SARS-CoV-2 infection and SLE: endothelial dysfunction, atherosclerosis, and thrombosis

• Published in: Clinical rheumatology 2023-10, Vol.42 (10), p.2691-2702
• Main Authors: Płazak, Wojciech, Drabik, Leszek
• Format: Article
• Language: English
• Subjects: Angiography; Antiphospholipid antibodies; Arteriosclerosis; Atherosclerosis; Autoimmune diseases; Autoimmunity; Cardiovascular disease; Cardiovascular Issues in Rheumatic Diseases; Carotid artery; Cell activation; Cerebral blood flow; Complement activation; Complement system; Computed tomography; Connective tissue diseases; Connective tissues; COVID-19; Embolism; Endothelial cells; Endothelium; Heart diseases; Ischemia; Leukocytes (neutrophilic); Lupus; Medical imaging; Medicine; Medicine & Public Health; Neutrophils; Nitric oxide; Pathophysiology; Pulmonary arteries; Pulmonary artery; Review; Review Article; Rheumatology; Scintigraphy; Severe acute respiratory syndrome coronavirus 2; Statins; Stenosis; Thromboembolism; Thrombosis; Traps
• ISSN: 0770-3198; 1434-9949; 1434-9949
• DOI: 10.1007/s10067-022-06497-1

An increased risk of atherosclerotic and thrombotic complications characterizes connective tissue diseases. Endothelial dysfunction is the basis for the initiation and progression of atherosclerosis and thrombosis. We present systemic lupus erythematosus (SLE) as a model rheumatic disease with endothelial dysfunction and discuss its mechanisms, factors that influence the early onset and rapid progression of atherosclerosis, and the increased risk of thromboembolic events. We focus on established methods to improve endothelium function, including statins, antiplatelet, and antithrombotic therapy. Hypercoagulable and hypofibrinolitic states and a hyperinflammatory response characterize severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. Several pathogenic mechanisms are typical for an acute phase of Covid-19 post-Covid syndrome and connective tissue diseases: endothelial dysfunction, elevated antiphospholipid antibody titer, activation of the complement system, and formation of extracellular neutrophil traps (NET). The current review discusses the mechanisms underlying SLE and the COVID-19 in the context of endothelial function, atherosclerosis, and thrombosis (Graphical abstract). Key Points • The pathophysiology of systemic lupus erythematosus (SLE) and Covid-19 shows some similarities, such as endothelial cell activation and dysfunction, the activation of complementary systems, the presence of antiphospholipid antibodies, and the formation of extracellular neutrophil traps. • Autoimmunity in both diseases creates the basis for hyperinflammatory, hypercoagulable, and hypofibrinolitic states and their thromboembolic complications. • This paper presents our perspective on the mechanisms behind the cardiovascular manifestations of SLE and COVID-19, with a particular emphasis on endothelial dysfunction. Graphical abstract Covid-19 and systemic lupus erythematosus—potential similarities in pathophysiology. Figures of the panel illustrate the clinical manifestations of endothelial dysfunction, atherosclerosis, and thromboembolism, including coronary artery disease ([A] coronary angiography with left anterior descending artery stenosis and [B] scintigraphy with reduced perfusion in the myocardial apical segments), stroke ([C] carotid angiography, left carotid artery occlusion) and pulmonary embolism ([D]computed tomography with thrombus in the right pulmonary artery).