The prognostic value of serial troponin measurements in patients admitted for COVID-19.
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ABSTRACT: Aims
Myocardial injury (MI) in coronavirus disease-19 (COVID-19) is quite prevalent at admission and affects prognosis. Little is known about troponin trajectories and their prognostic role. We aimed to describe the early in-hospital evolution of MI and its prognostic impact.Methods and results
We performed an analysis from an Italian multicentre study enrolling COVID-19 patients, hospitalized from 1 March to 9 April 2020. MI was defined as increased troponin level. The first troponin was tested within 24 h from admission, the second one between 24 and 48 h. Elevated troponin was defined as values above the 99th percentile of normal values. Patients were divided in four groups: normal, normal then elevated, elevated then normal, and elevated. The outcome was in-hospital death. The study population included 197 patients; 41% had normal troponin at both evaluations, 44% had elevated troponin at both assessments, 8% had normal then elevated troponin, and 7% had elevated then normal troponin. During hospitalization, 49 (25%) patients died. Patients with incident MI, with persistent MI, and with MI only at admission had a higher risk of death compared with those with normal troponin at both evaluations (P < 0.001). At multivariable analysis, patients with normal troponin at admission and MI injury on Day 2 had the highest mortality risk (hazard ratio 3.78, 95% confidence interval 1.10-13.09, P = 0.035).Conclusions
In patients admitted for COVID-19, re-test MI on Day 2 provides a prognostic value. A non-negligible proportion of patients with incident MI on Day 2 is identified at high risk of death only by the second measurement.
SUBMITTER: Nuzzi V
PROVIDER: S-EPMC8426962 | biostudies-literature |
REPOSITORIES: biostudies-literature
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| S-EPMC7766903 | biostudies-literature
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| S-EPMC7811154 | biostudies-literature
Project description:BackgroundIncreases in cardiac troponin (cTn) in coronavirus disease 2019 (COVID-19) have been associated with worse prognosis. Nonetheless, data about the significance of cTn in elderly subjects with COVID-19 are lacking.MethodsFrom a registry of consecutive patients with COVID-19 admitted to a hub hospital in Italy from 25/02/2020 to 03/07/2020, we selected those ≥ 60 year-old and with cTnI measured within three days from the molecular diagnosis of SARS-CoV-2 infection. When available, a second cTnI value within 48 h was also extracted. The relationship between increased cTnI and all-cause in-hospital mortality was evaluated by a Cox regression model and restricted cubic spline functions with three knots.ResultsOf 343 included patients (median age: 75.0 (68.0-83.0) years, 34.7% men), 88 (25.7%) had cTnI above the upper-reference limit (0.046 µg/L). Patients with increased cTnI had more comorbidities, greater impaired respiratory exchange and higher inflammatory markers on admission than those with normal cTnI. Furthermore, they died more (73.9%vs. 37.3%, P < 0.001) over 15 (6-25) days of hospitalization. The association of elevated cTnI with mortality was confirmed by the adjusted Cox regression model (HR = 1.61, 95%CI: 1.06-2.52, P = 0.039) and was linear until 0.3 µg/L, with a subsequent plateau. Of 191 (55.7%) patients with a second cTnI measurement, 49 (25.7%) had an increasing trend, which was not associated with mortality (univariate HR = 1.39, 95%CI: 0.87-2.22, P = 0.265).ConclusionsIn elderly COVID-19 patients, an initial increase in cTn is common and predicts a higher risk of death. Serial cTn testing may not confer additional prognostic information.
| S-EPMC8185447 | biostudies-literature
Project description:Background and aimsMyocardial injury defined by elevation of cardiac troponins (cTn) in the course of coronavirus disease 2019 (COVID-19) pandemic has been reported, though not fully characterized yet. Using the Turkish nationwide centralized COVID-19 database, we sought to determine whether cTn measured within 24 h of admission may help identify 30-day all-cause mortality in hospitalized patients.MethodsThis retrospective cohort study was conducted at all hospitals in Turkey between March 11, 2020, and June 22, 2020. All hospitalized COVID-19 patients (≥18 years) who had cTn measurements within 24 h of admission were included. The primary outcome was 30-day all-cause mortality.ResultsA total of 14,855 COVID-19 patients (median age 49 years and 54% male) from 81 provinces of Turkey were included. Of these, 2020 patients (13.6%) were transferred to intensive care unit, 1165 patients (7.8%) needed mechanical ventilation, and 882 patients (5.9%) died during hospitalization. The prevalence of cTn positivity was 6.9% (n = 1027) in the hospitalized patients. cTn positivity was 5% in those patients alive at 30-day, and 44% in those who died. In multivariable Cox proportional hazard regression model, age, lactate dehydrogenase, and cTn were the strongest predictors of 30-day mortality, irrespective of cTn definition as a continuous, ordinal variable, or dichotomic variables.ConclusionsA single measurement of cTn at admission in patients with COVID-19 is associated with 30-day all-cause mortality and may have an important prognostic role for optimizing risk stratification.
| S-EPMC8052510 | biostudies-literature
Project description:BackgroundAlthough studies assessing cardiovascular comorbidities and myocardial injury in Coronavirus disease 2019 (COVID-19) patients have been published, no reports focused on clinical outcomes of myocardial injury in patients with and without chronic coronary syndromes (CCS) are currently available.MethodsIn this study, consecutive COVID-19 patients admitted to four different institutions were screened for enrolment. Patients were divided into two groups (CCS vs. no-CCS). Association with in-hospital mortality and related predictors represented the main study outcome; myocardial injury and its predictors were deemed secondary outcomes.ResultsA total of 674 COVID-19 patients were enrolled, 112 (16.6%) with an established history of CCS. Myocardial injury occurred in 43.8% patients with CCS vs. 14.4% patients without CCS, as confirmed by high-sensitivity cardiac troponin (hs-cTn) elevation on admission or during hospitalization. The mortality rate in the CCS cohort was nearly three-fold higher. After adjusting for disease severity, myocardial injury resulted significantly associated with in-hospital mortality in the no-CCS group but not in CCS patients.ConclusionsPatients with CCS and COVID-19 showed high mortality rate. Myocardial injury may be a bystander in CCS patients and COVID-19, while in patients without known history of CCS, myocardial injury has a significant role in predicting poor outcomes.
| S-EPMC7601151 | biostudies-literature
Project description:We isolated neutrophils from 11 healthy controls, 12 COIVD-19 patients in ICU and 12 COVID-19 patients from ward and submitted the isolated RNA for RNA sequencing. We then performed gene expression profiling analysis using data obtained from RNA-seq of 3 different cohorts. .
2024-06-01 | GSE234207 | GEO
Project description:BackgroundThe need to determine prognostic factors that can predict a particularly severe or, conversely, the benign course of COVID-19 is particularly perceived in the Emergency Department (ED), considering the scarcity of resources for a conspicuous mass of patients. The aim of our study was to identify some predictors for 30-day mortality among some clinical, laboratory, and ultrasound variables in a COVID-19 patients population.MethodsProspective single-center pilot study conducted in an ED of a University Hospital. A consecutive sample of confirmed COVID-19 patients with acute respiratory failure was enrolled from March 8th to April 15th, 2020.Results143 patients were enrolled. Deceased patients (n = 65) were older (81 vs. 61 years, p <0.001), and they had more frequently a history of heart disease, neurological disease, or chronic obstructive pulmonary disease (p-values = 0.026, 0.025, and 0.034, respectively) than survived patients. Troponin I and presepsin had a significant correlation with a worse outcome. Troponin achieved a sensitivity of 77% and a specificity of 82% for a cut-off value of 27.6 ng/L. The presepsin achieved a sensitivity of 54% and a specificity of 92% for a cut-off value of 871 pg/mL.ConclusionIn a population of COVID-19 patients with acute respiratory failure in an ED, presepsin and troponin I are accurate predictors of 30-day mortality. Presepsin is highly specific and could permit the early identification of patients who could benefit from more intensive care as soon as they enter the ED. Further validation studies are needed to confirm this result.
| S-EPMC8477102 | biostudies-literature
Project description:BackgroundThe outbreak of novel coronavirus pneumonia 2019 (COVID-19) has caused millions of deaths worldwide. It is well documented that troponin predicts the prognosis of patients. Myoglobin is not only an important marker of myocardial injury, but it indicates systemic muscle damage. However, its relationship with COVID-19 was rarely reported. The present study compared the predictive value of troponin and myoglobin on the final prognosis of COVID-19 patients by analyzing the clinical characteristics and serum levels of myoglobin and troponin in severe/critical COVID-19 patients.MethodsWe enrolled 499 consecutive eligible hospitalized patients with severe/critical COVID-19 from February 14 to March 24, 2020 at Leishenshan Hospital, Wuhan, China. Clinical characteristics and laboratory data were collected and compared between the patients who died and survived. We analyzed the receiver operating characteristic curves of myoglobin and troponin. Then, the patients were divided into myo+ group, myo- group, tro+ group, and tro- group, and survival curves were analyzed. The prognostic predictable values of myoglobin and troponin were further analyzed using Cox multifactorial analysis.ResultsMyoglobin and troponin were significantly elevated in the death group (134.4 [interquartile range (IQR) 24.80, 605] vs 38.02 [IQR 3.87, 11.73] ng/ml, p < 0.001), and troponin was also significantly elevated in the death group (0.01 [IQR 0.01, 0.01] vs 0.04 [IQR 0.02, 0.15] ng/ml, p < 0.001). The ROC curves demonstrated that the area under the curve when using myoglobin to predict patient death was 0.911, with a threshold of 1.17, which was equivalent to troponin. Kaplan-Meier survival analysis revealed a significantly lower survival curve in the myo+ group than the myo- group. Multifactor Cox survival analysis showed that troponin was no longer significant (HR = 0.98, 95% CI 0.92-1.03, p = 0.507), but elevated myoglobin was an independent predictor of death in COVID-19 patients (HR = 1.001, 95% CI 1.001-1.002, p < 0.001). The analysis of the Cox model for predicting patient death and plotting decision curves suggested that the single factor myoglobin model was superior to troponin, and the predictive value of the multifactor model was superior to the single-factor analyses.ConclusionsIn severe/critical COVID-19 patients, myoglobin and troponin were predictors of mortality and the probability of conversion to critical illness, and myoglobin may be superior to troponin for predictive value.
| S-EPMC8378829 | biostudies-literature
Project description:BackgroundThe outbreak of novel coronavirus pneumonia 2019 (COVID-19) has caused millions of deaths worldwide. It is well documented that troponin predicts the prognosis of patients. Myoglobin is not only an important marker of myocardial injury, but it indicates systemic muscle damage. However, its relationship with COVID-19 was rarely reported. The present study compared the predictive value of troponin and myoglobin on the final prognosis of COVID-19 patients by analyzing the clinical characteristics and serum levels of myoglobin and troponin in severe/critical COVID-19 patients.MethodsWe enrolled 499 consecutive eligible hospitalized patients with severe/critical COVID-19 from February 14 to March 24, 2020 at Leishenshan Hospital, Wuhan, China. Clinical characteristics and laboratory data were collected and compared between the patients who died and survived. We analyzed the receiver operating characteristic curves of myoglobin and troponin. Then, the patients were divided into myo+ group, myo- group, tro+ group, and tro- group, and survival curves were analyzed. The prognostic predictable values of myoglobin and troponin were further analyzed using Cox multifactorial analysis.ResultsMyoglobin and troponin were significantly elevated in the death group (134.4 [interquartile range (IQR) 24.80, 605] vs 38.02 [IQR 3.87, 11.73]ng/ml, p<0.001), and troponin was also significantly elevated in the death group (0.01 [IQR 0.01, 0.01] vs 0.04 [IQR 0.02, 0.15]ng/ml, p<0.001). The ROC curves demonstrated that the area under the curve when using myoglobin to predict patient death was 0.911, with a threshold of 1.17, which was equivalent to troponin. Kaplan-Meier survival analysis revealed a significantly lower survival curve in the myo+ group than the myo- group. Multifactor Cox survival analysis showed that troponin was no longer significant (HR=0.98, 95% CI 0.92-1.03, p=0.507), but elevated myoglobin was an independent predictor of death in COVID-19 patients (HR=1.001, 95% CI 1.001-1.002, p<0.001). The analysis of the Cox model for predicting patient death and plotting decision curves suggested that the single factor myoglobin model was superior to troponin, and the predictive value of the multifactor model was superior to the single-factor analyses.ConclusionsIn severe/critical COVID-19 patients, myoglobin and troponin were predictors of mortality and the probability of conversion to critical illness, and myoglobin may be superior to troponin for predictive value.
| S-EPMC7914026 | biostudies-literature
Project description:IntroductionSeveral serum inflammatory markers are associated with poor clinical outcomes in community-acquired pneumonia (CAP). However, the prognosis and early treatment response in hospitalized CAP patients based on serial neutrophil-to-lymphocyte ratio (NLR) measurement has never been investigated.MethodsWe performed a retrospective observational study for 175 consecutive patients hospitalized with CAP between February 2016 and February 2018. NLR, C-reactive protein (CRP) and procalcitonin levels were measured on admission day (D1) and on hospital day 4 (D4). The Pneumonia Severity Index (PSI) was also assessed on admission. The primary endpoint was all-cause death within 30 days after admission. The secondary endpoint was early treatment response such as intensive care unit (ICU) admission during hospitalization and clinical unstability on day 4.ResultsThe 30-day mortality rate was 9.7%. In multivariate analysis, NLR D4 (OR: 1.11; 95% CI: 1.04-1.18; P = 0.003) and its incremental change (NLR D4/D1 >1) (OR: 7.10; 95% CI: 2.19-23.06; P = 0.001) were significant predictors of 30-day mortality. NLR D4 and its incremental change were significant predictors of ICU admission and clinical unstability on day 4 in multivariate analyses. Adding of incremental NLR change significantly improved the prognostic ability of the PSI. The additive value of incremental NLR change for the prognostic ability of the PSI was larger than that of incremental CRP change.ConclusionSerial NLR measurement represents useful laboratory tool to predict the prognosis and early treatment response of hospitalized CAP patients.
| S-EPMC8049261 | biostudies-literature