Cardiac Biomarkers: What Is and What Can Be

Jacob, Rachel; Khan, Mahmood

doi:10.1055/s-0039-1679104

Cited by 71 publications

(58 citation statements)

References 26 publications

(19 reference statements)

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“…The same applies for increased blood urea nitrogen and creatinine as well as proteinuria and hematuria for renal injuries [ 44 ]. Heart specific markers found in the publications are increased creatine kinase, troponin C and myohemoglobin levels as well as a decreased platelet count [ 45 ]. It is also noticeable that an increased number of coagulation factors such as decreased platelets, increased d -dimer level and increased fibrinogen [ 46 ] as well as inflammatory parameters such as c-reactive protein [ 47 ] and increased leucocyte level are associated with severity and fatality.…”

Section: Resultsmentioning

confidence: 99%

Risk factors for Covid-19 severity and fatality: a structured literature review

et al. 2020

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Purpose Covid-19 is a global threat that pushes health care to its limits. Since there is neither a vaccine nor a drug for Covid-19, people with an increased risk for severe and fatal courses of disease particularly need protection. Furthermore, factors increasing these risks are of interest in the search of potential treatments. A systematic literature review on the risk factors of severe and fatal Covid-19 courses is presented. Methods The review is carried out on PubMed and a publicly available preprint dataset. For analysis, risk factors are categorized and information regarding the study such as study size and location are extracted. The results are compared to risk factors listed by four public authorities from different countries. Results The 28 records included, eleven of which are preprints, indicate that conditions and comorbidities connected to a poor state of health such as high age, obesity, diabetes and hypertension are risk factors for severe and fatal disease courses. Furthermore, severe and fatal courses are associated with organ damages mainly affecting the heart, liver and kidneys. Coagulation dysfunctions could play a critical role in the organ damaging. Time to hospital admission, tuberculosis, inflammation disorders and coagulation dysfunctions are identified as risk factors found in the review but not mentioned by the public authorities. Conclusion Factors associated with increased risk of severe or fatal disease courses were identified, which include conditions connected with a poor state of health as well as organ damages and coagulation dysfunctions. The results may facilitate upcoming Covid-19 research.

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Section: Resultsmentioning

confidence: 99%

Risk factors for Covid-19 severity and fatality: a structured literature review

et al. 2020

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“…Classical EV markers [51] (Cd63, Pdcd6ip/Alix, Tsg101) were enriched in the EV fraction obtained from digest perfusate (Figure 2C). Importantly, during collagenase II‐based digestion, levels of cytoplasmic proteins (Actc1, Gapdh, Tuba1b) and clinical markers of cardiac damage [42,43,52] (Ldhb, Mb, Tnnt2) did not increase (Figure 2D/E), and we did not detect proteins activated in apoptotic processes (Casp3/9, Bax, Bak) (Table S2). Additionally, levels of Alb, Fga, and Hba were highest in wash fractions, suggesting successful perfusion of heart and depletion of abundant blood components from EV preparations (Figure 2F).…”

Section: Figurementioning

confidence: 88%

“…EVs have previously been isolated from hearts and cardiac tissues using mechanical dissociation [34,37,38,40] which invariably results in cell lysis and intracellular contamination of EV preparations. Indeed, other methods to isolate EVs from heart in this study involved tissue dicing, resulting in a high abundance of intracellular proteins associated with cardiac damage (troponins, lactate dehydrogenases, creatine kinases, myoglobin) [42–44] in isolated EVs (Figure S1). To avoid these issues associated with tissue mincing, we used collagenase II to gently hydrolyse the ECM and loosen cardiac tissue structure, a procedure commonly used for the isolation of cardiomyocytes [45–48].…”

Section: Figurementioning

confidence: 99%

“…However, tissue freezing and homogenisation results in tissue damage and cell disruption, thereby contaminating EV preparations with intracellular components and membrane debris. Additionally, MS profiling of EVs isolated using three different methods (Table S7), all utilising fresh (nonfrozen) tissue and mechanical disruption (Figure S1A/B), resulted in identification of cardiac damage markers (i.e., Ckmt2, Ckm, Mb, Ldha, Ldhb, Tnnc1, Tnni3, Tnnt2) [42–44] as highly abundant (top 10%) in each method, indicating cell stress/intracellular contamination of isolated EVs (Figure S1C). Comparatively, collagenase perfusion (cEV) resulted in none of these markers appearing in the top 10% most abundant proteins, whereas 20 inclusion markers for EVs (from international guidelines of EV research/reporting) were identified (i.e., Pdcd6ip/Alix, Anxa1, Anxa4) (Figure S1C) [51,76].…”

Section: Figurementioning

confidence: 99%

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Proteome characterisation of extracellular vesicles isolated from heart

et al. 2021

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Cardiac intercellular communication is critical for heart function and often dysregulated in cardiovascular diseases. While cardiac extracellular vesicles (cEVs) are emerging mediators of signalling, their isolation remains a technical challenge hindering our understanding of cEV protein composition. Here, we utilised Langendorffcollagenase-based enzymatic perfusion and differential centrifugation to isolate cEVs from mouse heart (yield 3-6 µg/heart). cEVs are ∼200 nm, express classical EV markers (Cd63/81/9 + , Tsg101 + , Pdcd6ip/Alix + ), and are depleted of blood (Alb/Fga/Hba) and cardiac damage markers (Mb, Tnnt2, Ldhb). Comparison with mechanically-derived EVs revealed greater detection of EV markers and decreased cardiac damage contaminants. Mass spectrometry-based proteomic profiling revealed 1721 proteins in cEVs, implicated in proteasomal and autophagic proteostasis, glycolysis, and fatty acid metabolism; essential functions often disrupted in cardiac pathologies. There was striking enrichment of 942 proteins in cEVs compared to mouse heart tissue -implicated in EV biogenesis, antioxidant activity, and lipid transport, suggesting active cargo selection and specialised function. Interestingly, cEVs contain marker proteins for cardiomyocytes, cardiac progenitors, B-cells, T-cells, macrophages, smooth muscle cells, endothelial cells, and cardiac fibroblasts, suggesting diverse cellular origin. We present a method of cEV isolation and provide insight into potential functions, enabling future studies into EV roles in cardiac physiology and disease.

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“…This issue deserves further investigation. Circulatory creatine kinase and its cardiac specific isozyme, CK-MB, are the additional markers of cardiac tissue damage (64). A rise in CK-MB level and/or activity during acute exercises such as intermittent training and marathon running indicate a significant cardiac stress (65)(66).…”

Section: Biomarkers Of Exercise Induced Oxidative Cardiac Injurymentioning

confidence: 99%

Melatonin, the advance-guard in oxidative myocardial assault instigated by exercise stress: a physiological and biochemical insight

2020

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Exercise conducted at an optimum training load is usually beneficial for the overall health of an individual. However, an unaccustomed intense exercise carried out by untrained individuals or elite athletes during over-training and/or competition-related stress often bear inevitable cardiovascular risks. Although many alterations occurring in the cardiovascular system during exercise are the results of training adaptations, sudden cardiovascular deaths reported in competitive athletes is a matter of grave concern. Several oxidative biomarkers that depict the underlying structural and functional impairment of the myocardial tissue have been identified in the individuals subjected to extensive exercise. The exercise-mediated cardiomyopathy is free radical related and also associated with pro-inflammatory response. In this review we will highlight the possible role of melatonin in obviating irrevocable oxidative cardiovascular injury triggered by extensive exercise stress. Melatonin effectively reduces exercise-induced lipid peroxidation, restores natural cellular antioxidant pool and supresses the innate immune cascade reaction that, otherwise, jeopardize cardiovascular integrity. Melatonin blocks the IKK/IκB/NFκB signaling as well as suppress iNOS and COX-2 mediated inflammation in cardiac tissue. In addition, melatonin reduces blood lactate accumulation and accelerates glucose utilization, thereby, promoting energy metabolism in athletes during their training and competition. Physical exertion associated overheating and the resultant sympathetic outflow impede cardiovascular homeostasis. Melatonin not only attenuates the sympathomedullary stimulation but also protects the cardiac cells from the cytotoxic effect of catecholamines. The available information regarding the efficacy of melatonin in amelioration of exercise-driven oxidative insult in cardiac tissue has been discussed and summarized.

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Cardiac Biomarkers: What Is and What Can Be

Cited by 71 publications

References 26 publications

Risk factors for Covid-19 severity and fatality: a structured literature review

Risk factors for Covid-19 severity and fatality: a structured literature review

Proteome characterisation of extracellular vesicles isolated from heart

Melatonin, the advance-guard in oxidative myocardial assault instigated by exercise stress: a physiological and biochemical insight

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