ABC | Volume 114, Nº5, May 2020

Viewpoint Nascimento et al. Anticoagulation in severe COVID-19 Arq Bras Cardiol. 2020; 114(5):829-833 production of inflammatory cytokines. The initial clinical findings of HPS are marked by those of the systemic inflammatory response syndrome. As HPS develops, the following might be observed: neurological findings, liver function changes, DIC, hepatosplenomegaly, pancytopenia, and high ferritin levels. Those findings can be triggered by infections, such as COVID-19, which shows, in some cases, a large release of cytokines, mainly interleukin 6, in association with systemic inflammatory response and DIC. Such conditions should be considered based on clinical and laboratory findings, and an early therapeutic approach should be defined to reverse them. 28 SARS-CoV-2 infection, in its most severe presentation, marked by organic dysfunction, such as acute respiratory failure, meets the diagnostic criteria for sepsis. 33 Recent observational studies have correlated the hypercoagulable state with the severe form of COVID-19, in which SIC and/or DIC seem to be present in most fatal cases. 3,21-23,34 The reduction in oxygen arterial pressure found in critical patients contributes directly and indirectly to the development of ischemic syndrome. 35 In line of this, results suggest that the prothrombotic pathophysiology already described in sepsis might be related to intrinsic aspects of the novel coronavirus, and, thus, the beneficial potential of the use of anticoagulants in selected groups of patients should be analyzed individually. A retrospective study conducted in the hospital of Tongji (Wuhan, China) has reported lower mortality in patients with severe COVID-19 who had used anticoagulants, unfractionated heparin or low-molecular weight heparin (LMWH), with a SIC score of ≥ 4 and/or very high D-dimer (> 6 times the upper limit of reference range). 36 Anticoagulant therapy in patients with severe COVID-19 and signs of SIC and/or very high D-dimer in association with other biomarkers of severity, in the absence of contraindication to anticoagulation, can be considered a therapeutic strategy for SARS-CoV-2 infection, based on expert consensus and a few retrospective studies. Moreover, that strategy requires the use of strict institutional protocols that enable surveillance and rapid intervention if complications occur. Figure 2 shows the algorithm to assess thrombogenesis in patients with COVID-19, as well as a suggestion of treatment. However, data are still insufficient to determine important aspects for the elaboration of a therapeutic plan, such as the best drug choice, its dosage and administration time schedule, as well as the duration of treatment. Further studies, mainly prospective, are required to better support the indication of anticoagulation for critical patients infected by the novel coronavirus. The possible benefit from attenuating the hypercoagulable state should be balanced against the risk of bleeding. Anticoagulant therapy might be more beneficial when initiated in the pre-thrombotic stage and not in advanced Figure 2 – The diagnosis of COVID-19 should be confirmed according to the World Health Organization recommendations.37 Patients with the severe form of that disease8,38 in addition to a sepsis-induced coagulopathy score ≥ 4 or disseminated intravascular coagulation and/or D-dimer levels > 6 times the upper limit of reference range might benefit from anticoagulant therapy. INR, international normalized ratio; SIC, sepsis-induced coagulopathy; ISTH, International Society on Thrombosis and Hemostasis; SOFA, sequential organ failure assessment; DIVC, disseminated intravascular coagulation; ULRR, upper limit of reference range. 831