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• W2926812473 abstract "Biomarkers in MedicineVol. 13, No. 5 CommentaryFree AccessCardiac troponins as biomarkers for cardiac diseaseClaudio Passino, Alberto Aimo, Silvia Masotti, Veronica Musetti, Concetta Prontera, Michele Emdin & Aldo ClericoClaudio Passino Fondazione CNR Regione Toscana G Monasterio & Scuola Superiore Sant'Anna, Pisa, ItalySearch for more papers by this author, Alberto Aimo Fondazione CNR Regione Toscana G Monasterio & Scuola Superiore Sant'Anna, Pisa, ItalySearch for more papers by this author, Silvia Masotti Fondazione CNR Regione Toscana G Monasterio & Scuola Superiore Sant'Anna, Pisa, ItalySearch for more papers by this author, Veronica Musetti Fondazione CNR Regione Toscana G Monasterio & Scuola Superiore Sant'Anna, Pisa, ItalySearch for more papers by this author, Concetta Prontera Fondazione CNR Regione Toscana G Monasterio & Scuola Superiore Sant'Anna, Pisa, ItalySearch for more papers by this author, Michele Emdin Fondazione CNR Regione Toscana G Monasterio & Scuola Superiore Sant'Anna, Pisa, ItalySearch for more papers by this author & Aldo Clerico*Author for correspondence: E-mail Address: clerico@ftgm.it Fondazione CNR Regione Toscana G Monasterio & Scuola Superiore Sant'Anna, Pisa, ItalySearch for more papers by this authorPublished Online:3 Apr 2019https://doi.org/10.2217/bmm-2019-0039AboutSectionsPDF/EPUB ToolsAdd to favoritesDownload CitationsTrack CitationsPermissionsReprints ShareShare onFacebookTwitterLinkedInReddit Keywords: acute coronary syndromecardiac troponinshigh sensitivity methodsmyocardial infarctionquality specificationreference populationrisk stratificationCardiovascular disease (CVD) is a leading cause of death, morbidity and hospitalization worldwide [1–3]. Patient risk stratification is a crucial goal, as it informs therapy and follow-up strategies, with the ultimate goal of impacting on the natural history of the disease. Laboratory biomarkers are regarded with interest as tools for prognostic stratification [4–7]. Over the last years, more than 100 new biomarkers have been evaluated under this respect, with more than 4000 clinical studies published [4,5].Assessing the prognostic accuracy of a novel cardiovascular biomarker is very complex [3,6,7]. According to the principles of Evidence-Based Laboratory Medicine, a biomarker should not only be an independent predictor of outcome in multiple regression models, but also influence patient management [8], which is the prerequisite for cost–efficacy [5,8]. As a result, very few novel laboratory biomarkers end up being recommended for risk prediction [5,9,10].Heart failure (HF) is the terminal form of many cardiac diseases [11]. Natriuretic peptides (NPs) and cardiac troponins (cTns) independently contribute to cardiovascular risk assessment because these biomarkers are involved in different pathophysiological mechanisms related to cardiac dysfunction and HF progression [11]. A large number of clinical studies demonstrated that plasma NPs and cTn are independent predictors of prognosis in HF [2,10,12–18]. Based on these findings, the 2017 American College of Cardiology Federation/American Heart Association/Heart Failure Society Association Guidelines confirmed that NPs and cTns are the first-line biomarkers for risk stratification in both acute and chronic HF [10].The use of cardiac-specific biomarkers for risk prediction in the general population is controversial and was not contemplated before 2010 [19], possibly because immunoassay methods able to measure the circulating levels of cTns in the majority of apparent healthy individuals (including both adult and pediatric ages) have been introduced only recently [20–25]. Here we discuss the recent evidence that circulating levels of cTns, measured with high-sensitivity (hs) methods, may be increased even in asymptomatic individuals. We believe that an initial myocardial remodeling could account for a rise in cTn, conferring a higher risk of developing HF to these subjects.cTns as cardiovascular risk biomarkers in the general populationOnly after the year 2006, the introduction in the clinical laboratory routine of immunoassays with increased analytical sensitivity (hs-methods) allowed the detection of increased levels of cTnI and cTnT in patients with cardiac diseases other than myocardial infarction (MI), in patients with extra-cardiac diseases (renal, pulmonary and inflammatory diseases), and even in some apparently healthy subjects [15–18,25,28–33]. Furthermore, several studies [34–53], including also three meta-analyses [45,52,53], demonstrated that the cardiovascular risk tend to increase also in some apparently healthy individuals of both sexes; in other words, for cTn values below the 99th percentile URL, which is the cut-off value recommended by all the international guidelines for the diagnosis of MI [54–56].In particular, in 2017 Willeit et al. [53] performed a meta-analysis including 28 studies, involving 154,052 participants. The cTnI values, measured by the Architect (14 studies) and Erenna (three studies) methods, were detectable in 82.6% of individuals, while those of cTnT in only 69.7% (ECLIA method, 11 studies).More recently, Welsh et al. [51] evaluated the distribution and association between cTnT (measured by ECLIA method), cTnI (measured by Architect method) and other cardiovascular risk factors in a large general population cohort (19,501 individuals, age range: 18–98 years). Detectable concentrations of cTnT and cTnI were found in 10,395 participants (53.3%) and 14579 (74.8%), respectively. Women and younger individuals were more likely to demonstrate undetectable concentrations of cTns [51]. More than 50% of women in the ≤50–59 year age-groups had undetectable cTnT and >50% of women in the ≤30–39 year age-groups had undetectable cTnI [51]. There were 296 male participants (3.6%) and 897 female participants (7.9%) with a cTnT result above the recommended 99th percentile (15.5 and 9.0 ng/l, respectively). For cTnI, 83 male participants (1.0%) and 115 female participants (1.0%) were above the recommended 99th percentile (34.2 and 15.6 ng/l, respectively) [51]. On average, higher troponin levels were found more frequently in older individuals with higher BMI, systolic blood pressure and creatinine values, with a history of CVD or diabetes, and use of cholesterol medications [51]. A composite 10-year CVD risk score calculated in participants without prevalent CVD and ≥35 years of age yielded not significantly different (p = 0.34) positive associations with both cTnT and cTnI [51].In the North-Trøndelag Health (HUNT) study [50], authors measured TnI with the Architect hs method in a cohort of a general population, including 9005 participants [50]. The prognostic accuracy of hs-TnI, assessed by C-statistics, was significantly greater than that of the standard model, also including C-reactive protein (0.753 vs 0.644) [50]. It is important to note that the tertile with the highest risk showed a cut-off value of 10 ng/l for women and 12 ng/l for men, which is a cTnI value below the 99th percentile suggested by the manufacturer [50].Analytical performance, pathophysiological considerations & clinical relevanceThe most important quality specifications concerning the ‘high-sensitivity’ methods for the cTn assay are related to estimation of 99th percentile URL. The 2018 Expert Opinion from the AACC and IFCC [55] recommends that high-sensitivity methods should satisfy two fundamental criteria. First, hs-methods should measure the 99th percentile URL with an imprecision (expressed as coefficient of variation, percent coefficient of variation [CV] %) ≤10%; second, these assays should be able to detect cTn concentration at or above the limit of detection (LoD) in at least 50% of healthy men and women.Marjot et al. [25] recently reported that the high-sensitivity methods for cTnI and cTnT are able to detect cardiac injury due to necrosis of just 40 mg of myocardium, equivalent to 0.015% of the heart, sufficient to increase serum concentrations above the 99th percentile URL. According to these data, cTn immunoassays with limit of detection less than 3 ng/l should be able to measure a cTn amount released from 6 to 8 mg of myocardial tissue [25,26]. Accordingly, the analytical sensitivity of these high-sensitivity cTnI methods is greatly higher than the spatial resolution of the most sensitive cardiac imaging techniques [25,26]. The intra-individual variation in healthy adult subjects of cTnI, evaluated with high-sensitivity method, is on average about 8–10% [27]. Considering these data as a whole, some authors suggested that the circulating levels of cTnI, measured with high-sensitivity immunoassays, in healthy adult subjects may be considered as a reliable estimate of the physiological turnover of human myocardial tissue [26].The 2018 fourth universal definition of myocardial infarction [56] states that: “the term myocardial injury should be used when there is evidence of elevated cTn values with at least one value above the 99th percentile upper reference limit.” Myocardial injury is a prerequisite for the diagnosis of MI, but also a distinct entity [57]. Indeed, several cardiac and systemic pathologies can result in myocardial injury without infarction. These conditions should be accurately distinguished from MI [56–58].The estimation of 99th percentile strongly depends not only on demographic and physiological variables of the reference population, but also on the analytical performances of cTn methods, and the mathematical algorithm used for calculating the 99th value [59,60]. cTnI values measured with the Architect method in an Italian reference population, including 675 healthy subjects (age range: 18–86 years, age: 50.1 ± 13.9 years, 348 women and 327 men) is not normally distributed with a 99th percentile value (28.0 ng/l) that is 15.6-fold higher than the median value (1.8 ng/l). These data confirm the results previously reported in the HUNT study for a Scandinavian general population including 3670 apparently healthy men and 4429 apparently healthy women [45].According to Callum G Fraser [61,62], the bidirectional Z-score Reference Change Value (RCV) between two results, with its 95% CI, can be calculated by considering both the analytical variability of the method (CVA) and the intra-individual variability (CVI), using Formula 1: (1) For example, the CVA estimated by the imprecision profile using standardized protocols [21,22], is 18.1% for a cTnI concentration of 2.0 ng/l, measured with the high-sensitivity cTnI method (hs-cTnI) Architect method. Furthermore, Van der Linden et al. [27] have recently reported that the CVI of cTnI measured with the Architect method is about 9% in adult healthy subjects. By using these values of CVA and CVI in the Formula 1, it is possible to estimate the RCV value as 56.0% and the absolute Δ change as 1.1 ng/l for a 95% probability. This means that, for a cTnI concentration of 2.0 ng/l, an increase or decrease of 1.1 ng/l should be considered significant with 95% probability. In a similar way, RCV and Δ change for the range of Architect cTnI concentrations from 2 to 40 ng/l can be calculated. These values are well in agreement with the absolute Δ changes in Architect cTnI values proposed by the 2016 ESC guidelines for the 0/1 h rule-in and rule-out algorithms for the diagnosis of non-ST segment elevation MI, considering also cTnI values below the upper reference levels [54]. When a population is considered instead of the single individual, these notions translate in the concept that increasingly cTn values reflect different degrees of cardiomyocyte renewal even when well below the 99th percentile values. It then comes as to no surprise that the cardiovascular risk in the general population seems to increase continuously and progressively from very low cTn values (for example, cTnI values of 4 ng/l for women and 6 ng/l for men in the HUNT study) [45].From a clinical perspective, the observation of an increment in hs-cTnI levels, even of only 3–5 ng/l over some months in a patient with a suspect of cardiomyopathy should suggest an initial myocardial remodeling, ultimately culminating in symptomatic HF [10,11]. Indeed, cTnI distribution in the reference population indicate that an individual with a cTnI concentration equal to the medial value (1.8 ng/l) should increase his/her myocardial renewal of about 16-fold in order to reach the 99th percentile value (i.e., 28.0 ng/l).Only very recently the introduction of high-sensitivity methods allowed the accurate detection of cTn levels in healthy adults [20–27]. Several studies [34–53] demonstrated that the cardiovascular risk progressively increases in the general population even for cTn values well below the 99th percentile, in other words, the recognized cut-off for the detection of myocardial injury and/or diagnosis of MI [56]. An early and effective treatment is needed to revert the initial myocardial remodeling and slow down HF progression [5,11,13,26]. High-sensitivity cTn methods enable to monitor myocardial renewal and remodeling, and to promptly identify patients at highest risk to HF development [26], possibly resulting in early diagnosis and improved prognosis.Financial & competing interests disclosureThe authors have no relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript. 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Letter regarding the article ‘Troponins and brain natriuretic peptides for the prediction of cardiotoxicity in cancer patients: a meta‐analysis.’15 April 2020 | European Journal of Heart Failure, Vol. 22, No. 7Head-to-head comparison of plasma cTnI concentration values measured with three high-sensitivity methods in a large Italian population of healthy volunteers and patients admitted to emergency department with acute coronary syndrome: A multi-center studyClinica Chimica Acta, Vol. 496 Vol. 13, No. 5 Follow us on social media for the latest updates Metrics History Received 22 January 2019 Accepted 21 February 2019 Published online 3 April 2019 Published in print April 2019 Information© 2019 Future Medicine LtdKeywordsacute coronary syndromecardiac troponinshigh sensitivity methodsmyocardial infarctionquality specificationreference populationrisk stratificationFinancial & competing interests disclosureThe authors have no relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript. This includes employment, consultancies, honoraria, stock ownership or options, expert testimony, grants or patents received or pending, or royalties.No writing assistance was utilized in the production of this manuscript.PDF download" @default.
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