Fluoroenzymometric method to measure cardiac troponin I in sera of patients with myocardial infarction

Zaninotto, Martina; Altinier, Sara; Lachin, Mattia; Carraro, Paolo; Plebani, Mario

doi:10.1093/clinchem/42.9.1460

Cited by 46 publications

(16 citation statements)

References 25 publications

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“…After 24 h, the rabbits were anesthetized exanguinated and the entire ischemic coronary artery removed and quickly frozen in liquid nitrogen for molecular biology determinations. The blood was collected in both acid-citrate dextrose (ACD) for P-selectin evaluation in the platelet surface and in a glass tube for sera isolation to determine troponin I. Sera troponin I was determined using a commercially available Dade-Behring immunoassay for human cardiac troponin I, which has been shown to react with rabbit cardiac troponin I (Zaninotto et al, 1996;O'Brien et al, 1997). The experimental procedure was approved by the institutional Animal Care and Use Committee.…”

Section: Experimental Designmentioning

confidence: 99%

Effect of clopidogrel on the expression of inflammatory markers in rabbit ischemic coronary artery

Molero

López‐Farré

Mateos-Cáceres

et al. 2005

British J Pharmacology

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1 Inflammation and platelet activation are critical phenomena in the setting of acute coronary syndromes. Platelets may contribute to increase ischemic injury by enhancing the inflammatory response of leukocytes and endothelial myocardial cells. Pharmacological inhibition of platelet activation prevents ischemic complications in patients with coronary diseases. Agents directed against the integrin glycoprotein IIb/IIIa (GP IIb/IIIa) receptor not only inhibit platelet aggregation but also have been demonstrated to limit the inflammatory response in acute coronary syndromes. The question then raised is if the inhibition of platelet activation by other mechanisms than the blockade of GP IIb/IIIa may also exert anti-inflammatory effects. The aim of the present study was to analyze if clopidogrel may exert anti-inflammatory effects during the acute phase of myocardial infarction. 2 A ligature was placed around the left anterior descending coronary artery of New Zealand White rabbits. After 15 min of ischemia, the myocardium was reperfused and the ischemic coronary artery was isolated 24 h after the ischemia. A group of ischemic rabbits was given a single oral dose of clopidogrel (20 mg kg À1 ) just after the arterial occlusion and the animal was recovered. Sham-operated animals served as control. 3 P-selectin expression was significantly increased in infarcted rabbits with respect to control rabbits. Clopidogrel administration reduced P-selectin expression with respect to untreated infarcted rabbits. CD40 ligand and tissue factor expression was increased in the ischemic coronary artery and reduced after clopidogrel administration. Clopidogrel also protected endothelial nitric oxide synthase protein expression in the ischemic coronary artery, a protein that has been found downregulated under inflammatory conditions. 4 In conclusion, inhibition of platelet activation by clopidogrel exerted anti-inflammatory effects on the ischemic coronary artery.

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Section: Experimental Designmentioning

confidence: 99%

Effect of clopidogrel on the expression of inflammatory markers in rabbit ischemic coronary artery

Molero

López‐Farré

Mateos-Cáceres

et al. 2005

British J Pharmacology

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“…Both troponin I and T have emerged as biochemical markers for the detection of myocardial cell damage in acute coronary syndromes, largely replacing creatine kinase and its fraction (MB) (1,2,9,19).…”

Section: Discussionmentioning

confidence: 99%

“…Although there is a substantial body of literature on cardiac troponin I in adults (2,12,13,19), there is essentially no information regarding normal neonatal values of this protein at birth. In our neonatal population, troponin I concentrations were frequently undetectable, similar to those of their healthy mothers and reference values for healthy adults (19 (22). In contrast to our results, in Soldin et al's study, 33% of neonatal patients (0-30 d of life) had troponin I concentrations in excess of the usual high cutoff for adults (0.1 mg/L) (23).…”

Section: Discussionmentioning

confidence: 99%

“…Troponin T levels were determined with an Elecsys 1020/2010 Systems analyser using the Elecsys Troponin T STAT Immunoassay (Roche Diagnostics GmbH 1 , Milan, Italy) (18). Troponin I levels were determined with a one-step enzyme immunoassay applied to R Â L Dimension analyser (Dade Behring 1 , Milan, Italy) (19). The lower limits of detection were 0.01 mg/L and 0.04 mg/L for troponin T and I, respectively (values declared by the manufacturers).…”

Section: Methodsmentioning

confidence: 99%

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Cardiac troponin I, cardiac troponin T and creatine kinase MB concentrations in umbilical cord blood of healthy term neonates

et al. 2003

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Aims: To measure and compare cardiac troponin I, cardiac troponin T and creatine kinase MB concentrations in the umbilical cord blood of healthy term infants and to investigate the relationship between maternal and neonatal troponin values at birth. Methods: Troponin I, troponin T and creatine kinase MB concentrations were measured from the umbilical cord samples of 85 healthy term neonates and in the blood samples of their respective mothers at birth. Results: Median (interquartile range) umbilical cord concentrations were 0 mug/L (0-0) for troponin I, 0 mug/L (0-0.019) for troponin T and 4.90 mug/L (3.90-6.61) for creatine kinase MB. Troponin I and T concentrations were higher than the detection limit for the assay in 2 (2.3%) and 41 (48.2%) neonates, respectively. Two mothers ( 2.3%) had cTnT levels above the detection limit; none of them had increased levels of cTnI.\ud \ud Conclusion: Probably owing to differences in expression and assay detection limits, cord blood troponin T concentrations are frequently over the detection limit at birth, while troponin I is mostly undetectable and comparable with that in healthy pregnant women. These cardiac regulatory proteins are of neonatal origin and are not influenced by maternal levels

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“…A more intensive detection process would probably have led to slightly lower marker sensitivity estimates than those reported. We did not study troponin assays, and cannot make conclusions about the diagnostic utility of early troponin testing; however, because troponins have similar release kinetics to CK-MB, 2,29,35,[49][50][51][52][53][54] it is likely that troponin assays would perform similarly at these early time intervals. Finally, the use of a core lab to perform assays may have introduced freeze/thaw artifact, which can potentially reduce detectable levels of biomarkers -particularly CK-MB.…”

Section: Limitationsmentioning

confidence: 99%

Diagnostic parameters of CK–MB and myoglobin related to chest pain duration

Innes

Christenson

Weaver

et al. 2002

CJEM

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ABSTRACT:Objective:Cardiac marker sensitivity depends on chest pain duration at the time of sampling. Our objective was to estimate the sensitivity, specificity, and likelihood ratios of early CK–MB and myoglobin assays in patients presenting to the emergency department (ED) with nondiagnostic ECGs, stratified by the duration of ongoing chest pain at the time of ED assessment.Methods:This was a prospective observational study carried out in 10 US and 2 Canadian EDs. Patients >25 years of age with ongoing chest pain and nondiagnostic ECGs were stratified by pain duration (0–4 h, 4–8 h, 8–12 h, >12 h). CK–MB and myoglobin assays were drawn at T = 0 (ED assessment) and T = 1 hr. Patients were followed for 7–14 days to identify all cases of acute myocardial infarction (AMI). ED test results were correlated with patient outcomes.Results:Of 5005 eligible patients, 565 had AMI. Pain duration was 0–4 h in 3014 patients, 4–8 h in 961, 8–12 h in 487, and >12 h in 543. Marker sensitivity increased with pain duration, ranging from 28%–77% for CK–MB and 39%–73% for myoglobin. The maximal sensitivity achieved by a T = 0 assay was 73%, and this was in patients with 8–12 or >12 h of ongoing pain. No combination of tests achieved 90% sensitivity in any pain duration strata.Conclusions:Regardless of chest pain duration, single assays and early serial markers (0+1 hr) do not rule out AMI; therefore, serial assays over longer observation periods are required. Likelihood ratios derived in this study will help physicians who use Bayesian analysis to determine post-test AMI likelihood in patients with chest pain.

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Fluoroenzymometric method to measure cardiac troponin I in sera of patients with myocardial infarction

Cited by 46 publications

References 25 publications

Effect of clopidogrel on the expression of inflammatory markers in rabbit ischemic coronary artery

Effect of clopidogrel on the expression of inflammatory markers in rabbit ischemic coronary artery

Cardiac troponin I, cardiac troponin T and creatine kinase MB concentrations in umbilical cord blood of healthy term neonates

Diagnostic parameters of CK–MB and myoglobin related to chest pain duration

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