High sensitivity troponin and COVID-19 outcomes

Authors: Nikolaos Papageorgiou,a,bCatrin Sohrabi,aDavid Prieto Merino,c,dAngelos Tyrlis,aAbed Elfattah Atieh,aBunny Saberwal,aWei-Yao Lim,aAntonio Creta,aMohammed Khanji,aReni Rusinova,aBashistraj Chooneea,aRaj Khiani,d,eNadeev Wijesuriya,e,fAnna Chow,e,fHaroun Butt,e,fStefan Browne,e,fNikhil Joshi,e,fJamie Kay,e,fSyed Ahsan,a and Rui Providenciaa,g



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.


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.


Myocardial injury, defined as positive troponin during admission was observed in 288 (66.4%) patients. Age (OR: 1.68 [1.49–1.88], p < .001), hypertension (OR: 1.81 [1.10–2.99], p = .020) and moderate chronic kidney disease (OR: 9.12 [95% CI: 4.24–19.64], 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: 1.27–4.56], p = .007, and OR: 6.81 [95% CI: 3.40–13.62], p < .001, respectively) and urgent renal replacement therapy (OR: 4.14 [95% CI: 1.34–12.78], 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: 3.40–13.47], p < .001), venous thromboembolism (OR: 11.99 [95% CI: 3.20–44.88], p < .001), development of atrial fibrillation (OR: 10.66 [95% CI: 1.33–85.32], p = .026) and death during admission (OR: 2.40 [95% CI: 1.34–4.29], 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 (5–13) negative, 14 (7–23) low-positive levels and 16 (10–23) high-positive (p < .001).


Admission and peak troponin appear to be predictors for cardiovascular and non-cardiovascular events and outcomes in COVID-19 patients, and their utilization may have an impact on patient management.

For More Information: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7970632/

Clinical utility of cardiac troponin measurement in COVID-19 infection

Authors: David C Gaze 1 2


The novel coronavirus SARS-CoV-2 causes the disease COVID-19, a severe acute respiratory syndrome. COVID-19 is now a global pandemic and public health emergency due to rapid human-to-human transmission. The impact is far-reaching, with enforced social distancing and isolation, detrimental effects on individual physical activity and mental wellbeing, education in the young and economic impact to business. Whilst most COVID-19 patients demonstrate mild-to-moderate symptoms, those with severe disease progression are at a higher risk of mortality. As more is learnt about this novel disease, it is becoming evident that comorbid cardiovascular disease is associated with a greater severity and increased mortality. Many patients positive for COVID-19 demonstrate increased concentrations of cardiac troponin, creating confusion in clinical interpretation. While myocardial infarction is associated with acute infectious respiratory disease, the majority of COVID-19 patients demonstrate stable cTn rather than the dynamically changing values indicative of an acute coronary syndrome. Although full understanding of the mechanism of cTn release in COVID-19 is currently lacking, this mini-review assesses the limited published literature with a view to offering insight to pathophysiological mechanisms and reported treatment regimens.

For More Information: https://pubmed.ncbi.nlm.nih.gov/32255359/

Troponin and BNP Use in COVID-19

Mar 18, 2020 Cardiology Magazine

Authors: James L. Januzzi Jr., MD, FACC

  1. What are the potential mechanisms underlying troponin elevation with COVID-19 infection? Rise and/or fall of troponin indicating myocardial injury is common among patients with acute respiratory infections and correlated with disease severity.  Abnormal troponin values are common among those with COVID-19 infection particularly when testing with a high sensitivity cardiac troponin (hs-cTn) assay. In a recent article summarizing clinical course of patients with COVID-19, detectable hs-cTnI was observed in most patients, and hs-cTnI was significantly elevated in more than half of the patients that died. The mechanisms explaining myocardial injury in those with COVID-19 infection are not fully understood, however in keeping with other severe respiratory illnesses, direct (“non-coronary”) myocardial damage is almost certainly the most common cause. Given presence of abundant distribution of ACE2 – the binding site for the SARS-CoV-2 – in cardiomyocytes, some have postulated that myocarditis might explain rise of hs-cTn in some cases, particularly as acute left ventricular failure has been described in some cases. Lastly, acute myocardial infarction (MI) – either Type 1 MI based plaque rupture triggered by the infection, or Type 2 MI based on supply-demand inequity – is always possible. Importantly, a rise and/or fall of hs-cTn is not sufficient to secure the diagnosis of acute MI, which should be based on clinical judgment, symptoms/signs, and ECG changes. Given the frequency and non-specific nature of abnormal troponin results among patients with COVID-19 infection, clinicians are advised to only measure troponin if the diagnosis of acute MI is being considered on clinical grounds and an abnormal troponin should not be considered evidence for an acute MI without corroborating evidence.
  2. What are the potential mechanisms underlying elevation of natriuretic peptides with COVID-19 infection? Natriuretic peptides are biomarkers of myocardial stress and are frequently elevated among patients with severe respiratory illnesses typically in the absence of elevated filling pressures or clinical heart failure. Much like troponin, elevation of BNP or NT-proBNP is associated with an unfavorable course among patients with ARDS. Patients with COVID-19 often demonstrate significant elevation of BNP or NT-proBNP. The significance of this finding is uncertain and should not necessarily trigger an evaluation or treatment for heart failure unless there is clear clinical evidence for the diagnosis.
  3. What testing should be performed in COVID-19 patients with acute myocardial injury or abnormal natriuretic peptide results?

For More Information: https://www.acc.org/latest-in-cardiology/articles/2020/03/18/15/25/troponin-and-bnp-use-in-covid19

Cardiac Troponin-I and COVID-19: A Prognostic Tool for In-Hospital Mortality

Authors: Baher Al Abbasi 1Pedro Torres 1Fergie Ramos-Tuarez 2Nakeya Dewaswala 1Ahmed Abdallah 1Kai Chen 1Mohamed Abdul Qader 1Riya Job 1Samar Aboulenain 1Karolina Dziadkowiec 1Huzefa Bhopalwala 3Jesus E Pino 2Robert D Chait 2


Background: The number of fatalities due to coronavirus disease 2019 (COVID-19) is escalating with more than 800,000 deaths globally. The scientific community remains in urgent need of prognostic tools to determine the probability of survival in patients with COVID-19 and to determine the need for hospitalization.

Methods: This is a retrospective cohort study of patients with a diagnosis of COVID-19 admitted to a tertiary center between March 2020 and July 2020. Patients age 18 years and older were stratified into two groups based on their troponin-I level in the first 24 h of admission (groups: elevated vs. normal). The aim of the study is to explore the utility of cardiac troponin-I level for early prognostication of patients with COVID-19.

Results: This cohort of 257 patients included 122/257 (47%) women with a mean age of 63 ± 17 years. Patients with an elevated troponin-I level were more likely to be older (77 ± 13 vs. 58 ± 16 years, P < 0.0001), have a history of hypertension (P < 0.0001), diabetes mellitus (P = 0.0019), atrial fibrillation or flutter (P = 0.0009), coronary artery disease (P < 0.0001), and chronic heart failure (P = 0.0011). Patients with an elevated troponin-I level in the first 24 h of admission were more likely to have higher in-hospital mortality (52% vs. 10%, P < 0.0001). Troponin-I level in the first 24 h of admission had a negative predictive value of 89.7% and a positive predictive value of 51.9% for all-cause in-hospital mortality.

Conclusions: Troponin-I elevation is commonly seen in patients with COVID-19 and is significantly associated with fatal outcomes. However, a normal troponin-I level in the first 24 h of admission had a high negative predictive value for all-cause in-hospital mortality, thereby predicting favorable survival at the time of discharge.

For More Information: https://pubmed.ncbi.nlm.nih.gov/33224386/

Can we predict the severe course of COVID-19 – a systematic review and meta-analysis of indicators of clinical outcome?

  1. Authors: Stephan Katzenschlager ,Alexandra J. Zimmer ,Claudius Gottschalk, Jürgen Grafeneder,Stephani Schmitz, Sara Kraker, Marlene Ganslmeier, Amelie Muth, Alexander Seitel, Lena Maier-Hein, Andrea Benedetti, Jan Larmann, Markus A. Weigand, Sean McGrath , Claudia M. Denkinger  



COVID-19 has been reported in over 40million people globally with variable clinical outcomes. In this systematic review and meta-analysis, we assessed demographic, laboratory and clinical indicators as predictors for severe courses of COVID-19.


This systematic review was registered at PROSPERO under CRD42020177154. We systematically searched multiple databases (PubMed, Web of Science Core Collection, MedRvix and bioRvix) for publications from December 2019 to May 31st 2020. Random-effects meta-analyses were used to calculate pooled odds ratios and differences of medians between (1) patients admitted to ICU versus non-ICU patients and (2) patients who died versus those who survived. We adapted an existing Cochrane risk-of-bias assessment tool for outcome studies.


Of 6,702 unique citations, we included 88 articles with 69,762 patients. There was concern for bias across all articles included. Age was strongly associated with mortality with a difference of medians (DoM) of 13.15 years (95% confidence interval (CI) 11.37 to 14.94) between those who died and those who survived. We found a clinically relevant difference between non-survivors and survivors for C-reactive protein (CRP; DoM 69.10 mg/L, CI 50.43 to 87.77), lactate dehydrogenase (LDH; DoM 189.49 U/L, CI 155.00 to 223.98), cardiac troponin I (cTnI; DoM 21.88 pg/mL, CI 9.78 to 33.99) and D-Dimer (DoM 1.29mg/L, CI 0.9 to 1.69). Furthermore, cerebrovascular disease was the co-morbidity most strongly associated with mortality (Odds Ratio 3.45, CI 2.42 to 4.91) and ICU admission (Odds Ratio 5.88, CI 2.35 to 14.73).

For More Information: https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0255154