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Articles |
1
Hennepin County Medical Center, Minneapolis, MN 55415.
2
Rush Presbyterian St. Luke's Medical Center, Chicago,
IL 60612.
3
Emory University Hospital, Atlanta, GA 30322.
4
University of Tennessee Memorial Hospital, Knoxville, TN
37920.
5
Columbia Presbyterian Medical Center, New York, NY
10032.
6
University of Maryland School of Medicine, Baltimore, MD
21201.
a Address correspondence to this author at: Hennepin County Medical Center, Clinical Laboratories 812, 701 Park Ave., Minneapolis, MN 55415. Fax 612-904-4229; e-mail fred.apple{at}co.hennepin.mn.us.
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Abstract |
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 Top Abstract IntroductionMaterials and MethodsResultsDiscussionReferences |
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0.5 µg/L, whereas the ROC curve-determined cutoff for AMI was
2.0 µg/L. This gave a diagnostic sensitivity of 91.8% and
specificity of 92.4% when tested in serial samples collected within
24 h of admission in 633 patients presenting with chest pain, of
which 122 had an AMI. The concordances of the AxSYM cTnI with the
Stratus cTnI, OPUS cTnI, and Access cTnI were 95.3%, 95.1%, and
94.3%, respectively, from patients with suspected AMI. The AxSYM cTnI
demonstrated excellent clinical specificity, 
96%, in skeletal muscle
injury, chronic renal disease, and same-day noncardiac surgery
patients. |
Introduction |
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TopAbstractIntroductionMaterials and MethodsResultsDiscussionReferences |
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Of the ~550 000 AMIs that occurred in the United States in 1997, only 45% presented with an ST-segment elevation on their ECGs (10). The triage of patients with chest pain without diagnostic evidence of AMI based on ST-segment alterations on an ECG presents a challenge to clinicians. Laboratory strategies have been developed to monitor both early and tissue-specific cardiac markers at admission and serially over a 9- to 12-h period following admission to assist in the triage and management of these patients (11)(12)(13)(14).Although the preferred AMI treatment options of thrombolytic therapy and angioplasty are not based on biochemical markers, recent evidence has suggested that increased risk of post-AMI morbidity and mortality after discharge may be assessed using cardiac troponin testing (15)(16). For cTnI to be successful, rapid random access assays must be available to provide 24-h service to clinicians for diagnostic decision making. The purpose of this study was to evaluate the analytical and clinical performance of the Abbott AxSYM Troponin-I immunoassay used in aiding clinicians in the diagnosis of and ruling out of AMI.
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Materials and Methods |
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TopAbstractIntroductionMaterials and MethodsResultsDiscussionReferences |
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patient samples
Specimens from 437 apparently healthy individuals were used to
estimate the reference range for cTnI for both the Abbott AxSYM
platform and the Dade Behring Stratus II platform, which was used for
direct clinical efficiency comparisons in this study. None of the
subjects had evidence of cardiac, renal, or skeletal muscle disease.
Serial serum or plasma (heparinized) specimens from 511 non-AMI
(excluding angina and unstable angina) patients (n = 1336 samples)
and from 122 AMI patients (n = 392 samples) presenting with chest
pain suggestive of myocardial ischemia were included. The diagnosis of
AMI was made according to modified WHO criteria, which include chest
pain duration, ST-segment ECG alterations, and cardiac markers
(1)(3). A minimum of two serial specimens were collected at
admission and approximately every 4–6 h following admission, dependent
on each hospital's protocol. Specimens were analyzed within 24 h
of collection or frozen at or below -10°C, and then thawed once
before analysis. All sites performed cTnI testing on the AxSYM and on
the Dade Behring Stratus II analyzers. Clinicians were blinded to the
AxSYM and Stratus cTnI results unless the Stratus cTnI was used as part
of the criteria for AMI rule out or rule in [in this study two sites,
Minnesota and Maryland, used cTnI as a diagnostic criterion, with
decision cutoffs of >0.8 µg/L (3) and >1.5 µg/L
(4), respectively].
Potential interfering conditions from skeletal muscle injury (n =
81), chronic renal failure (n = 111), and same-day surgery (n
= 99) patients were also evaluated by the AxSYM cTnI assay and compared
with the results obtained by the Stratus cTnI assay. Each patient
contributed one specimen. The clinical specificity was calculated for
each of these three populations, using the diagnostic cutoffs reported
in each manufacturer's package insert (2.0 µg/L for the AxSYM cTnI,
1.5 µg/L for the Stratus cTnI). In addition, peak cTnI concentrations
in 86 patients diagnosed with unstable angina were compared within
24 h of admission between the AxSYM and Stratus cTnI assays.
Measurable concentrations based on cTnI concentrations 0.5 µg/L for
the AxSYM and 0.4 µg/L for the Stratus were used as the reference
limits.
cTnI measurements
The AxSYM Troponin-I assay (Abbott Laboratories), a
microparticle enzyme immunoassay, is a two-site assay that uses an
anti-cTnI monoclonal antibody for capture and a polyclonal anti-cTnI
antibody for detection (17). The AxSYM system is a
continuous random access analyzer that measures a fluorescence product,
giving a first result, in 13 min, followed by additional continuous
results every minute. The Stratus cTnI assay system (Dade Behring) was
used according to the manufacturer's instructions. The assay time for
a first result is 8 min, followed by additional results every minute.
The interassay imprecision (CVs) values on the Stratus are <10% at
1.5 µg/L (the diagnostic cutoff) and 15% at 0.6 µg/L. The
detection limit is 0.35 µg/L. Two additional cTnI assay platforms,
the Beckman Access (Beckman Instruments) and the Behring OPUS (Behring
Diagnostics) were also used for clinical comparison, following
recommended manufacturer's guidelines. Previously established
diagnostic decision cutoff concentrations were used: 0.15 µg/L for
the Access (5) and 2.0 µg/L for the OPUS (6).
analytical performance
Reproducibility was determined on the AxSYM system following NCCLS
protocol EP5-T2. Three human serum panels and three porcine
gelatin-based controls were assayed in replicates of two at two
separate times per day for 20 days, using a single lot of reagents and
a single standard calibration per instrument. Within-run, between-run,
and between-day reproducibility were calculated using SAS Ver. 6.09
software (SAS Institute Inc). The within-run, between-run, and
between-day reproducibility were evaluated by calculating corresponding
CVs.
To determine the lowest measurable concentration of the AxSYM cTnI that could be distinguished from zero, each site tested 10 replicates of the A (0 µg/L) calibrator and 2 replicates of the B (2.5 µg/L) calibrator on 2 separate days. The lowest measurable concentration of cTnI was calculated for each analytical run by determining the mean value (in µg/L) that corresponded to the rate that was 2 SD from the mean rate of the A calibrator.
evaluation of cutoff concentrations
The 95th percentiles for the apparently healthy individuals and
the non-AMI patients were calculated. To determine the diagnostic
cutoff concentrations of AMI patients, the AMI and non-AMI populations,
excluding angina and unstable angina patients, were evaluated by
ROC curve analysis for the AxSYM and Stratus cTnI assays
(18). The relationship between cTnI concentrations measured
by the AxSYM and the Stratus was determined using 406 specimens whose
AxSYM cTnI concentration fell within the dynamic range (50 µg/L) of
the assay.
statistical comparisons
To compare the AxSYM and Stratus cTnI assays, Passing-Bablok
linear regression analysis was performed on a single test from each
sample over the dynamic range of both assays. Values below the minimal
detectable concentration of either assay were excluded from the data
analysis. Areas under the ROC curve for each assay were calculated
using the trapezoidal rule. The DeLong test for comparison of areas
under the curve was performed, and the P-value for the test
was calculated. Two-way frequency tables comparing the maximum value
for each AMI and non-AMI patient, comparing AxSYM and Stratus cTnI
concentrations, were analyzed. Diagnostic sensitivity and specificity
data are presented with 95% confidence intervals (CIs). All
statistical tests were two-tailed, with significance set at
P <0.05. SAS Ver. 6.09 software was used for all
statistical analyses.
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Results |
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TopAbstractIntroductionMaterials and MethodsResultsDiscussionReferences |
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, the total imprecision of the AxSYM Troponin I assay ranged
from 6.3% to 10.2% for the three human serum panels (I, II, and III)
and the three porcine gelatin-based controls (concentrations ranging
from 2.9 to 137.8 µg/L) evaluated over 20 days for four sites. Each
of the six sites performed determinations of the lower limit of
detection. The results ranged from 0.09 to 0.25 µg/L, with a mean of
0.14 µg/L and an SD of 0.05 µg/L.
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Regression analysis of paired cTnI measurements between the AxSYM and
the Stratus in 406 specimens collected from suspected AMI patients over
the dynamic range of both assays (Fig. 1
) showed the following: AxSYM cTnI = 3.50 (Stratus cTnI) -
1.10; r = 0.881. The 95% CI for the slope was
3.39–3.64 and for the intercept was -1.32 to -0.95. There were no
significant differences in slope or intercept when a subset (n =
259) of AxSYM cTnI concentrations <10 µg/L was compared with the
corresponding subset of Stratus cTnI concentrations (Fig. 2
: AxSYM cTnI = 3.67 (Stratus cTnI) - 1.17;
r = 0.782). The 95% CI for the slope was 3.33–4.00
and for the intercept was -1.40 to -1.03. Using subsets of the
overall patient population, two sites also compared the AxSYM cTnI with
two other cTnI assays, the Behring Opus (diagnostic cutoff <2.0
µg/L) and the Beckman Access (diagnostic cutoff <0.15 µg/L).
Comparisons of the assays showed the following: AxSYM cTnI =
1.79(Opus cTnI) - 0.00, r = 0.805, n = 32; AxSYM
cTnI = 105(Access cTnI) - 4.60, r = 0.604, n
= 50.
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Representative time vs cTnI concentration curves in the AMI patients,
comparing the AxSYM cTnI assay with the Stratus, Opus, and Access cTnI
assays are shown in Fig. 3
and demonstrate the different concentrations that can be
observed between assays.
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clinical performance
On the basis of the 95th percentile, expected AxSYM cTnI values
for apparently healthy individuals were 0.5 µg/L and for non-AMI
(excluding angina and unstable angina) patients were 2.4 µg/L. Fig. 4
shows the ROC curves displayed for both the AxSYM and Stratus
cTnI assays. The maximum value from serial specimens drawn within
24 h after presentation to the medical center or onset of chest
pain was used in the analysis. The AxSYM diagnostic cutoff of 2.0
µg/L was chosen to maximize clinical sensitivity at 91.8% (95% CI,
85.4–96.0%), with a corresponding clinical specificity of 92.4%
(95% CI, 89.7–94.5%). The Stratus diagnostic cutoff of 1.5 µg/L
gave a maximized clinical sensitivity of 90.2% (95% CI, 88.5–94.8%)
and specificity of 95.1% (95% CI, 92.9–96.8%). The areas under the
AxSYM and Stratus cTnI ROC curves were 0.9619 and 0.9450, respectively,
and were significantly different; P = 0.0039.
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Clinical sensitivities and specificities analyzed by timed intervals based on hours after presentation to each medical center and based on hours after the onset of chest pain are shown in Tables 2 and 3, respectively, for both the AxSYM and Stratus cTnI measurements. The analysis based on hours after presentation yielded clinical sensitivities ranging from 64.6% to 93.3% and specificities ranging from 93.8% to 94.6% for the AxSYM cTnI assay. For the Stratus cTnI assay, clinical sensitivities ranged from 54.9% to 92.2% and specificities ranged from 95.5% to 97.3%. The analysis based on chest pain time yielded clinical sensitivities ranging from 36.0% to 95.7% and specificities ranging from 90.6% to 96.4% for the AxSYM cTnI assay. For the Stratus cTnI assay, clinical sensitivities ranged from 24.0% to 93.5% and specificities from 93.2% to 99.2%. Because of the time delay between chest pain to admission [median 11.6 h (25th to 75th percentiles, 2.3–23.2 h)], clinical sensitivities for both assays were lower over the 12- to 24-h period for calculations based on time after onset of chest pain compared with calculations based on time after presentation to medical center.
Two-way frequency tables comparing the maximum AxSYM and Stratus cTnI values from each subject demonstrated >89% concordance: AMI patients (n = 122), 99.2%; non-AMI patients (n = 511), 90.8%; unstable angina patients (n = 86), 89.5%; all subjects (n = 1411), 94.9%.
When the maximum cTnI values from each patient were analyzed, there was only one AMI patient who showed a discordant result between the two assays. This AMI patient had an increased AxSYM cTnI of 4.0 µg/L compared with a Stratus cTnI of 1.4 µg/L. From 389 specimens (10.5% of AMI specimens) there was a 94.3% concordance for diagnosis between the AxSYM cTnI and Beckman Access cTnI measurements (data not shown). Furthermore, from 204 specimens (13.2% of AMI specimens) there was a 95.1% concordance for diagnosis between the AxSYM cTnI and Behring Opus cTnI measurements (data not shown).
Using the respective 95th percentiles calculated for healthy
individuals, we observed a 76.7% concordance for the unstable angina
patients between the AxSYM cTnI (cutoff <0.5 µg/L) and the Stratus
cTnI (cutoff <0.4 µg/L; no statistical differences). Twenty-four
percent (21 of 86) of the unstable angina patients demonstrated
increased concentrations for both cTnI assays. Although discordant
results were obtained for 20 patients between the two assays (Fig. 5
), no diagnostic follow ups were obtained to assess risk
stratification. These discordant values, however, were not biased
toward one of the assays. There was no statistical difference between
the two assays for specimens above and below the reference cutoffs
(McNemar test, P = 0.371).
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The AxSYM cTnI clinical specificities for the three patient groups
studied for potentially interfering clinical conditions were excellent,
at 96.0%, and were not statistically different from the Stratus cTnI
specificities: skeletal muscle injury patients, 96.3% (Stratus,
98.8%); chronic renal failure patients, 96.4% (Stratus, 98.2%);
same-day surgery patients, 96.0% (Stratus, 98.0%).
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Discussion |
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TopAbstractIntroductionMaterials and MethodsResultsDiscussionReferences |
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and 3
). These findings agree
with previous clinical studies that have shown that neither cTnI or
cTnT nor CK-MB mass provides early, sensitive detection for AMI
diagnosis (4)(5)(6). The diagnostic specificity of the AxSYM
cTnI was also highly concordant with the Dade Stratus cTnI,
demonstrating >90% specificity over the entire 24-h period following
either onset of chest pain or presentation to the hospital. The onset
of chest pain is often unreliable when a history is taken from a
patient. It is not uncommon for patients to experience multiple
episodes of chest pain, lasting hours to days, before presentation to
the hospital. Therefore, sample collection referenced to the time of
presentation to a medical center probably served as a more accurate
data representation for calculating sensitivity and specificity (Tables 2
and 3
). Our findings were in agreement with previously published
clinical studies using several different cTnI assay systems
(4)(5)(6).
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In addition to the comparison between the AxSYM and Stratus, small
subsets of patient samples were also compared between the AxSYM and
OPUS and AxSYM and Access immunoassays for cTnI measurements.
Acceptable correlations were observed between all assay systems.
However, there were substantial differences between absolute cTnI
concentrations, as indicated by both the slopes and diagnostic cutoff
concentrations: AxSYM (cutoff, 2.0 µg/L) vs Stratus (cutoff, 1.5
µg/L) slope = 3.50; AxSYM vs OPUS (cutoff, 2.0 µg/L)
slope = 1.79; AxSYM vs Access (cutoff, 0.15 µg/L) slope =
105. The 2- to 100-fold assay-dependent differences are consistent with
recently published data by Wu et al. (19) and proficiency
surveys by the College of American Pathologists (20), which
demonstrate that the largest concentration differences occur
proportional to the absolute increases in cTnI concentrations and are
likely influenced by the complex or oxidation state of the cTnI subunit
(19). Although absolute cTnI differences remain a concern
for laboratories and clinicians trying to compare and contrast
different assay systems, consistent clinical findings relative to
assay-dependent ROC curve-determined cutoffs for diagnostic efficiency
for AMI determination were found (Fig. 4
). There appears to be a need
to establish standardized cTnI protein materials and a unified
rationale for antibody selection in immunoassays to achieve consistency
or equivalence between absolute cTnI concentrations. However, in
the interim it appears that as long as one establishes a data base for
a single cTnI immunoassay, clinicians and laboratorians should be able
to utilize any analytically acceptable assay for cTnI measurement.
Discrepancies between the AxSYM and Stratus cTnI assays occurred in 20
of 86 unstable angina patients (Fig. 5
). Increased cTnI concentrations
are known to assist in risk stratification of unstable angina patients
(15)(16), supporting more aggressive medical and invasive
procedure management. Larger clinical outcome studies will be needed if
clinicians and laboratorians are to appropriately interpret cTnI
concentrations in the range between the upper reference limit (0.5
µg/L) for healthy individuals and the decision cutoff for AMI (2.0
µg/L) when assessing the role of the AxSYM in patient risk
stratification or diagnosis of non-Q-wave AMI. This was not a goal of
the present study. In the non-AMI patient groups studied, the AxSYM
cTnI demonstrated excellent clinical specificities, 96% for skeletal
muscle injury patients, same-day surgery patients, and chronic renal
disease patients.
The AxSYM cTnI assay demonstrated excellent analytical performance based on our examination of the limits of detection and quantification and assay imprecision. The lower limit of detection of 0.14 µg/L was well below the ROC curve AMI cutoff of 2.0 µg/L, a characteristic favorable for future studies involving risk stratification of unstable angina and non-Q-wave AMIs.
In conclusion, the Abbott AxSYM cTnI assay is a validated alternative to other cTnI, cTnT, and CK-MB assay systems in the worldwide marketplace for ruling in and ruling out AMI. Future studies on the use of cTnI to aid in the diagnosis and ruling out of AMI should address the following issues. First, the clinical utility of cTnI should be assessed in the subset of AMI patients with nondiagnostic ECGs because cardiac-specific markers are unnecessary in patients with diagnostic ECGs. Second, it would be helpful to compare the results of cTnI with other cardiac markers (i.e., CK-MB), although several studies have demonstrated the equivalence or superiority of cTnI over CK-MB. Third, precision studies should be conducted at cTnI decision concentrations such as at cutoff concentrations for AMI and the upper limit for apparently healthy individuals. Fourth, clinical follow up and/or additional analytical studies are necessary to resolve discrepant results between assays, specifically addressing potential interference from heterophilic antibodies (21) and rheumatoid factor. Addressing these issues will enhance the conduct of clinical and analytical studies to assess cTnI or future cardiac markers.
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Acknowledgments |
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Footnotes |
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References |
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