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Infective endocarditis is a rare disease in children. The etiology is mainly bacterial. However, viral infective endocarditis, possibly related to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has also been reported. The pathophysiological principle of the connection between the two entities seems to be attributed to the transient immune deficiency of the body during the infection. Additionally, SARS-CoV-2 is reported in the literature as a direct cardiopathic virus. Therefore, the new coronavirus seems to have the ability to affect both the intact cardiac tissue and the previously damaged one both during the acute episode and at a distance from it. Consequently, we propose to review the main pathophysiological aspects of pediatric cardiac damage caused by SARS-CoV-2. The ultimate goal is to deepen existing knowledge, broaden the horizon of understanding and analysis regarding the systemic damage induced by viral infections, and strengthen an information base from which to start a meta-analysis. Next, we performed a non-systematized screening of the specialized literature with reference to cases of endocarditis in the pediatric population, reported in the period 2020-2023. From the total of articles found, we chose to include in the review a number of 6 case reports, including a number of 7 patients (5 children and 2 adolescents). Analysis of reports suggests that SARS-CoV-2 infection could play a role in the development of endocarditis, either directly through active infection or indirectly through a post-infectious immune response. Also, pre-existing conditions and complex medical history predispose to an increased risk of developing a severe, complicated form of endocarditis. Also, the lack of data on the vaccination history and the failure to categorize the infection depending on the type of antibodies (IgM or IgG) in some studies represent a major bias in the reports. The latter make it difficult to evaluate the influence of vaccination and the impact of acute versus chronic infection on the course of cases., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2024 Lupu, Nedelcu, Budescu, Jechel, Starcea, Frasinariu, Ioniuc, Badescu, Salaru, Munteanu, Russu, Sascau, Statescu and Lupu.)

Alexandr Ceasovschih,1,2,* Victorita Sorodoc,1,2 Annabelle Shor,1,* Raluca Ecaterina Haliga,1,2,* Lynn Roth,3 Catalina Lionte,1,2 Viviana Onofrei Aursulesei,4,* Oana Sirbu,1,2,* Nicolae Culis,5 Albina Shapieva,6 Mohammed AR Tahir Khokhar,1 Cristian Statescu,7 Radu A Sascau,7 Adorata Elena Coman,1 Alexandra Stoica,1,2 Elena-Daniela Grigorescu,1 Maciej Banach,8 Costas Thomopoulos,9 Laurentiu Sorodoc1,2 1Faculty of Medicine, “Grigore T. Popa” University of Medicine and Pharmacy, Iasi, 700115, Romania; 2 2nd Internal Medicine Department, Sf. Spiridon Clinical Emergency Hospital, Iasi, 700111, Romania; 3Laboratory of Physiopharmacology, Department of Pharmaceutical Sciences, University of Antwerp, Wilrijk, 2610, Belgium; 4Department of Cardiology, Clinical Emergency Hospital “Sfantul Spiridon”, Iasi, 700106, Romania; 5Nottingham University Hospitals NHS Trust, Queen’s Medical Center, Nottingham, NG72UH, UK; 6Cardiac Electrophysiology Department, Petrovsky National Research Center of Surgery, Moscow, 119991, Russia; 7Department of Cardiology, Cardiovascular Diseases Institute “Prof. Dr. George I.M. Georgescu”, Iasi, 700503, Romania; 8Department of Preventive Cardiology and Lipidology, Medical University of Lodz (MUL), Lodz, 93338, Poland; 9Department of Cardiology, Elena Venizelou General Hospital, Athens, GR-11522, Greece*These authors contributed equally to this workCorrespondence: Victorita Sorodoc, 2nd Internal Medicine Department, Sf. Spiridon Clinical Emergency Hospital, Independentei 1 Street, Iasi, 700111, Romania, Tel +40232 240 822, Email vivisorodoc@yahoo.com Lynn Roth, Laboratory of Physiopharmacology, Department of Pharmaceutical Sciences, University of Antwerp, Wilrijk, 2610, Belgium, Email lynn.roth@uantwerpen.beAbstract: The Coronavirus Disease 2019 (COVID-19) pandemic was declared in early 2020 after several unexplained pneumonia cases were first reported in Wuhan, China, and subsequently in other parts of the world. Commonly, the disease comprises several clinical features, including high temperature, dry cough, shortness of breath, and hypoxia, associated with findings of interstitial pneumonia on chest X-ray and computer tomography. Nevertheless, severe forms of acute respiratory syndrome-related coronavirus 2 (SARS-CoV-2) are not limited to the respiratory tract but also may be extended to other systems, including the cardiovascular system. The bi-directional relationship between atherosclerosis and COVID-19 is accompanied by poor prognosis. The immune response hyperactivation due to SARS-CoV-2 infection causes an increased secretion of cytokines, endothelial dysfunction, and arterial stiffness, which promotes the development of atherosclerosis. Also, due to the COVID-19 pandemic, access to healthcare amenities was reduced, resulting in increased morbidity and mortality in patients at risk. Furthermore, as lockdown measures were largely adopted worldwide, the sedentary lifestyle and the increased consumption of processed nutrients or unhealthy food increased, and in the consequence, we might observe even 70% of overweight and obese population. Altogether, with the relatively low ratio of vaccinated people in many countries, and important health debt appeared, which is now and will be for next decade a large healthcare challenge. However, the experience gained in the COVID-19 pandemic and the new methods of patients’ approaching have helped the medical system to overcome this crisis and will hopefully help in the case of new possible epidemics.Keywords: vascular diseases, COVID-19, SARS-CoV-2, endothelial dysfunction, atherosclerosis, arterial stiffness, vaccines