Vol. 52 | No. 1 | January-June 2024 Back

Open Access

Impact of Age, Sex, and Cardiovascular Disease in Mortality in COVID-19 at the Medical City

Abstract

INTRODUCTION: COVID-19 (coronavirus disease 2019), which is caused by the human severe acute respiratory syndrome coronavirus 2 (SARS-COV-2), has reached a pandemic level. As a novel disease, local epidemiologic data are important to determine high-risk age groups, as well as risk factors that contribute to mortality. This study is a retrospective cohort study of 182 COVID-19–positive patients confirmed by real-time polymerase chain reaction. Baseline demographics and data on the preexisting cardiovascular comorbidities of 182 COVID-19 patients were collected by chart review and underwent statistical analysis using STATA 14 software (StataCorp, College Station, Texas). In the study, the majority of COVID-19 patients were 61 years or older (44.5%), with a higher prevalence of individuals 61 years or older among those who died (68.4%) compared with survivors (38.2%) (P = 0.005). In terms of gender, half of the patients were male (57.7%). In terms of cardiovascular disease, the most prevalent was hypertension (48.3%), followed by diabetes (28.0%). The prevalence of coronary artery disease (CAD) was significantly higher among patients who died (15.8%) compared with survivors (2.8%) (P = 0.022). In the univariate logistic regression analysis, older age was significantly associated with increased odds for mortality (odds ratio, 1.06; 95% confidence interval, 1.03–1.09). In terms of comorbidities, having CAD was significantly associated with increased odds for mortality (odds ratio, 6.6; 95% confidence interval, 1.7–24.6). Other variables were not significantly associated with mortality. In our study, advanced age and the presence of underlying CAD have been associated with an increased risk of in-hospital mortality among COVID-19 patients.

KEYWORDS: age, cardiovascular disease, COVID-19, mortality, sex

  1. World Health Organization Western Pacific. Coronavirus disease (COVID-19) outbreak. 2020. https://www.who.int/ westernpacific/emergencies/covid-19. Accessed May 11, 2020.
  2. World Health Organization Maldives. 2020. https://www. who.int/docs/default-source/maldives/novel-corona-virus update-mav-30jan.pdf?sfvrsn=a10dfb7b. Accessed May 11, 2020.
  3. United Nations Children’s Fund, World Health Organization, & International Federation of Red Cross. Key Messages and Actions for COVID-19 Prevention and Control in Schools. 2020. https://www.who.int/docs/default-source/ coronaviruse/key-messages-and-actions-for-covid-19- prevention-and-control-in-schools-march-2020.pdf. Accessed May 28, 2020.
  4. Yang X, Yu Y, Xu J, et al. Clinical course and outcomes of critically ill patients with SARS-CoV-2 pneumonia in Wuhan, China: a single-centered, retrospective, observational study. Lancet Respir Med 2020;8(5):475–481. doi:10.1016/ s2213-2600(20)30079-5.
  5. Gu T, Chu Q, Yu Z, et al. History of coronary heart disease increases the mortality rate of COVID-19 patients: a nested case-control study. 2020. medRxiv 2020.03.23.20041848. doi:10.1101/2020.03.23.20041848.
  6. Mehra M, Desai S, Kuy S, Henry T, Patel A. Cardiovascular disease, drug therapy, and mortality in COVID-19. N Engl J Med 2020. doi:10.1056/nejmoa2007621.
  7. Franceschi C, Bonafè M, Valensin S, et al. Inflamm-aging. An evolutionary perspective on immunosenescence. Ann N Y Acad Sci 2000;908:244–254. https://doi. org/10.1111/j.1749-6632.2000.tb06651.x.
  8. Liu Y, Yan LM, Wan L, et al. Viral dynamics in mild and severe cases of COVID-19 [published online March 19, 2020]. Lancet Infect Dis 2020;20(6):656–657. https://doi. org/10.1016/S1473-3099(20)30232-2.
  9. Libby P, Tabas I, Fredman G, Fisher E. Inflammation and its resolution as determinants of acute coronary syndromes. Circ Res 2014;114:1867–1879.
  10. De la Vega R, Barquín RR, Boros S, Szabo A. Could attitudes toward COVID-19 in Spain render men more vulnerable than women? Glob Public Health 2020;15(9):1278–1291. https://doi.org/10.31234/osf.io/ dyxqn.
  11. Stopsack KH, Mucci LA, Antonarakis ES, Nelson PS, Kantoff PW. TMPRSS2 and COVID-19: serendipity or opportunity for intervention? Cancer Discov 2020;10:779– 782.

Open Access This article is licensed under a Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International License, which permits use, share — copy and redistribute the material in any medium or format, adapt — remix, transform, and build upon the material, as long as you give appropriate credit, provide a link to the license, and indicate if changes were made. You may do so in any reasonable manner, but not in any way that suggests the licensor endorses you or your use. You may not use the material for commercial purposes. If you remix, transform, or build upon the material, you must distribute your contributions under the same license as the original. You may not apply legal terms or technological measures that legally restrict others from doing anything the license permits. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit https://creativecommons.org/licenses/by-nc-sa/4.0/.