The Value of Cardiac Biomarkers in Predicting in-Hospital Death in COVID-19 Patients

Given the strong evidence of direct invasion of coronavirus to myocardial tissue, as well as increasing the patient's susceptibility to inflammatory and thrombotic phenomena, it has been hypothesized that elevated levels of cardiac enzymes can predict disease severity and its poor prognosis. We aimed to determine the value of cardiac prognostic biomarkers along with other laboratory parameters in predicting in-hospital mortality of COVID-19 patients. This prospective study was performed on 30 consecutive patients with the definitive diagnosis of severe COVID-19. On admission, along with recording demographic characteristics, intravenous blood samples were extracted from the patients after at least 8 hours of fasting to evaluate other laboratory parameters. Comparing laboratory parameters across the survived and non-survived groups showed significantly higher mean CK-MB level in non-survived group than alive group (70.90+/-29.79 versus 43.56+/-22.02, P=0.020). Also, positive troponin I was reported in 38.1% of non-survived group, while in none of the patients in survived group (P=0.031). Using the logistic regression model, raised CK-MB could effectively predict in-hospital death among COVID-19 patients (OR=1.047, P=0.043). Area under the ROC curve analysis showed high value of raised CK-MB for predicting in-hospital death among COVID-19 patients. Raised CK-MB level on admission can predict in-hospital death in patients with severe COVID-19.Copyright © 2023 Tehran University of Medical Sciences.

Mechanism of Cardiac Pathogenesis and Cardiotoxicity of Anti-COVID-19 Drugs

Novel coronavirus (nCoV-19) infection has been declared a pandemic by WHO. More than 223 countries are under the attack of this emergency situation. Primarily, pneumocytes encountered by the nCoV-19 via ACE-2 receptor cause pulmonary edema, damage to alveolar cells, production of inflammatory cells, and hypoxia. It has been found that patients with co-existing cardiovascular diseases are more prone to the infection, and severe cardiovascular dysfunction was further observed when infected with nCoV-19. There is no substantial mechanism available for the pathogenesis of this cardiovascular dysfunction;therefore, we herein present a possible mechanistic approach of cardiotoxicity by nCov-19 infection. The hypothesis of this study is based on immunopathology of nCoV-19 in pneumocytes, presence of ACE-2 on cardiomyocytes membrane, cytokine storm, genomic analysis of virus in cardiac tissue, and several reports published on the cardiovascular complications in nCoV-19 across the globe. We have also analyzed the cardiotoxic profile of recently used repurposed and investigational drugs and highlighted their possible cardiotoxic consequences and drug interactions with cardiovascular medicines, such as statins and anti-coagulants.Copyright © 2021 Bentham Science Publishers.

Use and Prognostic Implications of Cardiac Troponin in COVID-19.

Myocardial injury is common in patients with COVID-19 and is associated with an adverse prognosis. Cardiac troponin (cTn) is used to detect myocardial injury and assist with risk stratification in this population. SARS-CoV-2 infection can play a role in the pathogenesis of acute myocardial injury due to both direct and indirect damage to the cardiovascular system. Despite the initial concerns about an increased incidence of acute myocardial infarction (MI), most cTn increases are related to chronic myocardial injury due to comorbidities and/or acute nonischemic myocardial injury. This review will discuss the latest findings on this topic.

Cardiac Biomarkers in 2022 - A Vital Tool for Emergency Care

The role of cardiac biomarkers in diagnosing acute myocardial infarction is undoubted. In the 2020 guidelines of the European Society of Cardiology, the measurement of cardiac peptides to gain prognostic information has a class IIa indication in all patients with ACS. In emergency care, ruling out a non-ST elevation myocardial infarction requires documentation of normal levels of cardiac biomarkers, which remain stable or have very small variations within several hours. This review aims to summarize the current knowledge and recent progresses in the field of cardiac biomarker discovery, from their routine use in emergency rooms to their prognostic roles in modern risk assessment tools. Integrated approaches combining cardiac troponin with other biomarkers of ventricular dysfunction or inflammation, or with modern cardiac imaging in emergency care are also presented, as well as the role of modern algorithms for serial troponin measurement in the modern management of emergency departments.

Interleukin-6 is upregulated and may be associated with myocardial injury in some patients who have recovered from COVID-19.

Coronavirus disease (COVID-19) causes myocardial injury by inducing a cytokine storm in severe cases. Studies have reported that myocardial injury persists for a prolonged period during COVID-19 recovery, and cardiac troponin is a useful indicator of myocardial injury. The interleukin-6 (IL-6) level is known to be associated with the morbidity and mortality of COVID-19, but this association has not been studied during recovery. The current study examined the association between IL-6 levels and myocardial damage during COVID-19 recovery. Four of 209 patients (1.9%) who recovered from COVID-19 had elevated IL-6 levels. All 4 patients tested positive for high-sensitivity troponin T, and 3 patients had subclinical left ventricular (LV) dysfunction according to echocardiography. Positivity for IL-6 during COVID-19 recovery suggests ongoing myocardial damage due to inflammation.

Monthly transthoracic echocardiography in young adults for 6 months following SARS-CoV-2 infection.

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) can elicit acute and long-term effects on the myocardium among survivors, yet effects among otherwise healthy young adults remains unclear. Young adults with mild symptoms of SARS-CoV-2 (8M/8F, age: 21 ± 1 years, BMI: 23.5 ± 3.1 kg·m-2 ) underwent monthly transthoracic echocardiography (TTE) and testing of circulating cardiac troponin-I for months 1-6 (M1-M6) following a positive polymerase chain reaction test to better understand the acute effects and post-acute sequelae of SARS-CoV-2 on cardiac structure and function. Left heart structure and ejection fraction were unaltered from M1-M6 (p > 0.05). While most parameters of septal and lateral wall velocities, mitral and tricuspid valve, and pulmonary vein (PV) were unaltered from M1-M6 (p > 0.05), lateral wall s' wave velocity increased (M1: 0.113 ± 0.019 m·s-1 , M6: 0.135 ± 0.022 m·s-1 , p = 0.013); PV S wave velocity increased (M1: 0.596 ± 0.099 m·s-1 , M6: 0.824 ± 0.118 m·s-1 , p < 0.001); the difference between PV A wave and mitral valve (MV) A wave durations decreased (M1: 39.139 ± 43.715 ms, M6: 18.037 ± 7.227 ms, p = 0.002); the ratio of PV A duration to MV A duration increased (M1: 0.844 ± 0.205, M6: 1.013 ± 0.132, p = 0.013); and cardiac troponin-I levels decreased (M1: 0.38 ± 0.20 ng·ml-1 , M3: 0.28 ± 0.34 ng·ml-1 , M6: 0.29 ± 0.16 ng·ml-1 ; p = 0.002) over time. While young adults with mild symptoms of SARS-CoV-2 lacked changes to cardiac structure, the subclinical improvements to cardiac function and reduced inflammatory marker of cardiac troponin-I over 6 months following SARS-CoV-2 infection provide physiologic guidance to post-acute sequelae and recovery from SARS-CoV-2 and its variants using conventional TTE.

Independent Predictors of Mortality in COVID-19 Myocardial Injury: The Role of Troponin Levels, GRACE Score, SOFA Score, and TIMI Score.

Background Coronavirus disease 2019 (COVID-19) infection is associated with troponin elevation, which is associated with increased mortality. However, it is not clear if troponin elevation is independently linked to increased mortality in COVID-19 patients. Although there is considerable literature on risk factors for mortality in COVID-19-associated myocardial injury, the Global Registry of Acute Coronary Events (GRACE), Thrombolysis in Myocardial Infarction (TIMI), and Sequential Organ Failure Assessment (SOFA) scores have not been studied in COVID-19-related myocardial injury. This data is important in risk-stratifying COVID-19 myocardial injury patients. Methodology Of the 1,500 COVID-19 patients admitted to our hospitals, 217 patients who had troponin levels measured were included. Key variables were collected manually, and univariate and multivariate cox regression analysis was done to determine the predictors of mortality in COVID-19-associated myocardial injury. The differences in clinical profiles and outcomes of COVID-19 patients with and without troponin elevation were compared. Results Mortality was 26.5% in the normal troponin group and 54.6% in the elevated troponin group. Patients with elevated troponins had increased frequency of hypotension (p = 0.01), oxygen support (p < 0.01), low absolute lymphocyte (p < 0.01), elevated blood urea nitrogen (p < 0.01), higher C-reactive protein (p < 0.01), higher D-dimer (p < 0.01), higher lactic acid (p < 0.01), and higher Quick SOFA (qSOFA), SOFA, TIMI, and GRACE (all scores p < 0.01). On univariate cox regression, troponin elevation (hazard ratio (HR) = 1.85, 95% confidence interval (CI) = 1.18-2.88, p < 0.01), TIMI score >3 (HRv = 1.79, 95% CI = 1.11-2.75, p = 0.01), and GRACE score >140 (HR = 2.27, 95% CI = 1.45-3.55, p < 0.01) were highly associated with mortality, whereas cardiovascular disease (HR = 1.40, 95% CI = 0.89-2.21, p = 0.129) and cardiovascular risk factors (HR = 1.15, 95% CI = 0.73-1.81, p = 0.52) were not. After adjusting for age, use of a non-rebreather or high-flow nasal cannula, hemoglobin <8.5 g/dL, suspected or confirmed source of infection, and qSOFA and SOFA scores (HR = 1.18, 95% CI = 1.07-1.29, p < 0.01) were independently associated with mortality, whereas troponin (HR = 1.08, 95% CI = 0.63-1.85, p = 0.76), TIMI score (HR = 1.02, 95% CI = 0.99-1.06, p = 0.12) and GRACE scores (HR = 1.01, 95% CI = 0.99-1.02, p = 0.10) were not associated with mortality. Conclusions Our study shows that troponin, GRACE score, and TIMI score are not independent predictors of mortality in COVID-19 myocardial injury. This may be because troponin elevation in COVID-19 patients may be related to demand ischemia rather than acute coronary syndrome-related. This was shown by the association of troponin with a higher degree of systemic inflammation and end-organ dysfunction. Therefore, we recommend SOFA scores in risk-stratifying COVID-19 patients with myocardial injury.

Admission high-sensitivity cardiac troponin levels as a prognostic indicator for in-hospital mortality rates in the elderly and very elderly COVID-19 patients.

BACKGROUND: Elevation of cardiac troponin (cTn) is associated with the worst prognosis not only in cardiovascular disease but also in non-cardiovascular disease. The aim of this study is to verify if cTn has a prognostic role in elderly and very elderly coronavirus disease 2019 (COVID-19) patients. METHODS: This study enrolled consecutive COVID-19 elderly patients hospitalized at INRCA hospital, with available admission high sensitivity cardiac troponin T (HS-cTnT) level. Patients were divided into three groups based on HS-cTnT level: group A (Hs-cTnT ≤ 40 pg/ml), group B (Hs-cTnT 41-100 pg/ml), and group C (Hs-cTnT ≥ 101 pg/ml). The correlation between HS-cTnT levels and mortality rates was analyzed. RESULTS: 461 patients (mean age 86 years; 59% female) were divided into group A (261 patients), group B (129 patients), and group C (71 patients). Group C resulted significantly older, more affected by heart failure, chronic obstructive pulmonary disease, chronic kidney disease, and dementia, and with higher levels of creatinine, C-reactive protein, pro-calcitonin, interleukin-6, ferritin, NT-proBNP, D-dimer then group A and group B. Mortality rate increased significantly across groups (group A: 18.4%; group B: 36.4%; group C: 62.0%; p<0.001). Group C had a significant increase in mortality risk compared to group A, both univariate analysis (HR 3.78) and multivariate analysis (model 2 HR 3.10; model 3 HR 3.59; model 4 HR 1.72). CONCLUSION: HS-cTnT has demonstrated a prognostic role in elderly and very elderly COVID-19 patients. HS-cTnT is a simple and inexpensive laboratory exam that gives clinicians important information on mortality risk stratification.

High-Sensitivity Troponin I is an Indicator of Poor Prognosis in Patients with Severe COVID-19 Related Pneumonia.

Objective: Critical covid-19 patients have complications with acute myocardial injury is still unclear. We observed a series of critically ill patients, paying particular attention to the impact of myocardial injury at admission on short-term outcome. Methods: We prospectively collected and analyzed data from a series of severe covid-19 patients confirmed by real-time RT-PCR. Data were obtained from electronic medical records including clinical charts, nursing records, laboratory findings, and chest x-rays were from Feb 8, 2020, to April 7, 2020. The Acute Physiology and Chronic Health Evaluation (APACHE II) score, CURB-65 Pneumonia Severity Score, Sequential Organ Failure Assessment (SOFA) Score and pneumonia severity index (PSI) score were made within 24 hours of admission. Cardiac injury was diagnosed as hs-cTnI were above >28 pg/mL. The short-term outcome was defined as mortality in hospital. Results: A total of 100 patients met the diagnostic criteria of severe patients with COVID-19 during 2020.02.08-2020.04.07. The CURB 65, APACH2, SOFA, and PSI score were significantly higher in Critical group than in Severe group. Univariate regression analysis showed that oxygen flow, PO2/FiO2, SOFA and hs-cTnI were closely related to short-term outcome. The corresponding ROC of hs-cTnI, oxygen flow and SOFA for patient death prediction were 0.949, 0.906 and 0.652. hs-cTnI at 47.8 ng/liter predicted death, sensitivity 92.8%, specificity 92.9%; Oxygen flow at 5.5 liter/minute predicted death sensitivity 100%, specificity 77.9%; SOFA score at 5 predicted death sensitivity 100%, specificity 73.8%. Conclusion: Our cohort study demonstrated that inhaled oxygen flow, SOFA score, and myocardial injury at admission in critically ill COVID-19 patients were important indicators for predicting short-term death of patients, the hs-cTnI can be as a risk stratification, which may provide a simple method for the physicians to identify high-risk patients and give reasonable treatment in time.

COVID-19 Vaccine-Induced Myocarditis: A Systemic Review and Literature Search.

Myocarditis is one of the complications reported with COVID-19 vaccines, particularly both Pfizer-BioNTech and Moderna vaccines. Most of the published data about this association come from case reports and series. Integrating the geographical data, clinical manifestations, and outcomes is therefore important in patients with myocarditis to better understand the disease. A thorough literature search was conducted in Cochrane library, PubMed, ScienceDirect, and Google Scholar for published literature till 30 March 2022. We identified 26 patients eligible from 29 studies; the data were pooled from these qualifying case reports and case series. Around 94% of patients were male in this study, the median age for onset of myocarditis was 22 years and 85% developed symptoms after the second dose. The median time of admission for patients to hospitals post-vaccination was three days and chest pain was the most common presenting symptom in these patients. Most patients had elevated troponin on admission and about 90% of patients had cardiac magnetic resonance imaging (CMR) that showed late gadolinium enhancement. All patients admitted with myocarditis were discharged home after a median stay of four days. Results from this current analysis show that post-mRNA vaccination myocarditis is mainly seen in young males after the second dose of vaccination. The pathophysiology of vaccine-induced myocarditis is not entirely clear and late gadolinium enhancement is a common finding on CMR in these patients that may indicate myocardial fibrosis or necrosis. Prognosis remains good and all patients recovered from myocarditis, however further studies are advisable to assess long-term prognosis of myocarditis.

Cardiovascular Complications of Pregnancy-Associated COVID-19 Infections.

Cardiovascular complications are frequently present in coronavirus-2019 (COVID-19) infection. These include microvascular and macrovascular thrombotic complications such as arterial and venous thromboembolism, myocardial injury or inflammation resulting in infarction, heart failure, and arrhythmias. Data suggest increased risk of adverse outcomes in pregnant compared with nonpregnant women of reproductive age with COVID-19 infection, including need for intensive care unit admission, mechanical ventilation, and extracorporeal membrane oxygenation utilization. Current statements addressing COVID-19-associated cardiac complications do not include pregnancy complications that may mimic COVID-19 complications such as peripartum cardiomyopathy, spontaneous coronary artery dissection, and preeclampsia. Unique to pregnancy, COVID-19 complications can result in preterm delivery and modify management of the pregnancy. Moreover, pregnancy has often been an exclusion criterion for enrollment in research studies. In this review, we summarize what is known about pregnancy-associated COVID-19 cardiovascular complications.

An overview of prognostic value of neurologic and cardiac biomarkers in patients with COVID-19 sequelae.

Many studies conducted after the pandemic period revealed that, while COVID-19 primarily injured the lungs, it also affects other organs in the form of cardiovascular complications, metabolic derangements, renal damage, and so on. Although we know that inflammatory cascades, complement activation, and pro-inflammatory cytokines are all involved in vasculitic processes that cause organ damage, we do not know the exact mechanism of complications such as acute respiratory distress syndrome (ARDS), cardiovascular ischemia, deep vein thrombosis, pulmonary thromboembolism, and brain injuries (embolism) that are frequently observed in COVID 19. The currently available biomarkers do not predict the severity of the aforementioned complications. As a result, more specific biomarkers such as serum calcium binding protein (S100B), glial fibrillary acid protein (GFAP), myelin basic protein (MBP), neuron-specific enolase (NSE), hs-TNI, (highly sensitive cardiac troponin) - HBDH, (Hydroxybutyrate Dehydrogenase), CK-MB (creatine kinase myocardial band), ST2 (suppression of tumorigenicity 2) are in need for early detection & improved clinical outcome.

Inflammatory and Cardiac Biomarkers in Relation with Post-Acute COVID-19 and Mortality: What We Know after Successive Pandemic Waves.

BACKGROUND: Biomarkers were correlated with mortality in critically ill COVID-19 patients. No prediction tools exist for noncritically ill COVID-19 patients. We aimed to compare the independent prognostic value of inflammation and cardiac biomarkers for post-acute COVID-19 patients and the 30-day mortality rate in noncritically ill COVID-19 patients, as well as the relation with the virus variant involved. METHODS: This observational cohort study was conducted at an emergency clinical hospital between 1 October 2020 and 31 December 2021. We included consecutive patients with biomarkers determined within 24 h of presentation, followed up at least 30 days postdischarge. RESULTS: Post-acute COVID-19 was diagnosed in 20.3% of the cases and the all-cause 30-day mortality rate was 35.1% among 978 patients infected with variants of concern. Neutrophil-to-lymphocyte ratio (1.06 [95%CI, 1.01-1.11], p = 0.015) and NT-pro BNP were correlated with 30-daymortality, while the monocyte-to-lymphocyte ratio (2.77 [95%CI, 1.10-6.94], p = 0.03) and NT-pro BNP (1.68 [95%CI, 1.00-2.84], p = 0.05) were correlated with post-acute COVID-19. High-sensitivity to troponin was associated with 30-day mortality (1.55 [95%CI, 1.00-2.42], p = 0.05). A Cox proportional-hazards model confirmed that NT-pro BNP was independently associated with mortality. NT-pro BNP remained independently associated with 30-day mortality during follow-up (1.29 [95%CI, 1.07-1.56], p = 0.007) after adjustment for confounders. CONCLUSION: Inflammation and cardiac biomarkers, determined upon admission and predischarge, in a cohort of hospitalized noncritically ill COVID-19 patients throughout successive pandemic waves, showed a predictive value for post-acute COVID-19 and 30-day mortality.

Reducing patient risk and enhancing care through the development and implementation of a new chest pain pathway, expedited by and for the COVID-19 era

The COVID-19 pandemic raised major concerns relating to hospital capacity and cross-infection patients and staff in the Emergency Department (ED) of a metropolitan hospital servicing a population of ~500,000. We determined to reduce length of stay and admissions in patients presenting with symptoms of possible myocardial infarction;the most common presentation group. After establishing stakeholder consensus, the existing accelerated diagnostic pathway (ADP) based on the ED Assessment of Chest-pain Score (EDACS), electrocardiogram, and troponin measurements with a high-sensitivity assay (hs-cTn) on presentation and two hours later (EDACS-ADP) was modified to stream patients following an initial troponin measure as follows: (i) to a very-low risk group who could be discharged home without follow-up or further testing, and (ii) to a low-risk group who could be discharged with next-day follow-up community troponin testing. Simulations were run in an extensive research database to determine appropriate hs-cTnI and EDACS thresholds for risk classification. This COVID-ADP was developed in ~2-weeks and was implemented in the ED within a further 3-weeks. A comparison of all chest pain presentations for the 3 months prior to implementation of the COVID-ADP to 3 months following implementation showed that there was a 64.7% increase in patients having only one troponin test in the ED, a 30-minute reduction of mean length of stay of people discharged home from the ED, and a 24.3% reduction in hospital admissions of patients ultimately diagnosed with non-cardiac chest pain. © 2021 International Federation of Clinical Chemistry and Laboratory Medicine. All rights reserved.

Cardiac biomarkers in COVID-19: a narrative review

The diagnosis and risk stratification of coronavirus disease 2019 (COVID-19) is primarily based on discretionary use of laboratory resources. Several lines of evidence now attest that cardiovascular disease not only is a frequent complication of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection, but its pre-existence may increase the risk of morbidity, disability, and death in patients with COVID-19. To this end, routine assessment of biomarkers of cardiac injury (i.e., cardiac troponin I or T) and dysfunction (e.g., natriuretic peptides) has emerged as an almost essential practice in patients with moderate, severe, and critical COVID-19 illness. Therefore, this narrative review aims to provide an overview of cardiac involvement in patients with SARS-CoV-2 infection as well as the clinical background for including cardiac biomarkers within specific panels of laboratory tests for managing COVID-19 patients. © 2021 International Federation of Clinical Chemistry and Laboratory Medicine. All rights reserved.

Myocardial Injury Predicts Risk of Short-Term All-Cause Mortality in Patients With COVID-19: A Dose-Response Meta-Analysis.

Objective: Predictive value of myocardial injury as defined by elevated cardiac tropnins (cTns) in patients with COVID-19 has not been fully investigated. We performed a meta-analysis to evaluate the dose-response relationship between myocardial injury and short-term all-cause mortality. Methods: Pubmed, Embase, and the Cochrane Library database were searched for all the studies which evaluated the relationship between cTns and the risk of short-term all-cause mortality in patients with COVID-19. Results: Compared with patients without myocardial injury, the group with elevated cTns was associated with increased short-term mortality (11 studies, 29,128 subjects, OR 3.17, 95% CI 2.19-4.59, P = 0.000, I 2 = 92.4%, P for heterogeneity 0.00). For the dose-response analysis, the elevation of cTns 1 × 99th percentile upper reference limit (URL) was associated with increased short-term mortality (OR 1.99, 95% CI 1.53-2.58, P = 0.000). The pooled OR of short-term mortality for each 1 × URL increment of cTns was 1.25 (95% CI 1.22-1.28, P = 0.000). Conclusion: We found a positive dose-response relationship between myocardial injury and the risk of short-term all-cause mortality, and propose elevation of cTns > 1 × 99th percentile URL was associated with the increased short-term risk of mortality.

Use and Prognostic Implications of Cardiac Troponin in COVID-19.

Myocardial injury is common in patients with COVID-19 and is associated with an adverse prognosis. Cardiac troponin (cTn) is used to detect myocardial injury and assist with risk stratification in this population. SARS-CoV-2 infection can play a role in the pathogenesis of acute myocardial injury due to both direct and indirect damage to the cardiovascular system. Despite the initial concerns about an increased incidence of acute myocardial infarction (MI), most cTn increases are related to chronic myocardial injury due to comorbidities and/or acute nonischemic myocardial injury. This review will discuss the latest findings on this topic.

COVID-19 and Cardiovascular Disease: Clinical Implications of Biochemical Pathways

Coronavirus disease of 2019 (COVID-19) is a viral pandemic which has taken away more than over 4 million lives all over the world as of July 9, 2021, with the USA, India, and Brazil being the most affected countries. Apart from the respiratory tract, the cardiovascular (CV) system is one of the important organ systems affected by this complex multisystem disease. Various studies have confirmed that COVID-19 predisposes an individual to increased risk of CV complications. In fact, hospitalized patients have been consistently reported to have modulated levels of biomarkers demonstrating coagulation and acute cardiac injury. Understanding of molecular mechanisms underlying CV involvement is strongly believed to be the foundation for developing strategies for early diagnosis and management of COVID-19-affected individuals. We review here various molecular mechanisms underlying CV involvement in COVID-19 and discuss several biochemical prognostic markers, as they have evidently revealed their importance in predicting severe prognosis such as mortality, mechanical ventilation, and ICU admission among severe acute respiratory syndrome coronavirus 2-infected patients with or without previous history of myocardial injury. The therapeutic strategies that could be employed to treat and manage CV manifestations in COVID-19-positive individuals are also discussed.

The ratio of cardiac troponin T to troponin I may indicate non-necrotic troponin release among COVID-19 patients.

BACKGROUND: Although cardiac troponin T (cTnT) and troponin I(cTnI) are expressed to similar amount in cardiac tissue, cTnI often reach ten-times higher peak levels compared to cTnT in patients with myocardial necrosis such as in acute myocardial infarction (MI). In contrast, similar levels of cTnT and cTnI are observed in other situations such as stable atrial fibrillation and after strenuous exercise. OBJECTIVE: Examine cTnT and cTnI levels in relation to COVID-19 disease and MI. METHODS: Clinical and laboratory data from the local hospital from an observational cohort study of 27 patients admitted with COVID-19 and 15 patients with myocardial infarction (MI) that were analyzed with paired cTnT and cTnI measurement during hospital care. RESULTS: Levels of cTnI were lower than cTnT in COVID-19 patients (TnI/TnT ratio 0.3, IQR: 0.1-0.6). In contrast, levels of cTnI were 11 times higher compared to cTnT in 15 patients with MI (TnI/TnT ratio 11, IQR: 7-14). The peak cTnI/cTnT ratio among the patients with MI following successful percutaneous intervention were 14 (TnI/TnT ratio 14, IQR: 12-23). The 5 COVID-19 patient samples collected under possible necrotic events had a cTnI/cTnT ratio of 5,5 (IQR: 1,9-8,3). CONCLUSIONS: In patients with COVID-19, cTnT is often elevated to higher levels than cTnI in sharp contrast to patients with MI, indicating that the release of cardiac troponin has a different cause in COVID-19 patients.