By now cardiac pathology in children has been described in very rare cases beyond the systemic inflammatory disease and general case fatality is low. Tissue damage to lungs, heart and other organs induced by SARS-CoV-2 is induced by binding of the virus with its surface spike glycoprotein to the host ACE2 receptor. In the human heart the receptors are localized at the pericytes, and their injury can lead to secondary capillary endothelial dysfunction, responsible for cardiac pathology. [11] The lower number and immaturity of ACE2 in children has been speculated to be one of the reasons of milder nature of COVID-19. [12]
Clinical symptoms of myocardial damage of adults affected with COVID-19 are rhythm disorders, hypotension and cardiogenic shock. Biomarkers like troponin, creatine kinase and lactate dehydrogenase and high sensitive Troponin (cTnI) are elevated. Acute myocarditis has been suspected in adults as myocardial interstitial edema and diffuse late gadolinium enhancement could be documented. [13] It remains obscure whether all cardiac pathologies are related to primary viral attack of cardiomyocytes or whether it is the result of proinflammatory cytokines and systemic inflammatory response.
Fulminant acute myocardial necrosis and mononuclear cell infiltration has been described, but only rarely virus particles could be demonstrated in myocardial tissue. [14] Together with a timely delayed presentation of symptoms (10-15 days) these findings might be interpreted in favor to inflammation mediated myocardial injury rather than induced by the cytopathic effect of the virus. [15]
Hyperinflammation, imbalance of renin-angiotensin-aldosterone system, and a particular form of vasculopathy, thrombotic microangiopathy are reported to contribute to increased severity of COVID-19 not only in respiratory but also in cardiac failure. [16]
In this context also in children impaired cardiac function, vasculitis and septic shock as well as features of Kawasaki disease shock syndrome have been described with distinct differences in inflammatory markers. While coronary involvement was variable, depressed LV-function, pericardial effusion and arrhythmia were the main findings. [17,18] Actually the European Centre for Disease Prevention and Control (ECDC) judged this „multisystem inflammatory syndrome in children (MIS-C)“ as associated with but not caused by SARS-CoV-2 – infection.
Whether children with underlying cardiac diseases are more susceptible to cardiac injury remains obscure. From an US-cohort of 177 patients infected with SARS-Cov-2, 3% had a preexisting cardiac disease and hospital admission occurred a little more frequently but not the severity of the symptoms. [19] Nevertheless, and although not scientifically proven most children and adults with congenital heart disease presenting with severe cyanosis, pulmonary hypertension or heart failure should be monitored more closely during SARS-Cov-2 pandemic.
As in adults underlying cardiac diseases with decreased cardiac reserve and enhanced metabolic demand contribute to increased severity of respiratory symptoms and worse outcome. [20,21] Some risk factors in the adult population for higher susceptibility to COVID-19 outcome are partly rebutted, like arterial hypertension.
A comprehensive guidance document has been established that addresses all management aspects of cardiovascular diseases in adults during the COVID-19 pandemic. [6]