Weekly and 90-Minute Biological Variations in Cardiac Troponin T and Cardiac Troponin I in Hemodialysis Patients and Healthy Controls

Abstract BACKGROUND Myocardial infarction (MI) is diagnosed by the finding of a single cardiac troponin value above the 99th percentile and a significant time-dependent change in cardiac troponin concentration. The aim of this study was to determine the 90-min and weekly biological variations, the reference change value (RCV), and the index of individuality (II) of high-sensitivity cardiac troponin T (hs-cTnT) (Roche Diagnostics) and hs-cTnI (Abbott Diagnostics) in patients receiving hemodialysis (HD) and in healthy individuals. METHOD Blood samples were collected from 19 HD patients (on an HD-free day) and 20 healthy individuals at 90-min intervals over a 6-h period (between 08:30 and 14:30) and before the midweek HD treatment for 10 weeks. The within-person variation (CVi), between-person variation, RCV, and II were calculated. RESULTS During the 6-h sampling period, the concentrations of hs-cTnT (both groups) and hs-cTnI (HD patients only) decreased on average by 0.8% to 1.7% per hour, respectively. These declining trends were included in the calculation of a 90-min asymmetric RCV: −8%/+5% in HD patients (hs-cTnT), −18%/+21% in HD patients (hs-cTnI), −27%/+29% in healthy individuals (hs-cTnT), and −39%/+64% in healthy individuals (hs-cTnI). The II was low in both groups for both assays. The weekly CVi values were approximately 8% (hs-cTnT) and 15% (hs-cTnI) in both groups. CONCLUSIONS When using a cardiac troponin change of 20%–50% to diagnose an MI, the false-positive rate is likely to be lower for the hs-cTnT assay than for the hs-cTnI assay. The low II suggests that use of a diagnostic cutoff value can be omitted.

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Biological variation of cardiac troponins in chronic kidney disease

Annals of Clinical Biochemistry International Journal of Laboratory Medicine ◽

10.1177/0004563220906431 ◽

2020 ◽

Vol 57 (2) ◽

pp. 162-169

Author(s):

RA Jones ◽

J Barratt ◽

EA Brettell ◽

P Cockwell ◽

RN Dalton ◽

...

Keyword(s):

Myocardial Infarction ◽

Chronic Kidney Disease ◽

Kidney Disease ◽

Cardiac Troponin ◽

Troponin I ◽

Troponin T ◽

Biological Variation ◽

Cardiac Troponin I ◽

Cardiac Troponin T ◽

Reference Change Value

Background Patients with chronic kidney disease often have increased plasma cardiac troponin concentration in the absence of myocardial infarction. Incidence of myocardial infarction is high in this population, and diagnosis, particularly of non ST-segment elevation myocardial infarction (NSTEMI), is challenging. Knowledge of biological variation aids understanding of serial cardiac troponin measurements and could improve interpretation in clinical practice. The National Academy of Clinical Biochemistry (NACB) recommended the use of a 20% reference change value in patients with kidney failure. The aim of this study was to calculate the biological variation of cardiac troponin I and cardiac troponin T in patients with moderate chronic kidney disease (glomerular filtration rate [GFR] 30–59 mL/min/1.73 m2). Methods and results Plasma samples were obtained from 20 patients (median GFR 43.0 mL/min/1.73 m2) once a week for four consecutive weeks. Cardiac troponin I (Abbott ARCHITECT® i2000SR, median 4.3 ng/L, upper 99th percentile of reference population 26.2 ng/L) and cardiac troponin T (Roche Cobas® e601, median 11.8 ng/L, upper 99th percentile of reference population 14 ng/L) were measured in duplicate using high-sensitivity assays. After outlier removal and log transformation, 18 patients’ data were subject to ANOVA, and within-subject (CVI), between-subject (CVG) and analytical (CVA) variation calculated. Variation for cardiac troponin I was 15.0%, 105.6%, 8.3%, respectively, and for cardiac troponin T 7.4%, 78.4%, 3.1%, respectively. Reference change values for increasing and decreasing troponin concentrations were +60%/–38% for cardiac troponin I and +25%/–20% for cardiac troponin T. Conclusions The observed reference change value for cardiac troponin T is broadly compatible with the NACB recommendation, but for cardiac troponin I, larger changes are required to define significant change. The incorporation of separate RCVs for cardiac troponin I and cardiac troponin T, and separate RCVs for rising and falling concentrations of cardiac troponin, should be considered when developing guidance for interpretation of sequential cardiac troponin measurements.

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Kinetics of high-sensitivity cardiac troponin T or troponin I compared to creatine kinase in patients with revascularized acute myocardial infarction

Clinical Chemistry and Laboratory Medicine (CCLM) ◽

10.1515/cclm-2014-0475 ◽

2015 ◽

Vol 53 (5) ◽

Cited By ~ 16

Author(s):

Kamila Solecki ◽

Anne Marie Dupuy ◽

Nils Kuster ◽

Florence Leclercq ◽

Richard Gervasoni ◽

...

Keyword(s):

Myocardial Infarction ◽

Acute Myocardial Infarction ◽

Cardiac Troponin ◽

Troponin I ◽

Troponin T ◽

High Sensitivity ◽

Cardiac Troponin T ◽

Significant Difference ◽

Kinetics Of

AbstractCardiac biomarkers are the cornerstone of the biological definition of acute myocardial infarction (AMI). The key role of troponins in diagnosis of AMI is well established. Moreover, kinetics of troponin I (cTnI) and creatine kinase (CK) after AMI are correlated to the prognosis. New technical assessment like high-sensitivity cardiac troponin T (hs-cTnT) raises concerns because of its unclear kinetic following the peak. This study aims to compare kinetics of cTnI and hs-cTnT to CK in patients with large AMI successfully treated by percutaneous coronary intervention (PCI).We prospectively studied 62 patients with anterior AMI successfully reperfused with primary angioplasty. We evaluated two consecutive groups: the first one regularly assessed by both CK and cTnI methods and the second group by CK and hs-cTnT. Modeling of kinetics was realized using mixed effects with cubic splines.Kinetics of markers showed a peak at 7.9 h for CK, at 10.9 h (6.9–12.75) for cTnI and at 12 h for hs-cTnT. This peak was followed by a nearly log linear decrease for cTnI and CK by contrast to hs-cTnT which appeared with a biphasic shape curve marked by a second peak at 82 h. There was no significant difference between the decrease of cTnI and CK (p=0.63). CK fell by 79.5% (76.1–99.9) vs. cTnI by 86.8% (76.6–92.7). In the hs-cTnT group there was a significant difference in the decrease by 26.5% (9–42.9) when compared with CK that fell by 79.5% (64.3–90.7).Kinetic of hs-cTnT and not cTnI differs from CK. The role of hs-cTnT in prognosis has to be investigated.

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