Anti-troponin antibodies following myocardial infarction

O’Donohoe, Tom J.; Ketheesan, Natkunam; Schrale, Ryan G.

doi:10.1016/j.jjcc.2016.07.018

Cited by 16 publications

(13 citation statements)

References 99 publications

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“…9 This is consistent with studies indicating a 0–27.6% prevalence of cardiac troponin autoantibodies, depending on underlying cardiac disease. 10 The pretest probability based on clinical information and local prevalence will determine how PEG, the discrepancy between assays, or other macrotroponin detection methods is most helpful in the local setting.…”

Section: Discussionmentioning

confidence: 99%

Practical approaches to the detection of macrotroponin

Lam

Kyle

2023

Ann Clin Biochem

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Introduction: Macrotroponin is increasingly recognised as a cause of confusion in interpreting high-sensitivity cardiac troponin (hs-cTnI) results. In this study, we sought to evaluate two practical approaches to detecting macrotroponin. These two approaches are PEG precipitation and SVM (support vector machine) analysis to classify discrepancies between hs-cTn assays. Method: Residual serum and heparin plasma specimens (n=483) with initially elevated hs-cTnI from hospital and community laboratories were retested on multiple hs-cTn platforms before and after PEG precipitation and Protein A immunoglobulin depletion. SVM analysis was conducted to identify a linear equation that best discriminated specimens with macrotroponin using a combination of results from two different hs-cTn assays. Findings: The diagnostic performance of PEG precipitation was carried out using Protein A immunoglobulin depletion as the reference comparator. When a cutoff residual activity after PEG precipitation of ≤ 20% was used, this threshold carried a high specificity of 92% (confidence interval 83 – 98%; n = 189) using the Siemens hs-cTnI Vista assay and 95% specificity (86% - 98%; n = 242) using the Abbott hs-cTnI Architect assay. SVM analysis generated a linear equation identifying macrotroponin specimens from results obtained on two hs-cTn assays. This approach can be highly specific, comparable to PEG precipitation when certain assay combinations and concentrations are used. Conclusion: We describe and identify practical alternatives to detecting macrotroponin. These approaches can be optimised for high specificity, reducing the need for more complex laboratory methods.

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Section: Discussionmentioning

confidence: 99%

Practical approaches to the detection of macrotroponin

Lam

Kyle

2023

Ann Clin Biochem

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“…Evermore sensitive assays for cardiac troponins have demonstrated that these biomarkers may be detectable in several clinical conditions, as well as in a significant proportion of healthy subjects (59,60). Anticardiac troponin autoantibodies have also been described in different settings (namely in healthy subjects and after MI) (6). Although the possible role of autoimmunity mediated by autoantibodies against cardiac troponin has raised interest, this phenomenon has still not been fully elucidated (3,4).…”

Section: Discussionmentioning

confidence: 99%

“…Given these data, and the fact that there are still gaps in our knowledge, especially concerning remodelling mechanisms (6,39), a reappraisal of anti-cardiac troponin autoantibodies in this setting seems important.…”

Section: Discussionmentioning

confidence: 99%

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Anti-cardiac troponin antibodies in clinical human disease: a systematic review

Vilela¹,

Bettencourt‐Silva²,

Costa³

et al. 2017

Ann. Transl. Med.

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Anti-cardiac troponin antibodies have been studied in different types of clinical diseases and in healthy populations. A systematic review of published data on anti-troponin antibodies was carried out (search performed on PubMed, ISI Web of Knowledge and Scopus databases). From title and abstract analysis, thirty-three articles were included that met the pre-specified criteria; after full-text analysis, nine articles were excluded. Most studies assessed anti-troponin I antibodies. The prevalence of anti-cardiac troponin antibodies in healthy individuals ranged from 0.0% to 20.0%. The prevalence of anti-troponin I autoantibodies in dilated cardiomyopathy (DCM) ranged from 7.0% to 22.2%. Other conditions under study were myocardial infarction, ischemic cardiomyopathy (ICM), peripartum cardiomyopathy (PPCM), Chagas disease, Emery-Dreifuss muscular dystrophy (EDMD) and renal transplantation. In the different patient populations studied, anti-cardiac troponin antibodies have been shown to be either positively or negatively associated with prognostic and clinical features. In what concerns a possible value as biomarkers, these assays have not emerged up to the present moment as important aids for practical clinical decisions in cardiac or other types of patients. In what concerns pathophysiology, anti-cardiac troponin autoantibodies may play a role in different diseases. It can be speculated that these antibodies could be involved in perpetuating some degree of cardiac injury after an event, such as myocardial infarction or PPCM. The major function of the heart is its contractile function, and cardiac muscle contains sarcomeres, which include different types of molecules, of which actin and myosin are essential for strength generation during contraction. Other molecules, such as cardiac troponins, play a role of regulation concerning cardiac muscle contraction. Cardiac troponins I and T have been shown to be different molecules than the corresponding ones in skeletal muscle, and have gained importance as cardiac biomarkers (1,2).Research has shown that antibodies against cardiac troponins exist in different settings, and questions about their role in the cardiovascular pathological continuum have emerged over the last years. The possible role of cardiac troponin autoantibodies in disease processes [and particularly in dilated cardiomyopathy (DCM) and ischemic cardiomyopathy (ICM)] has gained interest (3-6).Animal models in mice have demonstrated that anticardiac troponin I autoantibodies are capable of inducing heart dilatation and dysfunction, apparently through interactions with the calcium balance in cardiomyocytes (7). Okazaki et al. showed that in mice antibodies to cardiac troponin I stained the surface of cardiomyocytes, implying the presence of troponin I on the cell surface (differing from cardiac troponin T) (7). Göser et al. immunized mice with cardiac troponin I, leading to severe inflammation of the myocardium, cardiomegaly, fibrosis and 30% mortality over 270 days (8). However, in a study carri...

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“…In 2017, Fan et al also reported that cTnIAAbs are independent predictors of left ventricular remodelling in patients with ST-elevation myocardial infarction [8]. Due to the unknown mechanisms underlying these effects, the clinical relevance for cTnIAAb positive AMI patients remained unclear [9]. However, findings reported by Wu et al, who identified cTnIAAb to be involved in apoptosis, could explain the negative effects observed for cTnIAAb positive patients.…”

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confidence: 99%