Abstract
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.
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