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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.

Background This study aimed to investigate the clinical features and prognosis of diabetes and myocardial injury in patients admitted to the emergency department. Methods We analyzed the clinical data of all consecutive patients admitted to the emergency department during the years 2012 and 2013 with at least 1 cardiac Troponin I (cTnI Ultra Siemens, Advia Centaur) determination, and were classified according to the status of diabetes mellitus (DM) and myocardial injury (MI). Clinical events were evaluated in a 4-year follow-up. Results A total of 3622 patients were classified according to the presence of DM (n = 924 (25.55%)) and MI (n = 1049 (28.96%)). The proportion of MI in patients with DM was 40% and 25% in patients without DM. Mortality during follow-up was 10.9% in non-DM patients without MI, 21.3% in DM patients without MI, 40.1% in non-DM patients with MI, and 52.8% in DM patients with MI. A competitive risk model was used to obtain the Hazard Ratio (HR) for readmission for myocardial infarction or heart failure. There was a similar proportion of readmission for myocardial infarction and heart failure at a four-year follow-up in patients with DM or MI, which was much higher when DM was associated with MI, with respect to patients without DM or MI. The HR (95% Coefficient Interval) for myocardial infarction in the DM without MI, non-DM with MI, and DM with MI groups with respect to the non-DM without MI group was 2511 (1592–3960), 2682 (1739–4138), and 5036 (3221–7876), respectively. The HR (95% CI) for the risk of readmission for heart failure in the DM without MI, non-DM with MI, and DM with MI groups with respect to the non-DM without MI group was 2663 (1825–3886), 2562 (1753–3744) and 4292 (2936–6274), respectively. Conclusions The association of DM and MI in patients treated in an Emergency Service identifies patients at very high risk of mortality and cardiovascular events.

The aim of our study was to analyse the short-term prognostic value of different biomarkers in patients with COVID-19. We included patients admitted to emergency department with COVID-19 and available concentrations of cardiac troponin I (cTnI), D-dimer, C-reactive protein (CRP) and lactate dehydrogenase (LDH). Patients were classified for each biomarker into two groups (low vs. high concentrations) according to their best cut-off point, and 30-day all-cause death was evaluated. After multivariate adjustment, cTnI ≥21 ng/L, D-dimer ≥1112 ng/mL, CRP ≥10 mg/dL and LDH ≥334 U/L at admission were associated with an increased risk of 30-day all-cause death (hazard ratio (HR) 4.30; 95% CI 1.74–10.58; p = 0.002; HR 3.35; 95% CI 1.58–7.13; p = 0.002; HR 2.25; 95% CI 1.13–4.50; p = 0.021; HR 2.00; 95% CI 1.04–3.84; p = 0.039, respectively). The area under the curve for cTnI was 0.825 (95% CI 0.759–0.892) and, in comparison, was significantly better than CRP (0.685; 95% CI 0.600–0.770; p = 0.009) and LDH (0.643; 95% CI 0.534–0.753; p = 0.006) but non-significantly better than D-dimer (0.756; 95% CI 0.674–0.837; p = 0.115). In patients with COVID-19, increased concentrations of cTnI, D-dimer, CRP and LDH are associated with short-term mortality. Of these, cTnI provides better mortality risk prediction. However, differences with D-dimer were non-significant.

Resumen Introduccion y objetivos La elevacion de la troponina cardiaca como marcador de dano miocardico es un predictor pronostico en pacientes con COVID-19. Sin embargo, se desconoce su rendimiento en pacientes coetaneos con sospecha de COVID-19 pero con prueba de reaccion en cadena de la polimerasa negativa. Metodos Estudio de cohortes retrospectivo que incluyo a todos los pacientes consecutivos atendidos en un hospital universitario con sospecha de COVID-19, confirmada o descartada mediante prueba de reaccion en cadena de la polimerasa, todos ellos con determinaciones de troponina cardiaca I. Se analizo el impacto de la positividad de la troponina cardiaca I en la mortalidad a 30 dias. Resultados Un total de 433 pacientes quedaron distribuidos en los siguientes grupos: COVID-19 confirmada (n = 186), el 22% de ellos con dano miocardico (n = 41), y COVID-19 descartada (n = 247), el 21,5% de ellos con dano miocardico (n = 52). Los grupos de COVID-19 confirmada y descartada tuvieron similares edad, sexo y antecedentes cardiovasculares. La mortalidad en el grupo de COVID-19 confirmada frente al de descartada fue significativamente superior (el 19,9 frente al 5,3%; p Conclusiones Se detecta dano miocardico en 1 de cada 5 pacientes con infeccion por COVID-19 confirmada o descartada. En ambas circunstancias, el dano miocardico es predictor de mortalidad a 30 dias en similar grado.