8.6  N-3 PUFAs have the potential to ameliorate coagulopathy
Laboratory examinations from COVID-19 patients indicate serious coagulopathy has occurred in some individuals. This is reflected by widespread microvascular thrombosis and consumption of coagulation factors as evidenced by markers such as thrombocytopenia, prolongation of the prothrombin, elevation of D-dimer, increased fibrin degradation product levels and decreased fibrinogen levels (Tang et al., 2020). In a study with 184 Dutch ICU COVID-19 patients, 38% were reported to have abnormal blood clotting and 33% with identified clots (Klok et al., 2020). Importantly, blood clots may cause lung emboli, cardiovascular complications or stroke. In addition, long-term bed rest has been linked to increased risk of venous thromboembolism in severe SARS-CoV-2 infected patients (Iba, et al., 2019; Zhang et al., 2020). Accordingly, the active application of anticoagulants (such as heparin) for patients with severe SARS-CoV-2 infection has been recommended and appears to be associated with better prognosis (Tang, Bai, et al., 2020). Tang et al. recently published a study indicating anticoagulant therapy, mainly with low molecular weight heparin, is associated with better prognosis in severe SARS-CoV-2 infected patients (Tang, Bai, et al., 2020).
N-3 PUFAs contain polar lipids that exhibit potent antithrombotic effects against platelet-activating factor and other prothrombotic pathways, including thrombin, collagen, and adenosine diphosphate (Lordan et al., 2020; Tsoupras et al., 2019; Tsoupras, O'Keeffe, Lordan, Redfern, & Zabetakis, 2019). Increased levels of n-3 PUFAs may alter platelet phospholipid membrane composition and affect platelet function, which can be predicted to alter the progression and thrombotic complications of CVD. Adili et al. outlined that EPA and DHA act on the platelet membrane to reduce platelet aggregation and TX release via COX-1 and 12-LOX, which metabolize fatty acids into a group of beneficial oxylipins in platelets that contribute significantly to the regulation of platelet function in hemostasis and thrombosis (Adili, Hawley, & Holinstat, 2018). This is supported by Park and Harris who demonstrated healthy subjects supplemented with EPA for 4 weeks had reduced platelet activation, an early step in platelet aggregation (Park & Harris, 2002). While the evidence is limited, it appears EPA is more active than DHA in altering platelet function because it is a COX substrate. However, DHA appears to decrease TxA2 and PGH2 receptor affinity (Park & Harris, 2002). Although dietary supplementation of EPA and DHA has been shown to reduce platelet activation and aggregation in healthy subjects, a higher recommended dose of n-3 PUFAs may be needed in platelet hyperactivity prothrombotic conditions such as in CVD (Adili et al., 2018). These anticoagulant properties of n-3 PUFAs suggest potential effects on the platelet aggregation in severe cases of SARS-CoV-2 infected subjects. Our current level of knowledge only permits speculation on whether n-3 PUFAs can mitigate the coagulopathy associated with severe COVID-19.