high sensitivity troponin and covid 19 outcomes CORD-Papers-2022-06-02 (Version 1)

Title: High sensitivity troponin and COVID-19 outcomes
Abstract: BACKGROUND: Recent reports have demonstrated high troponin levels in patients affected with COVID-19. In the present study we aimed to determine the association between admission and peak troponin levels and COVID-19 outcomes. METHODS: This was an observational multi-ethnic multi-centre study in a UK cohort of 434 patients admitted and diagnosed COVID-19 positive across six hospitals in London UK during the second half of March 2020. RESULTS: Myocardial injury defined as positive troponin during admission was observed in 288 (66.4%) patients. Age (OR: 1.68 [1.491.88] p < .001) hypertension (OR: 1.81 [1.102.99] p = .020) and moderate chronic kidney disease (OR: 9.12 [95% CI: 4.2419.64] p < .001) independently predicted myocardial injury. After adjustment patients with positive peak troponin were more likely to need non-invasive and mechanical ventilation (OR: 2.40 [95% CI: 1.274.56] p = .007 and OR: 6.81 [95% CI: 3.4013.62] p < .001 respectively) and urgent renal replacement therapy (OR: 4.14 [95% CI: 1.3412.78] p = .013). With regards to events and after adjustment positive peak troponin levels were independently associated with acute kidney injury (OR: 6.76 [95% CI: 3.4013.47] p < .001) venous thromboembolism (OR: 11.99 [95% CI: 3.2044.88] p < .001) development of atrial fibrillation (OR: 10.66 [95% CI: 1.3385.32] p = .026) and death during admission (OR: 2.40 [95% CI: 1.344.29] p = .003). Similar associations were observed for admission troponin. In addition median length of stay in days was shorter for patients with negative troponin levels: 8 (513) negative 14 (723) low-positive levels and 16 (1023) high-positive (p < .001). CONCLUSIONS: Admission and peak troponin appear to be predictors for cardiovascular and non-cardiovascular events and outcomes in COVID-19 patients and their utilisation may have an impact on patient management.
Published: 2021-03-08
Journal: Acta cardiologica
DOI: 10.1080/00015385.2021.1887586
DOI_URL: http://doi.org/10.1080/00015385.2021.1887586
Author Name: Papageorgiou Nikolaos
Author link: https://covid19-data.nist.gov/pid/rest/local/author/papageorgiou_nikolaos
Author Name: Sohrabi Catrin
Author link: https://covid19-data.nist.gov/pid/rest/local/author/sohrabi_catrin
Author Name: Prieto Merino David
Author link: https://covid19-data.nist.gov/pid/rest/local/author/prieto_merino_david
Author Name: Tyrlis Angelos
Author link: https://covid19-data.nist.gov/pid/rest/local/author/tyrlis_angelos
Author Name: Atieh Abed Elfattah
Author link: https://covid19-data.nist.gov/pid/rest/local/author/atieh_abed_elfattah
Author Name: Saberwal Bunny
Author link: https://covid19-data.nist.gov/pid/rest/local/author/saberwal_bunny
Author Name: Lim Wei Yao
Author link: https://covid19-data.nist.gov/pid/rest/local/author/lim_wei_yao
Author Name: Creta Antonio
Author link: https://covid19-data.nist.gov/pid/rest/local/author/creta_antonio
Author Name: Khanji Mohammed
Author link: https://covid19-data.nist.gov/pid/rest/local/author/khanji_mohammed
Author Name: Rusinova Reni
Author link: https://covid19-data.nist.gov/pid/rest/local/author/rusinova_reni
Author Name: Chooneea Bashistraj
Author link: https://covid19-data.nist.gov/pid/rest/local/author/chooneea_bashistraj
Author Name: Khiani Raj
Author link: https://covid19-data.nist.gov/pid/rest/local/author/khiani_raj
Author Name: Wijesuriya Nadeev
Author link: https://covid19-data.nist.gov/pid/rest/local/author/wijesuriya_nadeev
Author Name: Chow Anna
Author link: https://covid19-data.nist.gov/pid/rest/local/author/chow_anna
Author Name: Butt Haroun
Author link: https://covid19-data.nist.gov/pid/rest/local/author/butt_haroun
Author Name: Browne Stefan
Author link: https://covid19-data.nist.gov/pid/rest/local/author/browne_stefan
Author Name: Joshi Nikhil
Author link: https://covid19-data.nist.gov/pid/rest/local/author/joshi_nikhil
Author Name: Kay Jamie
Author link: https://covid19-data.nist.gov/pid/rest/local/author/kay_jamie
Author Name: Ahsan Syed
Author link: https://covid19-data.nist.gov/pid/rest/local/author/ahsan_syed
Author Name: Providencia Rui
Author link: https://covid19-data.nist.gov/pid/rest/local/author/providencia_rui
sha: ff6558dcf6cd2658d93d56968dbf007216649c05
license: no-cc
license_url: [no creative commons license associated]
source_x: Medline; PMC
source_x_url: https://www.medline.com/https://www.ncbi.nlm.nih.gov/pubmed/
pubmed_id: 33685354
pubmed_id_url: https://www.ncbi.nlm.nih.gov/pubmed/33685354
pmcid: PMC7970632
pmcid_url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7970632
url: https://doi.org/10.1080/00015385.2021.1887586 https://www.ncbi.nlm.nih.gov/pubmed/33685354/
has_full_text: TRUE
Keywords Extracted from Text Content: renal macrovascular Renal left ventricular kidney ECMO fibrinogen hsTrop Barts Health NHS Trust CRP Figure 2 cardiac CK cardiovascular D-Dimers Shi COVID-19 heart SARS-CoV-2 Wuhan cohorts thrombin Coronavirus disease 2019 patient creatinine angiotensin-converting enzyme inhibitors ( pulmonary chronic/baseline D-dimers atrial men bloods Guo Diet pulmonary embolism D-Dimer CKD O2 troponin T thromboplastin vein People 22/04/2020 C-reactive [4] coronary artery myocardium Wuhan APTT ACE-I blood myocardial infarction/ myocardial LDH creatine kinase COVID-19 [9 statin [6] [7] [8] . patients haemoglobin people Patients INR lactate dehydrogenase RRT Patient blood cell ventricular NT-proBNP glomerular COVID-19 patients UK Troponin troponin
Extracted Text Content in Record: First 5000 Characters:Coronavirus disease 2019 (COVID-19) caused by SARS-CoV-2 is a global pandemic [1] . So far, it has affected more than 100 million people worldwide, and is associated with multi-organ dysfunction and high mortality rates [1] . Studies suggest that some patients present to hospital and have a relatively benign course, being discharged within a few days. However, for other patients the disease course is more aggressive, requiring multiple interventions, while they experience higher mortality and longer in-hospital stay [2] . It would be therefore of importance to have a biomarker which could help in distinguishing between these two groups of patients, not only for prognosis, but also, potentially, for treatment decisions. Troponin is a marker of myocardial injury, but it is also found to be raised in several conditions. Recent reports demonstrated high troponin levels in patients affected by COVID-19. These were found to have higher mortality rates during the initial outbreak in Wuhan cohorts [3, 4] . In addition, higher mortality rates have been observed in the UK, as an older and multiethnic population with more comorbidities was affected by the disease [5] . It is still unknown which patients are more likely to develop myocardial injury in the setting of COVID-19, and whether or not, after adjustment for confounders associated with rise in troponin, myocardial injury can be used as an independent predictor of the disease in Western multi-ethnic populations. Yet, it remains to be determined if admission troponin can be used as a predictor, and if the magnitude of troponin rise translates into different outcome rates (i.e. whether patients with higher rise in troponin levels experience a more severe disease progression than those with negative or mildly increase in troponin levels). We aimed to assess: (1) the risk factors for myocardial injury; (2) the impact of myocardial injury on different COVID-19 associated outcomes and (3) whether admission troponin, peak troponin and magnitude of troponin rise have a similar prognostic capacity. In this multi-centre study, we assessed the association between high-sensitivity troponin (hsTrop) and COVID-19 intra-hospital clinical trajectory (comprising mortality, utilisation of procedures, and cardiovascular and non-cardiovascular outcomes) in a UK cohort of 434 patients admitted and diagnosed positive, across six hospitals in London, UK. All patients admitted to the participant hospitals from the 16th to the 30th of March 2020 with a diagnosis of COVID-19 and having at least one troponin measurement were considered eligible for analysis. This observational study was approved by the Clinical Effectiveness Unit at Barts Health NHS Trust (Project ID: 11103; Title: COVID-19 and cardiovascular disease (CVD) outcomes) and by the Quality Governance Department at Royal Free London NHS Trust (Cardiovascular Implications of Outcomes of Patients With COVID-19; 22/04/2020). Patient demographic characteristics, laboratory results, procedures, comorbidities, procedures and outcomes were extracted from the electronic records and paper notes. In order for patients to be included in the study, these should be diagnosed COVID-19 positive, as confirmed by polymerase chain reaction (PCR) swab. Patients with two positive swabs and older than 16 years were included in the study. Troponin T levels were measured with a high-sensitivity assay on and during admission as per Trusts' protocols. Routine bloods were obtained from patients on and during admission. Routine hospital laboratory methods were used for the analysis. These were available on the electronic systems and included: full blood count parameters, high-sensitivity troponin T, C-reactive protein (CRP), lactate dehydrogenase (LDH), N-terminal pro B-type natriuretic peptide (NT-proBNP), international normalised ratio (INR), creatine kinase (CK), D-Dimers, activated partial thromboplastin time (APTT), fibrinogen, thrombin time and creatinine. Glomerular filtration rate (eGFR) was estimated using the Modification of Diet in Renal Disease (MDRD) Study equation. Patients were classified as having moderate CKD when eGFR was less than 60 ml/min. Troponin measurements were performed based on clinical indication or based on local protocols for risk stratification of COVID-19 patients. The term "myocardial injury" was used for patients with positive troponin levels (defined as 15 ng/mLthe 99th percentile in the normal population according to our lab). Peak troponin for each patient was measured and based on these values, three troponin levels were defined, utilising tertiles to define the cutoffs, as: "negative" if <15 ng/mL (no myocardial injury according to our definition above), "low-positive" if levels 15 ng/mL and <47 ng/mL and "high-positive" level if 47 ng/mL. The study primary endpoint was defined as all-cause mortality. Secondary outcomes were: (i) pneumonia, (ii) acute kidney injury (defined as a 50% increase in creatinine compared
Keywords Extracted from PMC Text: creatinine myocardium thromboplastin LDH thrombin heart pulmonary embolism Coronavirus disease 2019 Shi APTT D-dimers Diet troponin T bloods Guo troponin 's T People CK pulmonary NT-proBNP ventricular blood cell D-Dimers fibrinogen INR statin Troponin SARS-CoV-2 Patients chronic/baseline O2 people Renal ACE-I blood myocardial kidney macro-vascular CRP patient Figure 2 glomerular CKD ECMO lactate dehydrogenase Wuhan Wuhan cohorts renal COVID-19 patients creatine kinase RRT COVID-19 [9 cardiac COVID-19 angiotensin-converting enzyme inhibitors ( patients coronary artery haemoglobin C-reactive " UK ≥15 myocardial infarction/ischaemic vein cardiovascular atrial [4]
Extracted PMC Text Content in Record: First 5000 Characters:Coronavirus disease 2019 (COVID-19) caused by SARS-CoV-2 is a global pandemic [1]. So far, it has affected more than 100 million people worldwide, and is associated with multi-organ dysfunction and high mortality rates [1]. Studies suggest that some patients present to hospital and have a relatively benign course, being discharged within a few days. However, for other patients the disease course is more aggressive, requiring multiple interventions, while they experience higher mortality and longer in-hospital stay [2]. It would be therefore of importance to have a biomarker which could help in distinguishing between these two groups of patients, not only for prognosis, but also, potentially, for treatment decisions. Troponin is a marker of myocardial injury, but it is also found to be raised in several conditions. Recent reports demonstrated high troponin levels in patients affected by COVID-19. These were found to have higher mortality rates during the initial outbreak in Wuhan cohorts [3,4]. In addition, higher mortality rates have been observed in the UK, as an older and multi-ethnic population with more comorbidities was affected by the disease [5]. It is still unknown which patients are more likely to develop myocardial injury in the setting of COVID-19, and whether or not, after adjustment for confounders associated with rise in troponin, myocardial injury can be used as an independent predictor of the disease in Western multi-ethnic populations. Yet, it remains to be determined if admission troponin can be used as a predictor, and if the magnitude of troponin rise translates into different outcome rates (i.e. whether patients with higher rise in troponin levels experience a more severe disease progression than those with negative or mildly increase in troponin levels). We aimed to assess: (1) the risk factors for myocardial injury; (2) the impact of myocardial injury on different COVID-19 associated outcomes and (3) whether admission troponin, peak troponin and magnitude of troponin rise have a similar prognostic capacity. Routine bloods were obtained from patients on and during admission. Routine hospital laboratory methods were used for the analysis. These were available on the electronic systems and included: full blood count parameters, high-sensitivity troponin T, C-reactive protein (CRP), lactate dehydrogenase (LDH), N-terminal pro B-type natriuretic peptide (NT-proBNP), international normalised ratio (INR), creatine kinase (CK), D-Dimers, activated partial thromboplastin time (APTT), fibrinogen, thrombin time and creatinine. Glomerular filtration rate (eGFR) was estimated using the Modification of Diet in Renal Disease (MDRD) Study equation. Patients were classified as having moderate CKD when eGFR was less than 60 ml/min. Troponin measurements were performed based on clinical indication or based on local protocols for risk stratification of COVID-19 patients. The term "myocardial injury" was used for patients with positive troponin levels (defined as ≥15 ng/mL – the 99th percentile in the normal population according to our lab). Peak troponin for each patient was measured and based on these values, three troponin levels were defined, utilising tertiles to define the cut-offs, as: "negative" if <15 ng/mL (no myocardial injury according to our definition above), "low-positive" if levels ≥15 ng/mL and <47 ng/mL and "high-positive" level if ≥47 ng/mL. The study primary endpoint was defined as all-cause mortality. Secondary outcomes were: (i) pneumonia, (ii) acute kidney injury (defined as a 50% increase in creatinine compared to chronic/baseline levels), (iii) myocardial injury (defined as high-sensitivity troponin above the 99th percentile of normal), (iv) acute heart failure, (v) acute atrial fibrillation episode, (vi) stroke, (vii) venous thromboembolic disease (including pulmonary embolism and/or deep vein thrombosis) and (viii) utilisation of procedures (non-invasive ventilation, mechanical ventilation, ECMO and renal replacement therapy). Descriptive statistics are presented as proportions for binary variables and median and inter-quartile for continuous variables. Parametric (Student's T) or equivalent non-parametric tests (Mann–Whitney) were used where appropriate for comparisons of continuous variables among groups. Proportions were compared with a Chi2 test. Binary logistic regression was used to assess for predictors of myocardial injury using the forward likelihood ratio (LR) method, with probability for stepwise .05. Significant predictors identified through univariate analysis are added in the multivariable model through a stepwise process with predictors entering at each step as long as they significantly improve the predictive capacity of the model. The association of troponin levels with each pre-defined procedure and clinical outcome was assessed with a separate logistic regression. Each model was adjusted for the clinical variables that showed significant association with myoca
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