Patients with COVID-19 infection have an increased risk of cardiovascular complications and thrombotic events. Statins are known for their pleiotropic anti-inflammatory, antithrombotic and immunomodulatory effects.
Studies in patients with cardiovascular disease have demonstrated reduced C-reactive protein, providing convincing evidence of the anti-inflammatory benefits of statins along with their cholesterol-lowering effects. In COVID-19 patients, the same anti-inflammatory activity might improve outcomes in those patients with increasingly severe illness, worsening respiratory failure, and increasing D-dimer and IL-6 levels: all factors associated with increased mortality.
Earlier studies suggested the possible effectiveness of statin therapy in decreasing influenza-related hospitalizations and deaths. During the 2009 H1N1 pandemic, statin therapy was associated with reduced disease severity among hospitalized patients. Features including relatively good lung compliance despite poor oxygenation, the lack of pulmonary vasoconstriction with resultant significant shunting, and thrombotic microangiopathy suggest that vascular endothelial dysfunction plays a vital role in the pathogenesis of COVID-19 infections. Statin treatment might improve endothelial and vascular function in these patients. In fact, a combination of statin/ARB treatments was used in an unconventional and poorly documented experience to target the host response and prevent endothelial barrier damage in Ebola patients during the outbreak in West Africa.
The JUPITER trial, which studied relatively healthy patients with high CRP levels, reported a significantly decreased rate of deep vein thrombosis in those who received rosuvastatin compared to placebo (Glynn et al., 2009). Another study found statin therapy was associated with a 50% reduction in recurrent pulmonary embolism (Biere-Rafi et al., 2013).
It is believed that statins might mitigate the effects of COVID-19 infection in selected patients based on the understanding of its associated coagulopathy, endothelial dysfunction, and dysregulated inflammation.
Source: M.A. Albert, et al, Effect of statin therapy on C-reactive protein levels: the pravastatin inflammation/CRP evaluationJAMA, 286 (1) (2001), pp. 64-70, 10.1001/jama.286.1.64
F. Arsian, G. Pasterkamp, D.P. de Kleijn, Unraveling pleiotropic effects of statins: bit by bit, a slow case with perspective
Circ Res, 103 (4) (2008), pp. 334-336, 10.1161/CIRCRESAHA.108.182220