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.

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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?

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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.

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More than 1,000 COVID-19 deaths recorded as US returns to April levels

Authors: BY MYCHAEL SCHNELL – 08/18/21 07:27 AM EDT

The U.S. recorded more than 1,000 COVID-19 deaths on Tuesday as numbers reach levels last seen in April, largely due to the highly infectious delta variant spreading rapidly throughout the country.

The 1,017 coronavirus deaths reported on Tuesday equate to roughly 42 fatalities an hour, according to a Reuters tally of state data.

The U.S. has recorded more than 620,000 deaths since the beginning of the pandemic, according to the Centers for Disease Control and Prevention (CDC).

The U.S. is now averaging 769 daily coronavirus deaths, Reuters reported, which is the highest rate seen since mid-April.

The U.S. has consistently been seeing fewer than than 1,000 COVID-19 deaths per day since mid-March, when large swaths of the country started getting vaccinated. Before that, the country was recording more than 1,000 deaths daily.

Infections are also currently on the rise in the U.S.

According to the Reuters tally, the U.S. has recorded an average of more than 100,000 new daily cases for the past 12 days, marking a six-month high.

The increase in COVID-19 cases and deaths is driven largely by the delta variant, which is more infectious than previous versions of the virus and has taken hold as the dominant strain in the country.

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COVID-19-associated diarrhea

World J Gastroenterol. 2021 Jun 21; 27(23): 3208–3222.Published online 2021 Jun 21. doi: 10.3748/wjg.v27.i23.3208PMCID: PMC8218355PMID: 34163106

Authors: Klara MegyeriÁron DernovicsZaid I I Al-Luhaibi, and András Rosztóczy


Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) recently emerged as a highly virulent respiratory pathogen that is known as the causative agent of coronavirus disease 2019 (COVID-19). Diarrhea is a common early symptom in a significant proportion of patients with SARS-CoV-2 infection. SARS-CoV-2 can infect and replicate in esophageal cells and enterocytes, leading to direct damage to the intestinal epithelium. The infection decreases the level of angiotensin-converting enzyme 2 receptors, thereby altering the composition of the gut microbiota. SARS-CoV-2 elicits a cytokine storm, which contributes to gastrointestinal inflammation. The direct cytopathic effects of SARS-CoV-2, gut dysbiosis, and aberrant immune response result in increased intestinal permeability, which may exacerbate existing symptoms and worsen the prognosis. By exploring the elements of pathogenesis, several therapeutic options have emerged for the treatment of COVID-19 patients, such as biologics and biotherapeutic agents. However, the presence of SARS-CoV-2 in the feces may facilitate the spread of COVID-19 through fecal-oral transmission and contaminate the environment. Thus gastrointestinal SARS-CoV-2 infection has important epidemiological significance. The development of new therapeutic and preventive options is necessary to treat and restrict the spread of this severe and widespread infection more effectively. Therefore, we summarize the key elements involved in the pathogenesis and the epidemiology of COVID-19-associated diarrhea.

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Literature Review of COVID-19 G.I. Complications

Authors: Md. Rayhan Mahmud, University of Helsinki, Md Karim Uddin, University of Helsinki, Md. Sajjad Hossain, Jagannath University – Bangladesh, Sharmin Akter, Jagannath University – Bangladesh

Gastrointestinal Symptoms Associated With Unfavorable Prognosis of COVID-19 Patients: A Retrospective

The roles of nausea and vomiting in COVID-19: did we miss something?ArticleFull-text available

ACE2 imbalance as a key player for the poor outcomes in COVID-19 patients with age-related comorbidities – Role of gut microbiota dysbiosis

COVID-19 and the gastrointestinal tract: More than meets the eye

Clinical Features of 2019 Novel Coronavirus Pneumonia Presented Gastrointestinal Symptoms But Without Fever Onset

Gastrointestinal symptoms associated with COVID-19: impact on the gut microbiome

Gastrointestinal Symptoms and outcomes in hospitalized COVID-19 patients

Gut microbiota and Covid-19- possible link and implications

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ABO blood group and COVID-19: a review on behalf of the ISBT COVID-19 working group

Authors: the ISBT COVID-19 Working Group School of Medicine


Growing evidence suggests that ABO blood group may play a role in the immunopathogenesis of SARS-CoV-2 infection, with group O individuals less likely to test positive and group A conferring a higher susceptibility to infection and propensity to severe disease. The level of evidence supporting an association between ABO type and SARS-CoV-2/COVID-19 ranges from small observational studies, to genome-wide-association-analyses and country-level meta-regression analyses. ABO blood group antigens are oligosaccharides expressed on red cells and other tissues (notably endothelium). There are several hypotheses to explain the differences in SARS-CoV-2 infection by ABO type. For example, anti-A and/or anti-B antibodies (e.g. present in group O individuals) could bind to corresponding antigens on the viral envelope and contribute to viral neutralization, thereby preventing target cell infection. The SARS-CoV-2 virus and SARS-CoV spike (S) proteins may be bound by anti-A isoagglutinins (e.g. present in group O and group B individuals), which may block interactions between virus and angiotensin-converting-enzyme-2-receptor, thereby preventing entry into lung epithelial cells. ABO type-associated variations in angiotensin-converting enzyme-1 activity and levels of von Willebrand factor (VWF) and factor VIII could also influence adverse outcomes, notably in group A individuals who express high VWF levels. In conclusion, group O may be associated with a lower risk of SARS-CoV-2 infection and group A may be associated with a higher risk of SARS-CoV-2 infection along with severe disease. However, prospective and mechanistic studies are needed to verify several of the proposed associations. Based on the strength of available studies, there are insufficient data for guiding policy in this regard.

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Role of neutrophil-epithelial interactions in SARS-CoV-2 infection

Authors: By Suchandrima BhowmikAug 15 2021Reviewed by Benedette Cuffari, M.Sc.

The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), which is the virus that causes coronavirus disease 2019 (COVID-19), is associated with high mortality and hospitalization rates. However, many patients who are infected with SARS-CoV-2 remain asymptomatic or develop mild symptoms.

In a recent study published on the preprint server bioRxiv*, researchers focus on the relationship between the pre-existing airway neutrophils and SARS-CoV-2 infection to determine the impact that neutrophils have on COVID-19.

An overview of neutrophils

Neutrophils are the first and predominant immune cells that are recruited to the respiratory tract in response to viral infection. Upon their arrival, neutrophils release various inflammatory mediators in an effort to rapidly eliminate the pathogen from the infected area.

Neutrophils are capable of recognizing infectious sites as well as act as sites of infections which, together, leads to an acute inflammatory response. An uncontrolled massive inflammatory response, which is also known as the cytokine storm, has been documented in patients with severe COVID-19.

“Despite their importance in anti-viral immunity and response to viral pathogens, neutrophils have been somewhat overlooked for their role in the pathogenesis of SARS-CoV-2 infection.”

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Intracellular localization of the SARS coronavirus protein 9b: evidence of active export from the nucleus

Authors: Igor Moshynskyy 1Sathiyanarayanan ViswanathanNatalia VasilenkoVladislav LobanovMartin PetricLorne A BabiukAlexander N Zakhartchouk


Open reading frame 9b (ORF 9b) encodes a 98 amino acid group-specific protein of severe acute respiratory syndrome (SARS) coronavirus (CoV). It has no homology with known proteins and its function in SARS CoV replication has not been determined. The N-terminal part of the 9b protein was used to raise polyclonal antibodies in rabbits, and these antibodies could detect 9b protein in infected cells. We analyzed the sub-cellular localization of recombinant 9b protein using fluorescence microscopy of live transfected cells and indirect immunofluorescence of transfected fixed cells. Our findings indicate that the 9b protein is exported outside of a cell nucleus and localizes to the endoplasmic reticulum. Our data also suggest that the 46-LRLGSQLSL-54 amino acid sequence of 9b functions as a nuclear export signal (NES).

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The Crystal Structure of ORF-9b, a Lipid Binding Protein from the SARS Coronavirus

Author links open overlay panelChristophMeier123A. RaduAricescu13ReneAssenberg2Robin T.Aplin2Robert J.C.Gilbert13Jonathan M.Grimes123David I.Stuart123


To achieve the greatest output from their limited genomes, viruses frequently make use of alternative open reading frames, in which translation is initiated from a start codon within an existing gene and, being out of frame, gives rise to a distinct protein product. These alternative protein products are, as yet, poorly characterized structurally. Here we report the crystal structure of ORF-9b, an alternative open reading frame within the nucleocapsid (N) gene from the SARS coronavirus. The protein has a novel fold, a dimeric tent-like β structure with an amphipathic surface, and a central hydrophobic cavity that binds lipid molecules. This cavity is likely to be involved in membrane attachment and, in mammalian cells, ORF-9b associates with intracellular vesicles, consistent with a role in the assembly of the virion. Analysis of ORF-9b and other overlapping genes suggests that they provide snapshots of the early evolution of novel protein folds.

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