AccuTnI

33340
Intended Use

The Access AccuTnI assay is a paramagnetic particle, chemiluminescent immunoassay for the
quantitative determination of cardiac troponin I (cTnI) levels in human serum and plasma
using the Access Immunoassay Systems to aid in the diagnosis and treatment of myocardial
infarction and cardiac muscle damage.
Cardiac troponin I determination aids in the risk stratification of patients with unstable angina
or non-ST segment elevation acute coronary syndromes with respect to relative risk of
mortality, myocardial infarction, or increased probability of ischemic events requiring urgent
revascularization procedures.

Summary and
Explanation

Coronary artery disease is not only a leading cause of death in men and women in the US, but is
also associated with other life-threatening complications.1,2,3 The development of symptoms of
coronary artery disease, which at times is unexpected and sudden, is associated with increased
risk for adverse cardiac events such as death, myocardial infarction (MI), or hospitalization
requiring urgent revascularization. Therefore, patients presenting with ischemic syndromes
require prompt management. Specific and sensitive cardiac markers (troponin I and T) have
been used in conjunction with other clinical findings and patient history information to better
identify subjects with MI.1,2,4,5,6 These specific cardiac markers have also been used to identify
those patients at higher risk for short- and long-term adverse cardiac events
(endpoints/outcomes).1,7,8,9,10
Cardiac troponin I is a contractile protein exclusively present in the cardiac muscle.11,12 It is one
of three subunits of the troponin complex (I, T, C), which with tropomyosin are bound to actin
in the thin filament of the myofibril. cTnI is found as free troponin I (free TnI) and complexed
with troponin C (binary IC), with troponin T (binary IT) or with both troponin C and troponin T
(ternary ITC). Its physiological role is to inhibit the ATPase activity of the actin-myosin
complex in the absence of calcium, and therefore, to prevent muscular contraction.13 Three
tissue isoforms have been identified:
Fast troponin I and slow troponin I with molecular weights of 19,800 Da each, expressed in
fast twitch and slow twitch skeletal muscle fibers, respectively.
cTnI with a molecular weight of 24,000 Da contains an additional 31 amino acid residues in
the N-terminal.
Sequencing of cTnI from mammals has shown important differences between the cardiac 14 and
skeletal 15 forms. All three troponin I isoforms are encoded by different genes. The human cTnI
exhibits only 52% and 54% amino acid sequence homology with the human fast and slow
skeletal troponin I, respectively. The Access AccuTnI monoclonal antibody pair is selected to be
cTnI specific. In addition, it has been well documented that skeletal muscle does not express
cTnI, either during development or in response to stimuli.16 Therefore, the absolute
cardiospecificity of cTnI allows distinction between cardiac and skeletal injuries, and allows
diagnosis of myocardial infarction distinct from muscle lesions (rhabdomyolysis,
polytraumatism) and non-cardiac surgery.16,17,18,19 Elevated troponin I levels have also been
documented in cases of unstable angina (UA) 20 and congestive heart failure (CHF).21
cTnI levels in acute myocardial infarction (AMI) exhibit similar rise and fall patterns to those
found in CK-MB. The collection of at least three blood samples during the early triage period
has been recommended. 22 cTnI is 13 times more abundant in the myocardium than CK-MB and
does not normally circulate in the blood, so the signal to noise ratio is more favorable for the

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detection of myocardial necrosis.23 Cumulative data from several studies indicate troponin I
levels are detectable (above quoted values for non-AMI samples) 36 hours after the onset of
chest pain. Troponin I levels peak at approximately 1216 hours and can remain elevated for
49 days post-AMI. These same studies noted that the time to peak concentration of cTnI
occurred later in patients who did not receive thrombolytic therapy.17,24,25
Unstable angina comprises a broad spectrum of patients with varying levels of risk for
suffering an adverse event such as death, MI, or other major cardiac complications requiring
hospitalization and potentially urgent revascularization (UR). However, it has been reported
that it is difficult to predict who will suffer an adverse event in those patients with UA and
without evidence of ST segment elevation (NSTEMI).1 The development and
commercialization of the more specific and sensitive cardiac troponin I (cTnI) immunoassays
have significantly contributed to the diagnosis of MI and to the risk stratification of patients
with NSTEMI/UA. The 2000/2002 American College of Cardiology (ACC) and the American
Heart Association (AHA) Guideline Update for the management of these patients strongly
recommends to include cTnI measurements for the risk stratification of patients presenting
with symptoms suggestive of acute coronary syndromes.2,6 In light of the potential adverse
outcomes faced by these patients such as cardiac death or nonfatal ischemic events, an
assessment of the prognosis should assist physicians in identifying and managing high risk
patients. Ultimately, the assessment of the prognosis will be useful in both selecting the site of
care and in identifying patients most likely to benefit from specific therapeutic interventions.
The 2002 ACC and the European Society of Cardiology (ESC) guidelines recommend that
individual laboratories define their own reference range and that an elevated value of cTnI be
defined as a measurement above the 99th percentile of a normal control group (i.e. the
99th percentile upper reference limit).4,5
Recent studies have shown that the predominant cTnI form present in blood of patients after
AMI is the binary troponin IC complex with smaller amounts of the ternary ITC complex,
binary IT complex and free cTnI.26,27,28,29 The pattern of release of these forms over the course of
AMI is still under investigation. The differential recognition of complexed and free cTnI forms
is common for many commercial methods.26,30,31 For some assays, the relative responses to the
various forms of cTnI are nearly equal, while other assays demonstrate a substantial difference.
The latter may lead to over- and under-estimation of the true concentration of troponin I in a
complex biological milieu. Equimolar binding, defined as the ability to recognize both the
complexed and free cTnI forms equally, allows an unbiased determination of the total cTnI
present in samples from the same subject over the course of AMI. The Access AccuTnI assay
recognizes the binary troponin IC or IT or ternary troponin ITC complexes and free cTnI
equally. In addition, the assay responds to both the phosphorylated and dephosphorylated
forms of cTnI complex equally.32
cTnI is highly susceptible to proteolysis and enzymatic modification. Substantial degradation
occurs both in-vivo and in-vitro. The C-terminal of the molecule is preferentially cleaved then
followed by the cleavage of the N-terminal.27,33,34 The Access AccuTnI assay utilizes
monoclonal antibodies directed against the more stable region of the molecule, and is therefore
less affected by degradation of cTnI.
Principles of
the Procedure

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The Access AccuTnI assay is a two-site immunoenzymatic (sandwich) assay. A sample is

added to a reaction vessel along with monoclonal anti-cTnI antibody conjugated to alkaline
phosphatase and paramagnetic particles coated with monoclonal anti-cTnI antibody. The
human cTnI binds to the anti-cTnI antibody on the solid phase, while the anti-cTnI antibody alkaline phosphatase conjugate reacts with different antigenic sites on the cTnI molecules. After
incubation in a reaction vessel, materials bound to the solid phase are held in a magnetic field
while unbound materials are washed away. Then, the chemiluminescent substrate
Lumi-Phos* 530 is added to the vessel and light generated by the reaction is measured with a
luminometer. The light production is directly proportional to the concentration of cTnI in the

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sample. The amount of analyte in the sample is determined from a stored, multi-point
calibration curve.
Product
Information

Warnings and
Precautions

Access AccuTnI Reagent Pack

Cat. No. 33340: 100 determinations, 2 packs, 50 tests/pack
Provided ready to use.
Store upright and refrigerate at 2 to 10C.
Refrigerate at 2 to 10C for a minimum of two hours before use on the instrument.
Stable until the expiration date stated on the label when stored at 2 to 10C.
Stable at 2 to 10C for 56 days after initial use.
Signs of possible deterioration are a broken elastomeric layer on the pack or control values
out of range.
If the reagent pack is damaged (i.e., broken elastomer), discard the pack.
R1a:

Paramagnetic particles coated with mouse monoclonal anti-human

cardiac troponin I (cTnI) suspended in TRIS buffered saline, with
surfactant, bovine serum albumin (BSA) matrix, < 0.1% sodium azide,
and 0.1% ProClin** 300.

R1b:

0.1 N NaOH

R1c:

Mouse monoclonal anti-human cTnI alkaline phosphatase conjugate

diluted in ACES buffered saline, with surfactant, BSA matrix, protein
(bovine, goat, mouse), < 0.1% sodium azide, and 0.25% ProClin 300.

For in vitro diagnostic use.

Patient samples and blood-derived products may be routinely processed with minimum risk
using the procedure described. However, handle these products as potentially infectious
according to universal precautions and good clinical laboratory practices, regardless of their
origin, treatment, or prior certification. Use an appropriate disinfectant for decontamination.
Store and dispose of these materials and their containers in accordance with local
regulations and guidelines.
Sodium azide may react with lead and copper plumbing to form highly explosive metal
azides. On disposal of liquids, flush with a large volume of water to prevent azide
build-up.35
Xi. Irritant: 0.25% ProClin 300.
R 43: May cause sensitization by skin contact.
S 28-37: After contact with skin, wash immediately with plenty of soap
and water. Wear suitable gloves.
The Material Safety Data Sheet (MSDS) is available upon request.

Specimen
Collection and
Preparation

1. Lithium heparin plasma is the recommended sample. Serum and plasma (heparin) are
acceptable samples. Heparin and serum samples should not be used interchangeably.22
Each laboratory should determine the acceptability of its own blood collection tubes and
serum separation products. Variations in these products may exist between manufacturers
and, at times, from lot-to-lot. The AMI cutoff value presented in the Clinical Performance
section applies to heparin plasma and serum samples. A study performed by Beckman
Coulter, Inc. comparing EDTA plasma samples to heparin plasma samples produced the
following correlation: y = 0.864x 0.049, r = 0.999.
2. Observe the following recommendations for handling, processing, and storing blood
samples (ensure sample tube manufacturer recommendations are followed):
Collect all blood samples observing routine precautions for venipuncture.36
Allow serum samples to clot completely before centrifugation.36

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 Keep tubes stoppered at all times.36

Store samples tightly stoppered at room temperature (15 to 30C) for no longer than
two hours.
Samples should be centrifuged and refrigerated within two hours of blood draw.
Serum or plasma should be physically separated from contact with cells as soon as
possible with a maximum time limit of two hours from the time of collection.
Remove any residual fibrin or cellular matter. Failure to do so can contribute to falsely
elevated results.
For plasma, avoid transferring material from the white blood cell/platelet layer located
just above the red blood cells. If a fixed angle rotor is used for centrifugation, care should
be taken to avoid resuspending platelets.
Turbid serum or plasma samples containing particulate matter should be transferred
from the original tube and recentrifuged prior to assay. A specimen (original tube) that
contains a separating device (gel barrier) is never to be recentrifuged.
If the assay will not be completed within 24 hours, or for shipment of samples, freeze at
-20C or colder.36
Samples may be stored for six months at -20C.
3. Use the following guidelines when preparing specimens:
Ensure residual fibrin and cellular matter has been removed prior to analysis.
Follow blood collection tube manufacturers recommendations for centrifugation.
4. Each laboratory should determine the acceptability of its own blood collection tubes and
serum separation products. Variations in these products may exist between manufacturers
and, at times, from lot-to-lot.
5. Thaw samples only once and centrifuge all thawed samples prior to analysis. Do not thaw in
a water bath.
Materials
Provided
Materials
Required But
Not Provided

Procedural
Comments

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R1

Access AccuTnI Reagent Packs

1. Access AccuTnI Calibrators

Provided at zero and approximately 0.3, 1.2, 5.0, 25 and 100 ng/mL (g/L).
Cat. No. 33345
2. Quality Control (QC) materials: commercial control material.
3. Access Sample Diluent A
Cat. No. 81908
4. Access Substrate
Cat. No. 81906
5. Access, Access 2, SYNCHRON LXi:
Access Wash Buffer II, Cat. No. A16792
UniCel DxI:
UniCel DxI Wash Buffer II, Cat. No. A16793
1. Refer to the appropriate system manuals and/or Help system for a specific description of
installation, start-up, principles of operation, system performance characteristics, operating
instructions, calibration procedures, operational limitations and precautions, hazards,
maintenance, and troubleshooting.
2. Mix contents of new (unpunctured) reagent packs by gently inverting pack several times
before loading on the instrument. Do not invert open (punctured) packs.
3. Use forty (40) L of sample for each determination in addition to the sample container and
system dead volumes. Refer to the appropriate system manuals and/or Help system for the
minimum sample volume required.

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4. The system default unit of measure for sample results is ng/mL. To change sample reporting
units to the International System of Units (SI units), g/L, refer to the appropriate system
manuals and/or Help system. To manually convert concentrations to the International
System, multiply ng/mL by multiplication factor 1.
5. Run the Access AccuTnI S0 and S1 Calibrators in quadruplicate, and the S2S5 Calibrators
in duplicate.
Procedure

Calibration
Details

Refer to the appropriate system manuals and/or Help system for information on managing
samples, configuring tests, requesting tests, and reviewing test results.
Run the Access AccuTnI S0 and S1 Calibrators in quadruplicate, and the S2S5 Calibrators in
duplicate.
An active calibration curve is required for all tests. For the Access AccuTnI assay, calibration is
required every 56 days. Refer to the appropriate system manuals and/or Help system for
information on calibration theory, configuring calibrators, calibrator test request entry, and
reviewing calibration data.

Quality Control

Quality control materials simulate the characteristics of patient samples and are essential for
monitoring the system performance of immunochemical assays. Because samples can be
processed at any time in a random access format rather than a batch format, quality control
materials should be included in each 24-hour time period.37 Include commercially available
quality control materials that cover at least two levels of analyte. More frequent use of controls
or the use of additional controls is left to the discretion of the user based on good laboratory
practices or laboratory accreditation requirements and applicable laws. Follow manufacturer's
instructions for reconstitution and storage. Each laboratory should establish mean values and
acceptable ranges to assure proper performance. Quality control results that do not fall within
acceptable ranges may indicate invalid test results. Examine all test results generated since
obtaining the last acceptable quality control test point for this analyte. Refer to the appropriate
system manuals and/or Help system for information about reviewing quality control results.

Results

Patient test results are determined automatically by the system software using a weighted four
parameter logistic curve (4PLC) math model. The amount of analyte in the sample is
determined from the measured light production by means of the stored calibration data. Patient
test results can be reviewed using the appropriate screen. Refer to the appropriate system
manuals and/or Help system for complete instructions on reviewing sample results.

Limitations of
the Procedure

1. Samples can be accurately measured within the analytic range of the lower limit of detection
and the highest calibrator value (approximately 0.01100 ng/mL [g/L]).
If a sample contains less than the lower limit of detection for the assay, report the results
as less than that value (i.e., < 0.01 ng/mL [g/L]).
If a sample contains more than the stated value of the highest Access AccuTnI
Calibrator (S5), report the result as greater than that value (i.e., > 100 ng/mL [g/L]).
Alternatively, dilute 1 volume of sample with 9 volumes of Access Sample Diluent A.
Refer to the appropriate system manuals and/or Help system for instructions on entering
a sample dilution in a test request. The system reports the results adjusted for the
dilution.
2. For assays employing antibodies, the possibility exists for interference by heterophile
antibodies in the patient sample. Patients who have been regularly exposed to animals or
have received immunotherapy or diagnostic procedures utilizing immunoglobulins or
immunoglobulin fragments may produce antibodies, e.g. HAMA, that interfere with
immunoassays. Additionally, other heterophile antibodies such as human anti-goat
antibodies may be present in patient samples.38,39

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Such interfering antibodies may cause erroneous results. Carefully evaluate the results of
patients suspected of having these antibodies.
3. Other potential interferences in the patient sample could be present and may cause
erroneous results in immunoassays. Some examples that have been documented in literature
include rheumatoid factor, endogenous alkaline phosphatase, fibrin, and proteins capable of
binding to alkaline phosphatase.40,41 Carefully evaluate the results of patients suspected of
having these types of interferences.
4. The Access AccuTnI results should be interpreted in light of the total clinical presentation of
the patient, including: symptoms, clinical history, clinical examination, electrocardiogram
(ECG), data from additional tests, and other appropriate information. Medical decisions
should not be based on a single AccuTnI determination at one time point.22
5. The Access AccuTnI assay does not demonstrate any hook effect up to
1,920 ng/mL (g/L).
Expected
Values

1. Each laboratory should establish its own reference ranges to assure proper representation of
specific populations and sample types, and to reflect current practice and criteria for AMI
diagnosis at their institution.
2. Myocardial infarction has been redefined by the National Academy of Clinical Biochemistry
(NACB) and the Joint European Society of Cardiology (ESC)/American College of
Cardiology (ACC) Committee.4,5,22 These organizations recommend the use of biochemical
markers in conjunction with the 97.5th percentile (NACB) or 99th percentile (ESC/ACC)
reference ranges to aid in the diagnosis of myocardial infarction and cardiac damage.
3. The 97.5th and 99th percentiles (upper reference limit) as determined using lithium heparin
plasma samples for a population of apparently healthy adults with no known cardiac
disease are shown in the following table:
n

Age Range

97.5th percentile

254

1988

0.03 ng/mL

99th percentile
0.04 ng/mL

(95% CI at this concentration is:

0.020.04)

(95% CI at this concentration is:

0.030.05)

Note: The 95% confidence interval of a measurement of concentration at a level of the upper
reference limit is calculated as two times the total %CV at the corresponding concentration.
The total imprecision at 0.03 and 0.04 ng/mL was determined to be 20 and 14% CV,
respectively, from the medians of nine determinations.32
4. World Health Organization (WHO) 42 requires two of the following criteria for confirmation
of AMI: evolutionary changes in the ECG or history of chest pain coupled with elevated
cardiac enzymes. After a myocardial infarction, cTnI concentrations are detectable 36 hours
after the onset of chest pain, peak at approximately 1216 hours, and can remain elevated for
49 days post-AMI.
5. Any condition resulting in myocardial injury can potentially elevate cTnI levels above the
expected normal range. Clinical studies have documented these conditions to include stable
or unstable angina pectoris, congestive heart failure, myocarditis, and cardiac surgery or
invasive testing.4,5,16,43,44
6. Non-atherosclerotic mechanisms such as arteritis, coronary artery dissection, coronary
embolism, and cocaine or amphetamine use may be responsible for acute ischemic
syndrome potentially leading to cTnI levels above the reference range for healthy
individuals.45,46,47
7. The diagnostic cut-off value above which a sample is considered positive for AMI using the
Access AccuTnI assay was determined by ROC analysis.48 See the Clinical Performance
section for further information.
8. The AMI cutoff value presented in the Clinical Performance section applies to heparin
plasma and serum samples.

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Specific
Performance
Characteristics

Clinical Performance

Three medical centers in the United States and Europe participated in a prospective study to
determine the clinical sensitivity and specificity of the Access AccuTnI assay in diagnosing
acute myocardial infarction (AMI). Patients who met the following criteria were considered
eligible for final analysis in this study.
Onset of chest discomfort within the past 24 hours prior to enrollment
Chest discomfort for 20 minutes or more
A minimum of two (2) heparin plasma samples within 24 hours
A final diagnosis, based on World Health Organization diagnostic criteria for AMI
A total of 328 patients (183 males and 145 females) were considered eligible for analysis, of
which 74 (23%) ruled-in for AMI and 254 (77%) ruled-out for AMI. Clinical sensitivity and
specificity were determined for peak cTnI results following presentation to the hospital or from
time of admission. Peak cTnI results are defined as the highest cTnI concentration observed in
the serial draws obtained from each patient.
Clinical Sensitivity and Specificity
Peak cTnI results from patients enrolled in this study were analyzed using Receiver Operating
Characteristics (ROC) curve methodology to determine the most appropriate cutoff for
diagnosing AMI. A series of cutoff values with their respective sensitivities and specificities are
shown in the following table.
A cutoff of 0.50 ng/mL cTnI is recommended for diagnosis of AMI, as this yields optimal
performance of 96% sensitivity and 94% specificity.

AccuTnI Cutoff
(ng/mL)

Sensitivity
(%)

n/N

95% Confidence
(%)

Specificity
(%)

n/N

95% Confidence
(%)

0.20

97

72 / 74

93100

90

229 / 254

8694

0.30

96

71 / 74

91100

92

233 / 254

8895

0.40

96

71 / 74

91100

93

236 / 254

9096

0.50

96

71 / 74

91100

94

240 / 254

9197

0.60

93

69 / 74

87100

94

240 / 254

9197

0.70

93

69 / 74

87100

95

242 / 254

9298

The above cutoff values apply to heparin plasma and serum samples.
Clinical Sensitivity and Specificity: Access AccuTnI Assay versus Another Commercially
Available Assay
Results are shown below comparing the Access AccuTnI Assay (0.50 ng/mL cutoff) to another
commercially available cTnI assay (using that manufacturer's recommended AMI cutoff).
Samples from 313 patients were tested with both methods in this study.
Sensitivity
(%)

Assay

n/N

95%
Confidence (%)

Specificity
(%)

n/N

95%
Confidence (%)

Access AccuTnI Assay

97

66 / 68

92100

95

232 / 245

9298

Another Commercially
Available cTnI Assay

87

59 / 68

7896

95

232 / 245

92 98

Clinical Sensitivity and Specificity Over Time

Recently published guidelines on detection of AMI by cardiac markers suggest a diagnosis
based on a single sample taken at hospital admission is not adequate; the collection of at least
three blood samples during the early triage period has been recommended.22 Studies in the
literature show cTnI levels are detectable 36 hours after myocardial damage. cTnI levels peak
at approximately 1216 hours and can remain elevated for 49 days.17
Following the published guidelines and literature, the table below summarizes sensitivity and
specificity of the Access AccuTnI assay (0.50 ng/mL cutoff) determined for multiple time
intervals after admission to the hospital. A total of 328 patients with serial samples were
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evaluated in this analysis. Results show expected, improved sensitivity over time, with peak
sensitivity in the 1224 hour time frame.
.

Hours After Admission

0 to 6

> 6 to12

> 12 to 24

> 24

Sensitivity (%)

46

93

98

91

Specificity (%)

96

94

93

88

Description of Non-AMI Patients with Elevated cTnI Values (Cardiac Muscle Damage)
A total of 68 non-AMI patients had AccuTnI values above the upper reference limit
(99th percentile) of the assay (0.04 ng/mL). Of these patients, 91% were found to have cardiac
conditions such as unstable angina, congestive heart failure, or myocarditis, or severe
non-cardiac conditions such as trauma or renal failure that may cause cardiac muscle injury.
These data correspond with findings in the cardiac literature that cTnI is elevated in the
presence of myocardial damage.4,5,16,43,44,45,46,47
Evaluation of Potential Interfering Clinical Conditions
Patients with skeletal muscle injury or chronic renal failure with no evidence of cardiac
involvement were evaluated to assess the clinical specificity of the Access AccuTnI assay. The
results below show that the assay is specific for cardiac muscle damage.
.

Skeletal Muscle Injury

Chronic Renal Failure

62

102

0.03

0.04

0.000.18

0.000.25

100

100

Number of Subjects
Median cTnI (ng/mL)
cTnI Range (ng/mL)
Number of Subjects Above the
AMI Cutoff (0.50 ng/mL)
Clinical Specificity (%)

Risk Stratification for NSTEMI/UA Patients

Results were analyzed from 1,736 patients diagnosed with NSTEMI/UA. Patients were seen in
follow-up at 30 days and every three months thereafter. Follow-ups were planned to continue
for an average of one year (minimum of six months). Over the duration of the study, patients
were monitored for adverse cardiac events which included death, MI, and recurrent ischemia at
rest leading to rehospitalization and UR. Blood samples were obtained from all patients and
were tested for cTnI concentrations by the Access AccuTnI assay.
Results were evaluated at Access AccuTnI cutoffs of 0.04 ng/mL (representing the 99th
percentile upper reference limit, as recommended by the ESC/ACC and AHA/ACC
guidelines), and 0.06 ng/mL (Access AccuTnI median concentration at the 10% CV).2,4,5,6,32,49
Cardiac troponin I concentrations at the 99th percentile upper reference limit and at the median
concentration at the 10% CV, generated using the Access AccuTnI assay, can be used to risk
stratify NSTEMI/UA patients for both short- (42 days) and longer-term (10 months) assessment
for potential adverse cardiac events (death, MI, UR). Cardiac troponin I levels provide useful
prognostic information and aid in the risk stratification of NSTEMI/UA patients. This
association was shown to be independent of the following covariates: risk factors for CAD,
prior history of CAD, drugs used in two weeks prior to enrollment, drugs used during
hospitalization, sex, race and age. The results from this study indicate that elevated AccuTnI
levels are independently and significantly associated with an increased risk of adverse cardiac
events in patients diagnosed with NSTEMI/UA.
The 99th percentile upper reference limit (0.04 ng/mL) and the median concentration at the
10% CV (0.06 ng/mL) are values obtained in individual studies. Each laboratory should
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establish its own reference ranges and appropriate cutoffs to assure proper representation of
specific populations and sample types, and to reflect current practice and criteria for risk
stratification at their institution.
The Access AccuTnI results should be interpreted in light of total clinical presentation of the
patient, including: medical history, physical examination, ECG, and biochemical cardiac marker
measurements.1,2,6,10
Analytical Performance

Methods Comparison
A comparison of lithium heparin plasma cTnI values using the Access AccuTnI assay on the
Access Immunoassay system and a commercially available immunoassay system gave the
following statistical data:
:

Range of
Observations
(ng/mL)

Intercept
(ng/mL)

Slope

Correlation
Coefficient
(r)

157

0.0344.89

-1.039

0.932

0.980

Dilution Recovery (Linearity)

Based on CLSI EP6-P,50 multiple dilutions of three samples containing various cTnI levels with
Access Sample Diluent A resulted in the following data:
Sample 1
(%)

Expected Concentration
(ng/mL)

Determined
Concentration
(ng/mL)

Recovery
(%)

Neat

N/A

2.39

N/A

80

1.91

1.89

99

60

1.43

1.42

99

40

0.96

0.94

98

20

0.48

0.48

100

10

0.24

0.25

104

Mean % Recovery

100

Expected Concentration
(ng/mL)

Determined
Concentration
(ng/mL)

Recovery
(%)

Neat

N/A

13.51

N/A

80

10.81

10.65

99

60

8.11

8.11

100

40

5.40

5.23

97

20

2.70

2.67

99

10

1.35

1.27

94

Mean % Recovery

98

Sample 2
(%)

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Expected Concentration
(ng/mL)

Determined
Concentration
(ng/mL)

Recovery
(%)

Neat

N/A

60.48

N/A

80

48.38

48.42

100

60

36.29

36.29

100

40

24.19

22.73

94

20

12.10

10.58

87

10

6.05

5.48

91

Mean % Recovery

94

Sample 3
(%)

Imprecision
Reproducibility of the Access AccuTnI assay was determined in a study using commercially
available and in-house human serum based control material with two lots of reagents. The
study included a total of 40 assays, 3 replicates per assay, over 20 days. Representative data
were calculated based on CLSI EP5-A guidelines and are presented in the following table:51,52
Sample

Mean (n=120)
(ng/mL)

Within Run
(%CV)

Between Run
(%CV)

Total Imprecision
(%CV)

Tri-level control 1 (commercial)

0.56

4.03

2.97

5.01

Tri-level control 2 (commercial)

7.31

3.06

4.12

5.13

Tri-level control 3 (commercial)

30.55

3.29

6.07

6.90

Control 2 (in-house)

0.42

4.42

2.71

5.19

Control 1 (in-house)

1.34

3.42

2.75

4.39

Analytical Specificity / Interferences

The following drugs were added to a lithium heparin plasma pool containing approximately
2 ng/mL purified cTnI complex. Each drug was tested at a minimum concentration (listed
below) of five times the therapeutic level. All cTnI values obtained in the presence of each
drug/interferent were 5% of the control. This study was based on CLSI EP7-P.53
Drug
Abciximab

2 mg/dL

Acetaminophen

20 mg/dL

Allopurinol

40 mg/dL

Ambroxol

40 mg/dL

Ampicillin

5 mg/dL

Ascorbic Acid

3 mg/dL

Aspirin

50 mg/dL

Atenolol

1 mg/dL

Caffeine

10 mg/dL

Captopril

5 mg/dL

Cinnarizine

40 mg/dL

Cocaine

1 mg/dL

Diclofenac

2 mg/dL

Digoxin

0.02 mg/dL

Dopamine

65 mg/dL

Erythromycin

20 mg/dL

Furosemide

40 mg/dL

Ibuprofen

40 mg/dL

Low molecular weight heparin

Methyldopa
Nifedipine

Access AccuTnI
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Concentration Added

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5 U/mL
2.5 mg/dL
6 mg/dL

2010 Beckman Coulter, Inc.

Drug

Concentration Added

Nitrofurantoin

6.4 mg/dL

Nystatin

0.7 mg/dL

Oxytetracycline

0.5 mg/dL

Phenytoin

10 mg/dL

Propranolol

0.5 mg/dL

Quinidine
Sodium heparin

2 mg/dL
8 U/mL

Theophylline

25 mg/dL

Trimethoprim

7.5 mg/dL

Verapamil

16 mg/dL

Samples containing up to 40 mg/dL bilirubin (conjugated), 1000 mg/dL fibrinogen,

1000 mg/dL Triolein (triglycerides), 500 mg/dL hemoglobin, or 6000 mg/dL of human serum
albumin do not affect the concentration of cTnI assayed. All cTnI values obtained in the
presence of each interferent were 10% of the control.
The following table describes the cross-reactivity of the assay with other myofibrillar proteins.
Each of the potential cross reactants was added to a lithium heparin plasma pool containing
approximately 2 ng/mL purified cTnI complex and assayed in replicates of 10. This study was
based on CLSI EP7-P.53
Analyte Added
(ng/mL)

Substance

Cross-Reactivity
(%)

Skeletal troponin I

1000

0.034

Cardiac troponin C

1000

-0.002

Recombinant human cardiac troponin T

1000

-0.004

Actin (rabbit)

1000

-0.003

Myosin

1000

0.001

Tropomyosin (rabbit)

1000

-0.008

Human CK-MB

1000

-0.001

Myoglobin

1000

-0.002

Analytical Sensitivity
The lowest detectable level of cTnI distinguishable from zero (Access AccuTnI Calibrator S0)
with 95% confidence is 0.01 ng/mL (g/L). This value is the mean signal of 10 replicates of the
zero calibrator plus two standard deviations. This value is determined by processing a
complete six point calibration curve, controls, and 10 replicates of the zero calibrator in multiple
assays.
Functional Sensitivity
The term functional sensitivity was originally used to define the lowest point in a TSH assay
measuring range where results could be derived with a consistently attainable total imprecision
of 20% CV.54
The functional sensitivity as determined by a total imprecision of 20% CV was found to be
0.03 ng/mL (median of nine experiments). Using a total imprecision of 10% CV, the median
concentration was 0.06 ng/mL.32

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Page 11

AccuTnI CALIBRATORS
33345
Intended Use

The Access AccuTnI Calibrators are intended to calibrate the Access AccuTnI assay for the
quantitative determination of cardiac troponin I (cTnI) levels in human serum and plasma
using the Access Immunoassay Systems to aid in the diagnosis and treatment of myocardial
infarction and cardiac muscle damage.
Cardiac troponin I determination aids in the risk stratification of patients with unstable angina
or non-ST segment elevation acute coronary syndromes with respect to relative risk of
mortality, myocardial infarction, or increased probability of ischemic events requiring urgent
revascularization procedures.

Summary and
Explanation

Traceability

Quantitative assay calibration is the process by which samples with known analyte
concentrations (i.e., assay calibrators) are tested like patient samples to measure the response.
The mathematical relationship between the measured responses and the known analyte
concentrations establishes the calibration curve. This mathematical relationship, or calibration
curve, is used to convert RLU (Relative Light Unit) measurements of patient samples to specific
quantitative analyte concentrations.
The measurand (analyte) in the Access AccuTnI Calibrators is traceable to the manufacturers
working calibrators. Traceability process is based on EN ISO 17511.
The assigned values were established using representative samples from this lot of calibrator
and are specific to the assay methodologies of the Access reagents. Values assigned by other
methodologies may be different. Such differences, if present, may be caused by inter-method
bias.

Product
Information

Access AccuTnI Calibrators

Cat. No. 33345: S0S5, 1 mL/vial
Provided ready to use.
Freeze upon receipt at -20C or colder.
Mix contents thoroughly by gently inverting before use. Avoid bubble formation.
Stable until the expiration date stated on the label when stored at -20C or colder.
After initial use, the thawed vials are stable at 2 to 10C for 60 days. Label the vials with the
date of thaw or the date of expiration.
Return calibrators to 2 to 10C after each use. Do not refreeze opened vials.
Signs of possible deterioration are control values out of range.
Refer to calibration card for exact concentrations.
r

Access AccuTnI
Page 12

S0:

Buffered bovine serum albumin (BSA) matrix with surfactant

< 0.1% sodium azide, and 0.1% ProClin** 300.

S1, S2, S3,

S4, S5:

Recombinant troponin complex at cTnI levels of approximately

0.3, 1.2, 5.0, 25 and 100 ng/mL (g/L) in buffered BSA matrix with
surfactant, < 0.1% sodium azide, and 0.1% ProClin 300.

Calibration
Card:

A34077F

2010 Beckman Coulter, Inc.

Warnings and
Precautions

For in vitro diagnostic use.

Patient samples and blood-derived products may be routinely processed with minimum risk
using the procedure described. However, handle these products as potentially infectious
according to universal precautions and good clinical laboratory practices, regardless of their
origin, treatment, or prior certification. Use an appropriate disinfectant for decontamination.
Store and dispose of these materials and their containers in accordance with local
regulations and guidelines.
Sodium azide may react with lead and copper plumbing to form highly explosive metal
azides. On disposal of liquids, flush with a large volume of water to prevent azide
build-up.35
Xi. Irritant: 0.1% ProClin 300.
R 43: May cause sensitization by skin contact.
S 28-37: After contact with skin, wash immediately with plenty of soap
and water. Wear suitable gloves.
The Material Safety Data Sheet (MSDS) is available upon request.

Procedure

Calibration
Details

Refer to the appropriate system manuals and/or Help system for information on calibration
theory, configuring calibrators, calibrator test request entry, and reviewing calibration data.
Run the Access AccuTnI S0 and S1 Calibrators in quadruplicate, and the S2S5 Calibrators in
duplicate.
The Access AccuTnI Calibrators are provided at six levels - zero and approximately 0.3, 1.2, 5.0,
25 and 100 ng/mL. Assay calibration data are valid up to 56 days.

Limitations of
the Procedure

If there is evidence of microbial contamination or excessive turbidity in a reagent, discard the

vial.

2010 Beckman Coulter, Inc.

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Page 13

SAMPLE DILUENT A
81908
Intended Use

The Access Sample Diluent A is intended for use with Access assays to dilute patient samples
containing analyte concentrations greater than the analyte specific S5 calibrator.

Summary and
Explanation

The analyte level in patient samples may exceed the level of the specific S5 calibrator. If a
quantitative value is required, it will be necessary to dilute the samples in order to determine
the analyte concentration.

Product
Information

Access Sample Diluent A

Cat. No. 81908: 4 mL/vial
Provided ready to use.
Allow the contents to stand for 10 minutes at room temperature.
Mix gently by inverting before use. Avoid bubble formation.
Stable until the expiration date stated on the vial label when stored at 2 to 10C.
Diluent

Warnings and
Precautions

Buffered BSA matrix with surfactant, < 0.1% sodium azide, 0.5%
ProClin** 300.

For in vitro diagnostic use.

Patient samples and blood-derived products may be routinely processed with minimum risk
using the procedure described. However, handle these products as potentially infectious
according to universal precautions and good clinical laboratory practices, regardless of their
origin, treatment, or prior certification. Use an appropriate disinfectant for decontamination.
Store and dispose of these materials and their containers in accordance with local
regulations and guidelines.
Sodium azide may react with lead and copper plumbing to form highly explosive metal
azides. On disposal of liquids, flush with a large volume of water to prevent azide
build-up.35
Xi. Irritant: 0.5% ProClin 300.
R 43: May cause sensitization by skin contact.
S 28-37: After contact with skin, wash immediately with plenty of soap
and water. Wear suitable gloves.
The Material Safety Data Sheet (MSDS) is available upon request.

Procedure

Access AccuTnI
Page 14

Samples can be accurately measured within the analytic range of the lower limit of detection
and the highest calibrator value of the specific assay. If a sample contains more analyte than the
stated value of the S5 calibrator, dilute the sample following dilution instructions in the specific
assay labeling under Limitations of the Procedure in the reagent pack section. Refer to the
appropriate system manuals and/or Help system for instructions on how to enter a sample
dilution in a test request.

A34077F

2010 Beckman Coulter, Inc.

Limitations of
the Procedure

If there is evidence of microbial contamination or excessive turbidity in the reagent, discard the
vial.

2010 Beckman Coulter, Inc.

A34077F

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Page 15

References

1
2

8
9

10
11
12
13
14
15
16
17
18
19
20
21
22

23
24

25

Access AccuTnI
Page 16

Heidenreich PA, Go A, Melsop KA, Alloggiamento T, McDonald KM, Hagan V, Hastie T, Hlatky MA. Prediction of
risk for patients with unstable angina. AHRQ Publication No. 01-E001 December, 2000; Number 31.
Braunwald E, Antman EM, Beasley JW, Califf RM, Cheitlin MD, Hochman JS, Jones RH, Kereiakes D, Kupersmith J,
Levin TN, Pepine CJ, Schaeffer JW, Smith EE, Steward DE, Theroux P. ACC/AHA guidelines for the management
of patients with unstable angina and non-ST-segment elevation myocardial infarction: Executive summary and
recommendations. A report of the American College of Cardiology/American Heart Association Task Force on
Practice Guidelines (Committee on the Management of Patients with Unstable Angina). Circulation 2000; 102(10):
1193-1209.
Cannon CP, McCabe CH, Wilcox RG, Langer A, Caspi A, Berink P, Loper-Sendon J, Toman J, Charlesworth A,
Anders RJ, Alexander JC, Skene A, Braumwald E. Oral glycoprotein IIb/IIIa inhibition with orbofiban in patients
with unstable coronary syndromes (OPUS-TIMI 16) trial. Circulation 2000; 102: 149-156.
Alpert JS, Thygesen K, et al. Myocardial infarction redefined - A consensus document of The Joint European Society
of Cardiology/American College of Cardiology Committee for the Redefinition of Myocardial Infarction. JACC
2000; 36(3): 959-969.
The Joint European Society of Cardiology/American College of Cardiology Committee. Myocardial Infarction
redefineda consensus document of the Joint European Society of Cardiology/American College of Cardiology
Committee for the Redefinition of Myocardial Infarction. European Heart Journal 2000; 21: 1502-1513.
Braunwald E, Antman EM, Beasley JW, Califf RM, Dheitlin MD, Hochman JS, Jones RH, Kereiakes D, Kupersmith J,
Levin TN, Pepine CJ, Schaeffer JW, Smith EE, Steward DE, Theroux P. ACC/AHA guideline update for the
management of patients with unstable angina and non-ST-segment elevation myocardial Infarction: a report of the
American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee on the
Management of Patients with Unstable Angina). 2002.
Antman EM, Tanasijevic MJ, Thompson B, Schactman M, McCabe CH, Cannon CP, Fischer GA, Fung AY,
Thompson C, Wybenga D, and Braunwald E. Cardiac-specific troponin I levels to predict the risk of mortality in
patients with acute coronary syndromes. N Engl J Med 1996; 335: 1342-1349.
Tanasijevic MJ, Cannon CP, Antman EM. The role of cardiac troponin-I (cTnI) in risk stratification of patients with
unstable coronary artery disease. Clin Cardiol 1999; 22: 13-16.
Morrow DA, Rifai N, Tanasijevic MJ, Wybenga DR, De Lemos JA, Antman EM. Clinical efficacy of three assays for
cardiac troponin I for risk stratification in acute coronary syndromes: A thrombolysis in myocardial infarction
(TIMI) IIB substudy. Clin Chem 2000; 46(4): 453-460.
Antman EM, Fox KM. Guidelines for the diagnosis and management of unstable angina and non-Q-wave
myocardial infarction: Proposed revisions. Am Heart J 2000; 139: 461-75.
Wilkinson JM, Grand RJA. Comparison of amino acid sequence of troponin I from different striated muscles.
Nature 1978; 271: 31-35.
Wade R, Eddy R, Shows TB, Kedes L. cDNA sequence, tissue-specific expression and chromosomal mapping of the
human slow-twitch skeletal muscle isoform of troponin I. Genomics 1990; 7: 346-357.
Perry SV. The regulation of contractile activity in muscle. Biochem Soc Trans 1979; 7: 593-617.
Cummins P, Perry V. Troponin I from human skeletal and cardiac muscles. Biochem J 1978; 171: 251-259.
Vallins JW, Brand NJ, Dabhaden N, et al. Molecular cloning of human cardiac troponin I using polymerase chain
reaction. FEBS Lett 1990; 270: 57-61.
Adams III JE, Bodor GS, Davila-Roman VG, Delmez JA, Apple FS, Ladenson JH, et al. Cardiac troponin I: a marker
with high specificity for cardiac injury. Circulation 1993; 88: 101-106.
Larue C, Calzolari C, Bertinchant JP, Leclercq F, Grolleau R, Pau B. Cardiac-specific immunoenzymometric assay of
troponin I in the early phase of acute myocardial infarction. Clin Chem 1993; 39: 972-979.
Bakker AJ, Koelemay MJW, Gorgels JPMC, van Vlies B, Smits R, Tijssen JGP, Haagen FDM. Failure of new
biochemical markers to exclude acute myocardial infarction at admission. Lancet 1993; 342: 1220-1222.
Mair J, Wagner I, Puschendorf B, Mair P, Lechleitner P, Diensti F, et al. Cardiac troponin I to diagnose myocardial
injury (letter). Lancet 1993; 341: 838-839.
Galvani M, Ottani F, Ferrini D et al. Prognostic influence of elevated values of cardiac troponin I in patients with
unstable angina. Circulation 1997; 95: 20532059.
Missov ED, De Marco T. Clinical insights on the use of highly sensitive cardiac troponin assays. Clin. Chem. Acta.
1999; 284: 175185.
Wu HBA, Apple FS, Gibler B, Jesse RL et al. National Academy of Clinical Biochemistry Standards of Laboratory
Practice: Recommendations for the use of cardiac markers in coronary artery disease. Clin. Chem 1999; 45(7):
1104-1121.
Adams JE, Schechtman KB, Landt Y, Ladenson JH, Jaffe AS. Comparable detection of acute myocardial infarction
by creatin kinase MB isoenzyme and cardiac troponin I. Clin. Chem. 1994; 40:1291-1295
Mair J, Morandell D, Genser N, Lechleitner P, Dienstl F, Puschendorf B. Equivalent early sensitivities of myoglobin,
creatine kinase MB mass, creatine kinase isoform ratios, and cardiac troponins I and T for acute myocardial
infarction. Clinical Chemistry 1995; 41: 1266-1272.
Mair J, Genser N, Morandell D, Maier J, Mair P, Lechleitner P, Calzolari C, Larue C, Ambach E, Dienstl F, Pau B,
Puschendorf B. Cardiac troponin I in the diagnosis of myocardial injury and infarction. Clinica Chimica Acta. 1996;
245: 1938.

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26 Wu AHB, Feng YJ, Moore R, Apple FS, McPherson PH, Buechler KF, Bodar G. Characterization of cardiac troponin
I forms in the blood of patients with acute myocardial infarction and comparison of assays for troponin T and I.
Clin Chem 1998; 44: 1198-1208.
27 Morjana NA. Degradation of human cardiac troponin I after myocardial infarction. Biotechnol. Appl. Biochem 1998;
28: 105-111.
28 Giuliani I, Bertinchant JP, Granier C, Laprade M, Chocron S, Toubin G, Etievent JP, Larue C, Trinquier S.
Determination of cardiac troponin I forms in the blood of patients with acute myocardial infarction and patients
receiving crystalloid or cold blood cardioplegia. Clin Chem 1999; 45: 213-222.
29 Katrukha AG, Bereznikova AV, Esakova TV, Pettersson K, Lovgren T, Severina ME, Pulkki K, Vuopio-Pulkki LM,
Gusev NB. Troponin I is released in bloodstream of patients with acute myocardial infarction not in free form but as
complex. Clin Chem 1997; 43: 1379-1385.
30 Datta P, Foster K, Dasgupta A. Comparison of immunoreactivity of five human cardiac troponin I assays toward
free and complexed forms of the antigen: implications for assay discordance. Clin Chem 1999; 45: 2266-2269.
31 Newman D, Olabiran Y, Bedzyk WD, Chance S, Gorman EG, Price C. Impact of antibody specificity and calibration
material on the measure of agreement between methods for cardiac troponin I. Clin Chem 1999; 45: 822-828.
32 Uettwiller-Geiger D, Wu AHB, Apple FS, Jevans AW, Venge P, Olson MD, Darte C, Woodrum DL, Roberts S, Chan
S. Multicenter evaluation of an automated assay for troponin I. Clin Chem 2002; 48(6): 869-76.
33 Lagugger R, Organ L, Collier C, Atar D, Van Eyk JE. Extensive troponin I and T modification detected in serum
from patients with acute myocardial infarction. Circulation 2000; 102: 1221-1226.
34 McDonough JL, Arrell DK, Van Eyk JE. Troponin I degradation and covalent complex formation accompanies
myocardial ischemia/reperfusion injury. Circ Res 1999; 84: 9-20.
35 DHHS (NIOSH) Publication No. 78-127, August 1976. Current Intelligence Bulletin 13 - Explosive Azide Hazard.
Available http://www.cdc.gov/niosh.
36 Approved Guideline Procedures for the Handling and Processing of Blood Specimens, H18-A3. 2004. Clinical and
Laboratory Standards Institute.
37 Cembrowski GS, Carey RN. Laboratory quality management: QC QA. ASCP Press, Chicago, IL, 1989.
38 Kricka L. Interferences in immunoassays still a threat. Clin Chem 2000; 46: 10371038.
39 Bjerner J, et al. Immunometric Assay Interference: Incidence and Prevention. Clin Chem 2002; 48: 613621.
40 Lum G, Solarz D, Farney L. False Positive Cardiac Troponin Results in Patients Without Acute Myocardial
Infarction. Labmedicine 2006; 37(9): 546-550.
41 Lingwood D, Ballantyne JS. Alkaline phosphataseimmunoglobulin conjugate binds to lipids in vitro, independent
of antibody selectivity. Journal of Immunological Methods 2006; 311: 174177
42 World Health Organization. Report of the Joint International Society and Federation of Cardiology/World Heath
Organization Task Force on Standardization of Clinical Nomenclature. Nomenclature and criteria for diagnosis of
ischemic heart disease. Circulation 1979; 59: 607-9.
43 JP Etievent, et. al. Use of Cardiac Troponin I as a Marker of Perioperative Myocardial Ischemia. Annual of Thorac
Surgery 1995; 59: 1192-1194.
44 TM Guest, et. al. Myocardial Injury in Critically Ill Patients. Journal of American Medical Association 1995; 273, 24:
19451949.
45 Braunwald E, Jones RH, Maek DB et al. Diagnosing and managing unstable angina; Circulation 1994; 90: 613-622.
46 Theroux P, Fuster V. Acute coronary syndromes. Unstable angina and non-Q-Wave myocardial infarction.
Circulation 1998; 97: 1195-1206.
47 Falk E, Shak PK. Pathology of acute coronary syndromes. In Braunwald E (ed). Atlas of Heart Diseases. Acute
myocardial infarction and other acute ischemic syndromes. Mosby-2001 book 1996; St Louis, 3.1-3.31.
48 Zweig MH, Campbell G. Receiver-Operating Characteristic (ROC) Plots: A fundamental Evaluation Tool in Clinical
Medicine. Clin. Chem. 1993; 39, 4: 561-577.
49 Apple FS, Wu AHB. Myocardial infarction redefined: Role of cardiac troponin testing. Clin. Chem 2001: 47(3);
377-379.
50 Evaluation of the Linearity of Quantitative Analytical Methods; Proposed Guideline, EP6-P. 1986. National
Committee for Clinical Laboratory Standards, V6, N19.
51 Approved Guideline Evaluation of precision performance of clinical chemistry devices, EP5-A. 1999. National
Committee for Clinical Laboratory Standards, V19, N2.
52 Krouwer JS, Rabinowitz R. How to improve estimates of imprecision. Clinical Chemistry 1984; 30: 290-292.
53 Interference testing in clinical chemistry, EP7-P. 1986. National Committee for Clinical Laboratory Standards, V6,
N13.
54 Spencer CA, et al. Interlaboratory/intermethod differences in functional sensitivity of immunometric assays of TSH
and impact on reliability of measurement of subnormal concentrations of TSH. Clin Chem 1995; 41: 367374.

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Page 17

Beckman Coulter, Access, AccuTnI, SYNCHRON LX, UniCel and DxI are trademarks of Beckman Coulter, Inc.; Beckman Coulter,
Access, AccuTnI, SYNCHRON LX, UniCel and DxI are registered in the USPTO and SIPO.
*Lumi-Phos is a trademark of Lumigen, Inc, a subsidiary of Beckman Coulter, Inc.
**ProClin is a trademark of Rohm and Haas Company or of its subsidiaries or affiliates.

Beckman Coulter Ireland Inc.

Mervue Business Park,
Mervue, Galway,
Ireland 353 91 774068

Manufactured by:
Beckman Coulter, Inc.
250 S. Kraemer Blvd.
Brea, CA 92821 U.S.A.
Printed in U.S.A.
Made in U.S.A.
Revised July 2010

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A34077F

2010 Beckman Coulter, Inc.