Lack of Association of Initial Viral Load in SARS-CoV-2 Patients with In-Hospital Mortality

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  • 1 Department of Cardiology, Joan XXIII University Hospital, Tarragona, Spain;
  • 2 Pere Virgili Health Research Institute (IISPV), Tarragona, Spain;
  • 3 Rovira i Virgili University, Tarragona, Spain;
  • 4 Clinical Laboratory, Catalan Institute of HealthTarragona, Spain;
  • 5 Infectious Disease Unit, Department of Internal Medicine, Joan XXIII University Hospital, Tarragona, Spain

Controversy exists in the literature regarding the possible prognostic implications of the nasopharyngeal SARS-CoV-2 viral load. We carried out a retrospective observational study of 169 patients, 96 (58.9%) of whom had a high viral load and the remaining had a low viral load. Compared with patients with a low viral load, patients with a high viral load did not exhibit differences regarding preexisting cardiovascular risk factors or comorbidities. There were no differences in symptoms, vital signs, or laboratory tests in either group, except for the maximum cardiac troponin I (cTnI), which was higher in the group with a higher viral load (24 [interquartile range 9.5–58.5] versus 8.5 [interquartile range 3–22.5] ng/L, P = 0.007). There were no differences in the need for hospital admission, admission to the intensive care unit, or the need for mechanical ventilation in clinical management. In-hospital mortality was greater in patients who had a higher viral load than in those with low viral load (24% versus 10.4%, P = 0.029). High viral loads were associated with in-hospital mortality in the binary logistic regression analysis (odds ratio: 2.701, 95% Charlson Index (CI): 1.084–6.725, P = 0.033). However, in an analysis adjusted for age, gender, CI, and cTnI, viral load was no longer a predictor of mortality. In conclusion, an elevated nasopharyngeal viral load was not a determinant of in-hospital mortality in patients with COVID-19, as much as age, comorbidity, and myocardial damage determined by elevated cTnI are.

Author Notes

Address correspondence to Alfredo Bardají, Cardiology Service, Tarragona Joan XXIII University Hospital, Rovira Virgili University, IISPV, Calle Dr Mallafré Guash 4, Tarragona 43005, Spain. E-mail: abardaji.hj23.ics@gencat.cat

Financial support: This project has been carried out, in part, with the help of a FIS grant on Health Research Projects, Strategic Action in Health 2017–2020, PI19/00705, and by a the grant COVID-19 6_17 (to Francesc Vidal), Direcció General de Recerca i Innovació en Salut (Departament de Salut) and BIOCAT, Generalitat de Catalunya.

Authors’ addresses: Anna Carrasquer, Óscar M. Peiró, Raul Sanchez-Gimenez, Nisha Lal-Trehan, Victor del-Moral-Ronda, Gil Bonet, and Alfredo Bardají, Department of Cardiology, Joan XXIII University Hospital, Pere Virgili Health Research Institute (IISPV), Rovira Virgili University, Tarragona, Spain, E-mails: carrasquer1987@gmail.com, opi220290@gmail.com, raul.sagi@hotmail.com, nishalal593@gmail.com, moral.ronda@gmail.com, gil.bonet.p@gmail.com, and abardaji.hj23.ics@gencat.cat. Cristina Gutierrez, Isabel Fort-Gallifa, Carla Martin-Grau, and Clara Benavent, Clinical Laboratory, Catalan Institute of Health, Tarragona, Spain, E-mails: cgutierrez.hj23.ics@gencat.cat, ifgallifa.hj23.ics@gencat.cat, cgmartin.hj23.ics@gencat.cat, and cbenavent.hj23.ics@gencat.cat. Francesc Vidal, Infectious Disease Unit, Department of Internal Medicine, Joan XXIII University Hospital, Pere Virgili Health Research Institute (IISPV), Rovira Virgili University, Tarragona, Spain, E-mail: abardaji.hj23.ics@gencat.cat.

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