RESUMEN
COVID-19 is caused by a coronavirus called SARS-CoV-2, which spread, all over the world. The virus is spreading very easily and sustainably between people. Information from the ongoing pandemic disease suggests that this virus is spreading more efficiently than influenza. Older adults and people who have severe underlying medical conditions like heart or lung disease or diabetes seem to be at higher risk for developing more serious complications from COVID-19 illness. Coronavirus constantly changes through mutation. When a virus has one or more new mutation, it has called a variant of concern. There is no data from Yemen to show what type of coronavirus variant is spread in Yemen. We believe it is a unique situation where almost all people have been affected by the coronavirus. We tested the cardiac center workers and we found all of them have positive results. No severe symptoms among our staff were reported and many of them suffered from mild to moderate symptoms, which does not need admission to the hospital. Young age among this worker sample may explain the mild severity of Covid-19 infection detected; another explanation is the frequent exposure to viral infection in Yemen and the type of coronavirus variant in Yemen. We conducted this review to describe the current situation and our experience during the pandemic and further studies are needed to identify the exact variant in Yemen and the immunity response for this coronavirus variant in the Yemeni Society.
RESUMEN
OBJECTIVES: Antimalarials have been associated with QT prolongation in COVID-19 patients but are generally safe in systemic lupus erythematosus (SLE).We compared the prevalence of QTc prolongation between COVID-19 and SLE patients treated with hydroxychloroquine (HCQ). METHODS: We included patients with SARS-CoV-2 infection confirmed by nasopharyngeal swab and patients taking HCQ for SLE. A prolonged QTc was defined as an increase in QTc intervals >60 ms (compared with baseline) or as a QTc of ≥500 ms. We performed the univariate and multivariate logistic regression to investigate the risk factors for QTc prolongation in COVID-19 patients. RESULTS: We enrolled 58 COVID-19 patients (median age 70.5 years, IQR 25), grouped into group A (patients with HCQ) group B (patients with HCQ + azithromycin) and group C (not received either drug). Fifty (26%) COVID-19 patients presented a QTc prolongation (12 QTc≥500 ms, 3 patients ΔQTc>60 ms). We did not find any differences in QTc prolongation among the three treatment groups. Baseline QTc (OR 111.5) and D-dimer (OR 78.3) were independently associated to QTc prolongation. Compared to the 50 SLE patients (median age 38.5 years, IQR 22), chronically treated with HCQ, COVID-19 patients showed significantly longer QTc (p<0.001). CONCLUSIONS: This is the first study demonstrating that, unlike COVID-19 patients, patients with SLE are not susceptible to HCQ-induced long QT syndrome and arrhythmia. The combined arrhythmogenic effect of SARS-CoV-2 infection and HCQ could account for the excess of QTc prolongation and fatal arrhythmias described in patients with COVID-19.