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INTRODUCTION: In late 2019, a novel strain of coronavirus, discovered in the city of Wuhan, China, was found to cause a disease later named coronavirus disease 2019, or COVID-19. In January 2020, COVID-19 first reached the Gulf region. Afterwards, the disease spread rapidly across the countries of the Gulf and the number of COVID-19 cases rose significantly. Now, more than a year later, there are only a limited number of studies regarding COVID-19 and its behavior in this region. In this article, we aim to assess the mortality caused by the disease in the Gulf region by calculating the Case Fatality Rates (CFR) for all of the Gulf Cooperation countries and comparing the results with those of Europe. METHODS: Data was obtained from the official statistics of the World Health Organization (WHO) from January to May 2020. From the data, the CFR was calculated for every Gulf and European country included in the study. Following the calculation, the results were compared and analyzed. To make our comparison more accurate, we added the total number of COVID-19 tests per 1000 population and the Health Access and Quality index for each individual country. RESULTS: CFRs in the Gulf region to May 12, 2020 were: United Arab Emirates (1.06%), Kuwait (0.69%), Saudi Arabia (0.62%), Oman (0.45%), Bahrain (0.15%), and Qatar (0.06%). Within Europe over the same time period, 10 countries had CFRs above 10%, with the majority above 3%. CONCLUSIONS: Compared to Europe, the COVID-19 mortality rate in the Gulf region has been much lower. The difference in age groups between the Gulf region and Europe may be the most important factor, mainly due to a younger population and a smaller elderly demographic in the Gulf region. Although age is a strong factor for the lower CFR in the Gulf, other factors must also be considered. These include the number of COVID-19 tests conducted per population, different country capabilities, and varying criteria for reporting COVID-19 deaths(Table-1)(Table-2).
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Ebstein's anomaly is a rare congenital heart disorder that causes displacement of the tricuspid valve towards the apex of the heart. Patients with this anomaly rarely survive beyond the age of 70 without surgical correction. When such patients survive till adulthood, they tend to present with atrial arrhythmias. Although radiofrequency ablation is harder to successfully complete due to disrupted anatomy of the heart, it can be the best choice for terminating arrhythmias in such patients. Here, we present a case of a 76-year-old patient with an uncorrected Ebstein's anomaly that presented with atrial flutter and was treated successfully with radiofrequency ablation.
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The objective of this study was to determine a safe and effective dose of granulocyte-colony stimulating factor (G-CSF) to mobilize hematopoietic stem cells in patients with advanced heart failure and to determine its effects on the cytokine profile. Patients with advanced heart failure (n = 6) and implantable defibrillators in situ were administered G-CSF after baseline echocardiographic and laboratory evaluation, using an escalating dose schedule designed to ensure safety. The peripheral CD34+ hematopoietic stem cell count increased from 3.6 +/- 0.5/microl to 38.7 +/- 13/microl (p= 0.022) after 5 days of 5 microg/kg/day G-CSF therapy. The baseline or peak white blood cell count did not predict the stem cell response. G-CSF increased plasma levels of interleukin-10. Left ventricular ejection fraction increased significantly in the 4 patients with ischemic cardiomyopathy 9 months after treatment. No major adverse effects attributable to the drug occurred during administration or 9 months of follow-up. Our results have shown that low-dose G-CSF significantly mobilized hematopoietic stem cells in advanced heart failure and improved left ventricular function in the ischemic subset of patients. G-CSF significantly increased plasma levels of the anti-inflammatory cytokine interleukin-10, without changing pro-inflammatory cytokine levels. In conclusion, these results indicate a novel mechanism of action for the potential therapeutic benefit of G-CSF in advanced ischemic cardiomyopathy.
