Objectives Management of the pandemic caused by the novel coronavirus SARS-CoV-2 challenges both scientists and physicians to rapidly develop, and urgently assess, effective diagnostic tests and therapeutic interventions. The initial presentation of the disease in symptomatic patients is invariably respiratory, with dry cough being the main symptom, but an increasing number of reports reveal multiple organ involvement. The aim of this review is to summarise the potential role of the renin-angiotensin system activated phagocytes in the pathogenesis of COVID-19 disease. Methods Data for this review were identified by searches of PubMed, and references from relevant articles using the search terms “SARS”, “COVID-19”, “renin-angiotensin-system”, “phagocyte”, “reactive free radical”, “antioxidant”, “ARDS”, “thrombosis”, “myocardial”, “ischaemia”, “reperfusion”, “microvascular”, and “ACE2”. Abstracts and reports from meetings were not included in this work. Only articles published in English between 1976 and 2020 were reviewed. Results The cellular target of SARS viruses is the angiotensin converting enzyme 2, a critical regulating protein in the renin-angiotensin system. The elimination of this enzyme by the viral spike protein results in excessive activation of phagocytes, migration into the tissues via the high endothelial venules, and an oxidative burst. In the case of an over-stimulated host immune response, not only devastating respiratory symptoms, but even systemic or multiorgan involvement may be observed. Conclusion Early-stage medical interventions may assist in returning the exaggerated immune response to a normal range; however, some therapeutic delay might result in excessive tissue damages, occasionally mimicking a systemic disease with a detrimental outcome.

The coronavirus pandemic has spread globally and resulted in the registered deaths of over 5.5 million people, with nearly 380 million infected, straining health systems focused on transmission suppression and supportive care because specific treatment options are limited. COVID-19 is a microvascular disease with dominant respiratory representation, but a significant number of patients experience multisystem or extrarespiratory organ involvement. Although severe acute respiratory syndrome coronavirus-2 has some degree of a direct cytopathic effect on cardiomyocytes, the oxidative burst on a microvascular level seems to be the key for both short- and long-term adverse health effects. Targeted diagnostics and treatment without substantial delay may reduce the amplified immune response; otherwise, considerable tissue damage may occur with unfavourable consequences, including acute and chronic cardiac syndromes. This paper reviews the pathomechanisms relevant to the short- and long-term cardiac effects of COVID-19. Data were identified by searching the PubMed database and reviewing references from relevant articles published in English; abstracts and meeting reports were excluded.