Cardiac troponin may be released by ischemia alone, without necrosis

Hickman, Peter E.; Potter, Julia M.; Aroney, Con; Koerbin, Gus; Southcott, Emma; Wu, Alan H.B.; Roberts, Michael S.

doi:10.1016/j.cca.2009.12.009

Cited by 224 publications

(207 citation statements)

References 40 publications

Supporting

Mentioning

192

Contrasting

Unclassified

Order By: Relevance

“…On the contrary, in marathon runners an earlier, shorter and lower peak of cTns is usually observed. The shorter peak observed in these cases after physical exercise with respect to those occurring in AMI subjects may depend on the release of cTnI and cTnT from the cytosolic compartment, corresponding to 5%-8% of the total cTn content of cardiomyocytes [8,75,91]. It has been suggested that enhanced membrane permeability promoted by the production of reactive oxygen species or alterations in calcium, pH, glucose/fat metabolism, or in communication between integrins, might explain the release of cTn into circulation after strenuous exercise [25,75].…”

Section: Mechanisms Of Troponin Release In Cardiac Patients and Healtmentioning

confidence: 96%

“…The shorter peak observed in these cases after physical exercise with respect to those occurring in AMI subjects may depend on the release of cTnI and cTnT from the cytosolic compartment, corresponding to 5%-8% of the total cTn content of cardiomyocytes [8,75,91]. It has been suggested that enhanced membrane permeability promoted by the production of reactive oxygen species or alterations in calcium, pH, glucose/fat metabolism, or in communication between integrins, might explain the release of cTn into circulation after strenuous exercise [25,75]. Other authors suggest alternative mechanisms: increased cardiovascular stress, inflammation, release of troponin degradation products in "blebs", dehydration, impaired renal clearance, and cTn expression in skeletal muscle [25], although the latter seems to occur only in the case of cTnT [92,93].…”

Section: Mechanisms Of Troponin Release In Cardiac Patients and Healtmentioning

confidence: 96%

“…Some pathophysiological factors should be borne in mind when comparing and explaining the differences in cTn release in ischemic and non-ischemic injury in patients with cardiac disease [74][75][76] and that in healthy patients following physical exercise. The kinetic profile of cTnI and cTnT circulating levels after strenuous exercise in apparently healthy subjects [25,40,[52][53][54][55][56][77][78][79][80][81][82][83][84][85][86][87][88][89][90] is different from that usually observed in patients with AMI.…”

Section: Mechanisms Of Troponin Release In Cardiac Patients and Healtmentioning

confidence: 99%

See 2 more Smart Citations

The 99th percentile of reference population for cTnI and cTnT assay: methodology, pathophysiology and clinical implications

Clerico

Zaninotto

Ripoli

et al. 2017

Clinical Chemistry and Laboratory Medicine (CCLM)

View full text Add to dashboard Cite

According to recent international guidelines, including the 2012 Third Universal Definiton of Myocardial Infarction by the Joint ESC/ACCF/AHA/WHF Task Force, an increase in cardiac troponin (cTn) levels over the 99th percentile upper reference limit (99th URL) should be considered clinically relevant, this cut-off being measured with an imprecision ≤10 CV%. In theory 99th URL values strongly depend not only on demographic and physiological variables (i.e. criteria for considering the reference population "healthy"), but also on the analytical performance of cTn methods and mathematical algorithms used for the calculation. The aim of the present article was therefore to review the methodological and pathophysiological factors affecting the evaluation and calculation of the 99th URL for cTn assay. The critical analysis made showed that no uniform procedure is followed, and nor have experts or regulatory bodies provided uniform guidelines for researchers or cTn assays manufacturers as an aid in "their quest to define normality". In particular, little attention has been paid to the way in which a healthy reference population is to be selected, or the criteria for calculating the 99th URL value for cTn assays, thus highlighting the need for international recommendations not only for demographic and physiological variables criteria for defining a healthy reference population, but also for calculating mathematical algorithms for establishing/ calculating clinical decision values. An expert consensus group, comprising laboratory and clinical scientists, biomedical statisticians, industrial and regulatory representatives, should be responsible for drawing up these guidelines.

show abstract

Section: Mechanisms Of Troponin Release In Cardiac Patients and Healtmentioning

confidence: 96%

Section: Mechanisms Of Troponin Release In Cardiac Patients and Healtmentioning

confidence: 96%

Section: Mechanisms Of Troponin Release In Cardiac Patients and Healtmentioning

confidence: 99%

See 1 more Smart Citation

The 99th percentile of reference population for cTnI and cTnT assay: methodology, pathophysiology and clinical implications

Clerico

Zaninotto

Ripoli

et al. 2017

Clinical Chemistry and Laboratory Medicine (CCLM)

View full text Add to dashboard Cite

show abstract

“…Another important, measurable parameter is the inter-individual variation, which reflects biological variations among healthy individuals from a defined population. A number of investigators measured intraand inter-individual variations using various cTn assays [15,[55][56][57][58][59][60]. The results ranged from 4% to 30% for intraindividual variations and from 30% to 200% for interindividual variations as summarized by Nordenskjöld and coworkers [60].…”

Section: What Constitutes the Rise And/or Fall In Ctn Concentrations?mentioning

confidence: 99%

“…Perhaps the only mechanism that would allow for limited release of cTn and leave behind viable cardiac cells is the formation of exosomes containing small amounts of the free, cytoplasmic cTn. Indeed, the formation of blebs in cardiac myocytes exposed to ischemia has been reported [15].…”

Section: Structure and Function Of Cardiac Troponinsmentioning

confidence: 99%

High sensitivity cardiac troponin assays in the clinical laboratories

Jarolím

2015

Clinical Chemistry and Laboratory Medicine (CCLM)

115

View full text Add to dashboard Cite

Abstract:Immunoassays measuring cardiac troponins I or T have become firmly established as critical tools for diagnosing acute myocardial infarction. While most contemporary assays provide adequate diagnostic performance, the increased sensitivity and precision of the new, high sensitivity assays that have already been introduced into clinical practice, provide the potential to further shorten intervals between blood draws or the time needed to detect the first significant troponin elevation. In addition to the relatively modest benefits at the diagnostic end, the high sensitivity assays and the investigational ultrasensitive cardiac troponin assays offer improvements for predicting major adverse cardiovascular events, development of heart failure or transition to end-stage kidney disease. These novel high sensitivity assays can measure troponin concentrations in 50%-100% of healthy individuals and therefore allow for the distribution of troponin values within a healthy cohort to be measured, patient's baseline troponin levels to be monitored, and clinicians to be alerted of deteriorating cardiorenal conditions. We envisage that the high sensitivity assays will become important tools for predicting each patient's risk of future adverse events and for guiding and monitoring corresponding adjustments of preventative therapeutic interventions.

show abstract

Cardiac troponins: Mechanisms of release and role in healthy and diseased subjects

et al. 2022

View full text Add to dashboard Cite

The cardiac troponins (cTns), cardiac troponin C (cTnC), cTnT, and cTnI are key elements of myocardial apparatus, fixed as protein complex on the thin filament of sarcomere and are involved in the regulation of excitationcontraction coupling of cardiomyocytes in the presence of Ca 2+ . Circulating cTnT and cTnI (cTns) increase following cardiac tissue necrosis, and they are consolidated biomarkers of acute myocardial infarction (AMI). However, the use of high sensitivity (hs)-immunoassay tests for cTnT and cTnI has made it possible to identify a multitude of other clinical conditions associated with increased circulating levels of cTns. cTns can be measured also in the peripheral circulation of healthy subjects or athletes, suggesting that different mechanisms are involved in the release of cTns in the blood independently of cardiac cell necrosis. In this review, the molecular/cellular mechanisms involved in cTns release in blood and the exploitation of cTnI and cTnT as biomarkers of cardiac adverse events, in addition to cardiac necrosis, are discussed.

show abstract

Cardiac troponin may be released by ischemia alone, without necrosis

Cited by 224 publications

References 40 publications

The 99th percentile of reference population for cTnI and cTnT assay: methodology, pathophysiology and clinical implications

The 99th percentile of reference population for cTnI and cTnT assay: methodology, pathophysiology and clinical implications

High sensitivity cardiac troponin assays in the clinical laboratories

Cardiac troponins: Mechanisms of release and role in healthy and diseased subjects

Contact Info

Product

Resources

About