Background: Patients with coronary artery disease (CAD) are at increased risk for cardiac death and respiratory failure following SARS-CoV-2 infection. Platelets are crucially involved in pathogenesis of CAD and might also contribute to pathophysiology of SARS-CoV-2 infection.

Methods and Results: We enrolled a cohort of 83 participants from February 2020 to July 2020 including 55 patients with pre-existing CAD and SARS-CoV-2 infection (CAD+SARS-CoV-2), and 28 patients with CAD. Clinical and cardiac examination including blood sampling, echocardiography, and electrocardiography was performed within 24 hours after hospital admission. Phenotyping of platelets was performed by flow cytometry, plasma levels of chemokines were analyzed by ELISA. Respiratory failure of patients was stratified by the Horovitz Index (HI) as moderately/severely impaired when HI ≤ 200mmHg. The clinical endpoint (EP) was defined as HI ≤ 200mmHg with subsequent mechanical ventilation within a follow-up of 60 days. CAD+SARS-CoV-2 patients display a significant enhanced platelet activation and hyper-inflammation early at time of hospital admission. Circulating platelet/leukocyte co-aggregates correlate with plasma levels of cytokines/chemokines like IL-6, CCL2 and CXCL10 as well as activation of platelets is associated with CCL5 and elevation of pulmonary artery pressure (PAPsys). Furthermore, subtilisin-like proprotein convertase furin is stored and released from activated platelets. Furin plasma levels are associated with poor clinical prognosis in SARS-CoV-2-positive CAD patients.

Conclusion: Patients with CAD and SARS-CoV-2 infection exhibit elevated systemic platelet activation and enhanced plasma levels of the subtilisin-like proprotein convertase furin which may contribute to the unfavourable clinical prognosis.