death. Also, a markedly increased level of D-dimer, a protein product of fibrin degradation, has been associated to mortality. Furthermore, activation of immune response due to virus infection may led to uncontrolled severe inflammation with damage to host cells and induction of endotheliitis and cellular apoptosis and pyroptosis. The use of low molecular weight heparin in early stage of the disease could prevent vascular complications and reduce the progression to severe stage of the disease. Aim of this paper was to summarize current evidence about vascular involvement in COVID-19 disease and potential antithrombotic therapy.

COVID-19 pneumonia: the impact of coagulopathy

The development of coagulopathy is emerging as one of the most significant poor prognostic features in COVID-19 pneumopathy. D-dimer, a protein product of fibrin degradation, has been found elevated in the most severe cases and correlated to mortality. Potentially involved factors in the impairment of coagulation caused by viral infection include the dysregulated inflammatory response, platelet and endothelial dysfunction with impaired fibrinolysis. Autoptic analysis in deaths fore severe COVID-19 disease revealed fibrin exudation in alveoli, blood vessel wall edema and hyaline thrombi in small vessels in other organs and tissues. Heparin is an anticoagulant molecule that also showed anti-inflammatory properties and a potential antiviral effect. The use of low molecular weight heparin could prevent thromboembolic complications in COVID-19 pneumopathy. However, the correct timing of prophylaxis according to the stage of COVID-19 disease and the appropriate therapeutic dosage to use in severe cases need further research.