Prevalence and prognostic implications of myocardial injury across different waves of COVID-19.

Introduction: The prognostic ability of myocardial injury across different waves of the COVID-19 pandemic is not well established. The purpose of this study was to evaluate the prevalence and prognostic implications of myocardial injury in the first and sixth wave of COVID-19. Methods: We conducted a retrospective observational study that included patients admitted to the emergency department with COVID-19 with data on concentrations of cardiac troponin during the first and sixth wave. We compared the prevalence of myocardial injury and its predictive capacity for 30-day all-cause death in both waves. Results and discussion: A total of 346 patients were included (1st wave 199 and 6th wave 147 patients). The prevalence of myocardial injury was 21% with non-significant differences between waves. Myocardial injury was associated, in both waves, with a higher prevalence of comorbidities and with an increased risk of 30-day all-cause death [1st wave HR: 3.73 (1.84-7.55); p < 0.001 and 6th wave HR: 3.13 (1.23-7.92); p = 0.016], with non-significant differences in predictive capacity between groups after ROC curve analysis [AUC: 1st wave 0.829 (95% CI: 0.764-0.895) and 6th wave 0.794 (95% CI: 0.711-0.876)]. As limitations, this is a retrospective study with a relatively small simple size and troponin assay was performed at the discretion of the emergency physician so selection bias could be present. In conclusion, the prevalence of myocardial injury and its prognostic capacity was similar in both waves despite vaccination programs. Myocardial injury predicts short-term mortality in all COVID-19 patients, so they should be treated intensively.

Clinical characteristics and prognostic implications of diabetes and myocardial injury in patients admitted to the emergency room.

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.

Biomarkers and short-term prognosis in COVID-19.

PURPOSE: The aim of our study was to analyse the short-term prognostic value of different biomarkers in patients with COVID-19. METHODS: 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. RESULTS: 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). CONCLUSIONS: 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.

[Prognostic implications of myocardial injury in patients with and without COVID-19 infection treated in a university hospital]. / Implicaciones pronósticas del daño miocárdico en pacientes con y sin diagnóstico confirmado de COVID-19 atendidos en un hospital universitario.

INTRODUCTION AND OBJECTIVES: Cardiac troponin, a marker of myocardial injury, is frequently observed in patients with COVID-19 infection. Our objective was to analyze myocardial injury and its prognostic implications in patients with and without COVID-19 infection treated in the same period of time. METHODS: The present study included patients treated in a university hospital with cardiac troponin I measurements and with suspected COVID-19 infection, confirmed or ruled out by polymerase chain reaction analysis. The impact was analyzed of cardiac troponin I positivity on 30-day mortality. RESULTS: In total, 433 patients were distributed among the following groups: confirmed COVID-19 (n = 186), 22% with myocardial injury (n = 41); and ruled out COVID-19 (n = 247), 21.5% with myocardial injury (n = 52). The confirmed and ruled out COVID-19 groups had a similar age, sex, and cardiovascular history. Mortality was significantly higher in the confirmed COVID-19 group than in the ruled out group (19.9% vs 5.3%, P < .001). In Cox multivariate regression analysis, cardiac troponin I was a predictor of mortality in both groups (confirmed COVID-19 group: HR, 3.54; 95%CI, 1.70-7.34; P = .001; ruled out COVID-19 group: HR, 5.57; 95%CI, 1.70-18.20; P = .004). The predictive model analyzed by ROC curves was similar in the 2 groups (P = .701), with AUCs of 0.808 in the confirmed COVID-19 group (0.750-0.865) and 0.812 in the ruled out COVID-19 group (0.760-0.864). CONCLUSIONS: Myocardial injury is detected in 1 in every 5 patients with confirmed or ruled out COVID-19 and predicts 30-day mortality to a similar extent in both circumstances.

Prognostic implications of myocardial injury in patients with and without COVID-19 infection treated in a university hospital.

INTRODUCTION AND OBJECTIVES: Cardiac troponin, a marker of myocardial injury, is frequently observed in patients with COVID-19 infection. Our objective was to analyze myocardial injury and its prognostic implications in patients with and without COVID-19 infection treated in the same period of time. METHODS: The present study included patients treated in a university hospital with cardiac troponin I measurements and with suspected COVID-19 infection, confirmed or ruled out by polymerase chain reaction analysis. The impact was analyzed of cardiac troponin I positivity on 30-day mortality. RESULTS: In total, 433 patients were distributed among the following groups: confirmed COVID-19 (n=186), 22% with myocardial injury (n=41); and ruled out COVID-19 (n=247), 21.5% with myocardial injury (n=52). The confirmed and ruled out COVID-19 groups had a similar age, sex, and cardiovascular history. Mortality was significantly higher in the confirmed COVID-19 group than in the ruled out group (19.9% vs 5.3%, P <.001). In Cox multivariate regression analysis, cardiac troponin I was a predictor of mortality in both groups (confirmed COVID-19 group: HR, 3.54; 95%CI, 1.70-7.34; P=.001; ruled out COVID-19 group: HR, 5.57; 95%CI, 1.70-18.20; P=.004). The predictive model analyzed by ROC curves was similar in the 2 groups (P=.701), with AUCs of 0.808 in the confirmed COVID-19 group (0.750-0.865) and 0.812 in the ruled out COVID-19 group (0.760-0.864). CONCLUSIONS: Myocardial injury is detected in 1 in every 5 patients with confirmed or ruled out COVID-19 and predicts 30-day mortality to a similar extent in both circumstances.

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

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.

Implicaciones pronósticas del daño miocárdico en pacientes con y sin diagnóstico confirmado de COVID-19 atendidos en un hospital universitario / Prognostic implications of myocardial injury in patients with and without COVID-19 infection treated in a university hospital

INTRODUCCIÓN Y OBJETIVOS: La elevación de la troponina cardiaca como marcador de daño miocárdico es un predictor pronóstico en pacientes con COVID-19. Sin embargo, se desconoce su rendimiento en pacientes coetáneos con sospecha de COVID-19 pero con prueba de reacción en cadena de la polimerasa negativa. MÉTODOS: Estudio de cohortes retrospectivo que incluyó a todos los pacientes consecutivos atendidos en un hospital universitario con sospecha de COVID-19, confirmada o descartada mediante prueba de reacción en cadena de la polimerasa, todos ellos con determinaciones de troponina cardiaca I. Se analizó el impacto de la positividad de la troponina cardiaca I en la mortalidad a 30 días. RESULTADOS: Un total de 433 pacientes quedaron distribuidos en los siguientes grupos: COVID-19 confirmada (n=186), el 22% de ellos con daño miocárdico (n=41), y COVID-19 descartada (n=247), el 21,5% de ellos con daño miocárdico (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 <0,001). En ambos grupos, el daño miocárdico fue predictor de mortalidad en el análisis multivariado de regresión de Cox (grupo de COVID-19 confirmada, HR=3,54; IC95%, 1,70-7,34; p = 0,001; grupo de COVID-19 descartada, HR=5,57; IC95%, 1,70-18,20; p = 0,004). El modelo predictivo analizado por curvas ROC fue similar en ambos grupos: COVID-19 confirmada, AUC=0,808 (0,750-0,865); COVID-19 descartada, AUC=0,812 (0,760-0,864) (p = 0,701). CONCLUSIONES: Se detecta daño miocárdico en 1 de cada 5 pacientes con infección por COVID-19 confirmada o descartada. En ambas circunstancias, el daño miocárdico es predictor de mortalidad a 30 días en similar grado

INTRODUCTION AND OBJECTIVES: Cardiac troponin, a marker of myocardial injury, is frequently observed in patients with COVID-19 infection. Our objective was to analyze myocardial injury and its prognostic implications in patients with and without COVID-19 infection treated in the same period of time. METHODS: The present study included patients treated in a university hospital with cardiac troponin I measurements and with suspected COVID-19 infection, confirmed or ruled out by polymerase chain reaction analysis. The impact was analyzed of cardiac troponin I positivity on 30-day mortality. RESULTS: In total, 433 patients were distributed among the following groups: confirmed COVID-19 (n=186), 22% with myocardial injury (n=41); and ruled out COVID-19 (n=247), 21.5% with myocardial injury (n=52). The confirmed and ruled out COVID-19 groups had a similar age, sex, and cardiovascular history. Mortality was significantly higher in the confirmed COVID-19 group than in the ruled out group (19.9% vs 5.3%, P <.001). In Cox multivariate regression analysis, cardiac troponin I was a predictor of mortality in both groups (confirmed COVID-19 group: HR, 3.54; 95%CI, 1.70-7.34; P=.001; ruled out COVID-19 group: HR, 5.57; 95%CI, 1.70-18.20; P=.004). The predictive model analyzed by ROC curves was similar in the 2 groups (P=.701), with AUCs of 0.808 in the confirmed COVID-19 group (0.750-0.865) and 0.812 in the ruled out COVID-19 group (0.760-0.864). CONCLUSIONS: Myocardial injury is detected in 1 in every 5 patients with confirmed or ruled out COVID-19 and predicts 30-day mortality to a similar extent in both circumstances