RESUMEN
Background and Aim: We aimed to evaluate cardiac manifestations of the multisystem inflammatory syndrome in children(MIS-C) and the changes in cardiac function during one year of follow-up. Method(s): All children diagnosed as MIS-C with cardiac involve-ment were enrolled in this prospective study. The diagnosis and severity of the disease of MIS-C was made according to the Centers for Disease Control and World Health Organization guidelines. Clinical findings, laboratory parameters including car-diac markers, electrocardiographic and echocardiographic findings at the time of diagnosis and during follow-up were evaluated. Cardiac magnetic resonance imaging (MRI) was performed on all children with echocardiographic abnormality. Result(s): Between April 1st 2020 and December 1st 2021,71 chil-dren were diagnosed with MIS-C and 44 of these patients had car-diac involvement (25 male and 19 female). 24 patients were followed up in the intensive care unit and all of these patients had myocardial involvement. All the patients had elevated NT-proBNP levels (median:5893pg/ml) whereas troponin-T levels were above upper limit in 13 patients. A significant positive cor-relation was found between troponin-T and NT-proBNP (plt;0.01). The NT-proBNP levels were also positively correlated with the severity of MIS-C (plt;0.05). On admission 22 patients had tachycardia and atrioventricular conduction disturbances and supraventricular tachycardia developed in 5 of these patients during follow-up. Bradycardia was observed in 18(40%) patients during hospitalization (4 of these occurred after tachycardia). Although 26 patients had an echocardiographic abnormality, only twelve patients had systolic dysfunction (9 with mild and 3 with moderate) and two patients had diastolic dysfunction. NT-proBNP and troponin-T were negatively correlated with ejection fraction ve fractional shortening (respectively, p = 0.003, p = 0.013). Cardiac MRI was normal in all patients except 3 patients who had myocardial late gadolinium enhancement of left ven-tricle. Pericardial effusion was observed in 14 patients. The echo-cardiographic abnormalities disappeared in 42 patients during follow-up, one patient died on the second day of hospitalization and and 1 patient has ongoing LV systolic dysfunction. Conclusion(s): Bradycardia and myocardial involvement is common during MIS-C. Although myocardial dysfunction can be observed during acute disease, commonly the disease does not cause perma-nent damage during one year of follow-up.
RESUMEN
The World Health Organization (WHO) has announced that Severe Acute Respiratory Syndrome Coronavirus-2 (SARS-CoV-2) and Coronavirus disease (COVID-19) is considered a worldwide pandemic. Rapidly rising numbers of patients have been reported in almost every country, along with the growing mortality rates. Uncontrolled growth in patient numbers may be due to reasons such as treatment options and vaccine availabilities and unidentified targets of SARS-CoV-2. Previous study has revealed that the molecular target of SARS-CoV-2 is analogous to SARS (2003), i.e. angiotensin-converting enzyme-2 (ACE-2). Therefore, the determination of ACE-2 may enrich existing information and facilitate development of drugs targeted toward SARS-CoV-2. This study aims to screen the expression of ACE-2 genes and their relationship to the types of SNP variants in SARS-CoV-2. We explored a series of observations using powerful databases, e.g. GTEx portal, HaploReg, 1000 Genome and Ensembl, to identify the gene variant of ACE-2. We showed that ACE-2 is highly expressed in the testes and small intestine, while its lowest level is observed in lymphocytes. Subsequently, we observed 17 gene variants containing a missense mutation potentially damaging protein level. Among these genes, single nucleotide polymorphism (SNP) rs370187012 shows the highest damage-level score, while the lowest effect is in SNP rs4646116. The highest frequency of the C allele was observed in European populations (1%). In addition to showing that ACE-2 is expressed in several organs, we concluded that the ACE-2 gene variation can be found in African, American, Southeast and East Asian, and European populations. The polymorphisms of ACE-2 impact on the ACE2 protein structure and the binding capacity of the ACE-2 receptor with the S-Protein of SARS-CoV-2.