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letter
. 2020 Jul 12;8(5):901. doi: 10.1016/j.jvsv.2020.06.007

Reply

Enrico M Marone 1,2, Luigi F Rinaldi 3
PMCID: PMC7354268  PMID: 32663524

The remarks made by Kow and Hasan1 regarding the use of low-molecular-weight heparin (LMWH) in hospitalized COVID-19 patients are greatly appreciated since they focus on one of the most important aspects concerning the treatment of this disease, namely, thromboprophylaxis. In fact, since our latest letter was published in this Journal, suggesting a close correlation between COVID-19 and deep venous thrombosis (DVT),2 a number of studies have followed, confirming this view and providing evidence of the fact that respiratory infection is also responsible for a systemic procoagulant activity,3, 4, 5 which can lead to different clinical manifestations ranging from DVT to septic intravascular coagulation, not only in the most critical cases (patients in intensive care unit) but in all in-hospital patients. In light of this evidence, heparin has become a cornerstone of the treatment against COVID-19, along with empirical antiviral and antibiotic therapy, but the correct dose to administer is still the subject of discussion.6 Most centers continue to administer a prophylactic dose of LMWH (100 mUI/kg daily), although our experience reports several cases of DVT and pulmonary embolism in COVID-19 patients with this posology, which justifies the use of anticoagulant doses (100 mUI/kg twice a day) when no absolute contraindication to anticoagulant therapy exists. This is, in our opinion, a correct approach, although there are other potential risks to be taken into account, for example, thrombocytopenia, a common alteration in COVID-19 patients that is a predictor of poor prognosis and can be worsened by LMWH.7 The decision is, in fact, a difficult one, and it is made even harder by the many things that we still ignore regarding the effects that the virus has on the hemostatic function. In this respect, constant and careful monitoring of platelet count and coagulation parameters (especially D-dimer and fibrinogen) throughout the entire clinical course is crucial to recognize and minimize complications.

In conclusion, we share the authors' view that COVID-19 is a powerful risk factor for DVT; moreover, in hospitalized patients, it is often associated with pre-existing comorbidities (advanced age, obesity) and immobilization that further enhance the thrombotic risk, and so all measures should be adopted to counteract the onset of DVT or other clinical manifestations of an altered hemostasis. To this purpose, further studies investigating the relationship between disease severity and the extent of coagulopathy will be necessary to select those patients who need more protection.

References

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