The COVID-19 pandemic is an unprecedented healthcare emergency causing mortality and illness across the world. Although primarily affecting the lungs, the SARS-CoV-2 virus also affects the cardiovascular system. In addition to cardiac effects, e.g. myocarditis, arrhythmias, and myocardial damage, the vasculature is affected in COVID-19, both directly by the SARS-CoV-2 virus, and indirectly as a result of a systemic inflammatory cytokine storm. This includes the role of the vascular endothelium in the recruitment of inflammatory leucocytes where they contribute to tissue damage and cytokine release, which are key drivers of acute respiratory distress syndrome (ARDS), in disseminated intravascular coagulation, and cardiovascular complications in COVID-19. There is also evidence linking endothelial cells (ECs) to SARS-CoV-2 infection including: (i) the expression and function of its receptor angiotensin-converting enzyme 2 (ACE2) in the vasculature; (ii) the prevalence of a Kawasaki disease-like syndrome (vasculitis) in COVID-19; and (iii) evidence of EC infection with SARS-CoV-2 in patients with fatal COVID-19. Here, the Working Group on Atherosclerosis and Vascular Biology together with the Council of Basic Cardiovascular Science of the European Society of Cardiology provide a Position Statement on the importance of the endothelium in the underlying pathophysiology behind the clinical presentation in COVID-19 and identify key questions for future research to address. We propose that endothelial biomarkers and tests of function (e.g. flow-mediated dilatation) should be evaluated for their usefulness in the risk stratification of COVID-19 patients. A better understanding of the effects of SARS-CoV-2 on endothelial biology in both the micro- and macrovasculature is required, and endothelial function testing should be considered in the follow-up of convalescent COVID-19 patients for early detection of long-term cardiovascular complications.
Takayasu arteritis, a rare granulomatous vasculitis affecting young people, is associated with considerable morbidity and premature mortality. In most patients the diagnosis is delayed until after the development of substantial arterial injury. Studies of noninvasive imaging techniques suggest that these approaches might facilitate earlier diagnosis and have a role in monitoring disease progress; however, they remain limited in their ability to accurately quantify inflammatory disease activity in the arterial wall. A lack of controlled clinical trial data complicates the choice of therapy for Takayasu arteritis, and clinical indices for monitoring disease activity are currently suboptimal. Increasing knowledge of the pathogenesis of the large vessel vasculitides might eventually lead to novel targeted therapies. Preliminary data from open-label trials of anti-tumor necrosis factor therapy are encouraging, but there is an urgent need for controlled clinical trials to establish optimum therapeutic approaches for this disease. These trials should include a prospective assessment of the use of noninvasive imaging modalities in the diagnosis and subsequent management of Takayasu arteritis.
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