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Multicenter clinical and analytical evaluation of the AxSYM troponin-I immunoassay to assist in the diagnosis of myocardial infarction.

The diagnosis of acute myocardial infarction (AMI) [7] as formally established by WHO requires at least two of the following criteria: a history of chest pain, evolutionary changes on the electrocardiogram (ECG), and increased cardiac enzymes, such as the creatine kinase (CK) MB isoenzyme (1). Cardiac troponin I (cTnI) and cardiac troponin T (cTnT) are being investigated as new standards for cardiac injury testing to rule in and rule out AMI (2-4). Recent clinical studies have demonstrated that measurement of cTnI is comparable to CK-MB for the sensitive and specific detection of AMI (4-6). cTnI, located exclusively in the myocardium, successfully differentiates cardiac from non-cardiac injury in patient groups that show falsely increased CK-MB concentrations attributable to skeletal muscle injury. Examples include patients with cocaine-induced chest pain (7), severe muscle trauma or disease (2), chronic renal disease (2, 8), and cardioversion (9).

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 (11-14). 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.

Materials and Methods

This study was performed at six clinical sites: Columbia Presbyterian Medical Center, New York, NY; Emory University Hospital, Atlanta GA; Hennepin County Medical Center, Minneapolis, MN; Rush Presbyterian St. Luke' s Medical Center, Chicago, IL; the University of Maryland Medical Center, Baltimore MD; and University of Tennessee Memorial Hospital, Knoxville, TN. All sites obtained approval for human subject research from their respective institutional review boards.


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[degrees]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 [micro]g/L (3) and >1.5 [micro]g/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 [micro]g/L for the AxSYM cTnI, 1.5 [micro]g/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 [greater than or equal to] 0.5 mg/L for the AxSYM and [greater than or equal to] 0.4 mg/L for the Stratus were used as the reference limits.


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 [micro]g/L (the diagnostic cutoff) and [less than or equal to] 15% at 0.6 [micro]g/L. The detection limit is 0.35 [micro]g/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 [micro]g/L for the Access (5) and 2.0 [micro]g/L for the OPUS (6).


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 [micro]g/L) calibrator and 2 replicates of the B (2.5 [micro]g/L) calibrator on 2 separate days. The lowest measurable concentration of cTnI was calculated for each analytical run by determining the mean value (in [micro]g/L) that corresponded to the rate that was 2 SD from the mean rate of the A calibrator.


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 ([less than or equal to] 50 mg/L) of the assay.



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.




As shown in Table 1, 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 [micro]g/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 [micro]g/L, with a mean of 0.14 [micro]g/L and an SD of 0.05 [micro]g/L.

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 [micro]g/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 [micro]g/L) and the Beckman Access (diagnostic cutoff <0.15 [micro]g/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.



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.


On the basis of the 95th percentile, expected AxSYM cTnI values for apparently healthy individuals were [less than or equal to] 0.5 [micro]g/L and for non-AMI (excluding angina and unstable angina) patients were [less than or equal to] 2.4 mg/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 [micro]g/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 [micro]g/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.

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 [micro]g/L compared with a Stratus cTnI of 1.4 [micro]g/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 [micro]g/L) and the Stratus cTnI (cutoff <0.4 [micro]g/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).

The AxSYM cTnI clinical specificities for the three patient groups studied for potentially interfering clinical conditions were excellent, at [greater than or equal to] 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%).


This study demonstrated that the Abbott AxSYM cTnI immunoassay was comparable clinically with the Dade-Behring Stratus cTnI immunoassay for the detection and ruling out of AMI. Our data show that the AxSYM cTnI assay demonstrated the expected temporal rise and fall pattern of cTnI over the 24-h period following admission, with >90% sensitivity and specificity at peak concentrations and with no significant difference compared with the Dade Stratus cTnI findings. As expected, the AxSYM cTnI and the Stratus cTnI were not early markers for detection of AMI, demonstrating sensitivities of 36.0% and 24.0%, respectively, from onset of chest pain and 64.6% and 54.9%, respectively, at presentation (Tables 2 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 (4-6). 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 (4-6).

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 [micro]g/L) vs Stratus (cutoff, 1.5 [micro]g/L) slope = 3.50; AxSYM vs OPUS (cutoff, 2.0 [micro]g/L) slope = 1.79; AxSYM vs Access (cutoff, 0.15 [micro]g/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 [micro]g/L) for healthy individuals and the decision cutoff for AMI (2.0 [micro]g/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, [greater than or equal to] 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 [micro]g/L was well below the ROC curve AMI cutoff of 2.0 [micro]g/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. This work was supported in part by Abbott Laboratories.

Received August 25, 1998; accepted November 30, 1998.


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(2.) Adams JE, Bodor GS, Davila-Roman V, Delinez JA, Apple FS, Ladenson JH, Jaffe AS. Cardiac troponin I: a marker with high specificity for cardiac injury. Circulation 1993;88:101-6.

(3.) Apple FS, Falahati A, Paulsen PR, Miller EA, Sharkey SW. Improved detection of minor ischemic myocardial injury with measurement of serum cardiac troponin I. Clin Chem 1997;43:2047-51.

(4.) Tucker JF, Collins RA, Anderson AJ, Hauser J, Kalas J, Apple FS. Early diagnostic efficiency of cardiac troponin I and T for acute myocardial infarction. Acad Emerg Med 1997;4:13-21.

(5.) Christenson RH, Apple FS, Morgan DL, Alonsozana GL, Mascotti K, Olson M, et al. Cardiac troponin I measurement with the ACCESS immunoassay system: analytical and clinical performance characteristics. Clin Chem 1998;44:52-60.

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(8.) McLaurin MD, Apple FS, Voss EM, Herzog CA, Sharkey SW. Cardiac troponin I, cardiac troponin T, and creatine kinase MB in dialysis patients without ischemic heart disease: evidence of cardiac troponin T expression in skeletal muscle. Clin Chem 1997;43:976-82.

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[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.

[7] Nonstandard abbreviations: AMI, acute myocardial infarction; ECG, electrocardiogram; CK, creatine kinase; cTnI, cardiac troponin I; cTnT, cardiac troponin T; and CI, confidence interval.

* 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
Table 1. Within-run and total imprecision (excluding between-instrument
variance components) of the AxSYM Troponin-I assay over 20 days
according to the NCCLS EP5-T2 protocol.

 Mean cTnl, [micro]g/L Within-run Total
 (n = 320) SD CV, % SD CV, %

Low control 2.9 0.18 6.2 0.24 8.1
Medium control 9.7 0.52 5.4 0.95 9.8
High control 33.6 1.55 4.6 2.12 6.3
Panel 1 2.9 0.18 6.2 0.29 10
Panel 2 29.5 1.30 4.4 2.23 7.5
Panel 3 137.8 6.12 4.4 8.93 6.5

Table 2. Clinical sensitivities and specificities by hours from
presentation to medical center for cTnI measured on the AxSYM and
Stratus analyzers.

Time Interval, h Samples (Pts) (a) Sensitivity, % 95% CI


(0 to <5) 113 (91) 64.6 (55.0-73.4)
(5 to <12) 77 (72) 92.2 (83.8-97.1)
(12 to <24) 112 (89) 89.3 (82.0-94.3)
>24 90 (54) 93.3 (86.1-97.5)


(0 to <5) 113 (91) 54.9 (45.2-64.2)
(5 to <12) 77 (72) 92.2 (83.8-97.1)
(12 to <24) 112 (89) 85.7 (77.8-91.6)
>24 90 (54) 87.8 (79.2-93.1)

Time Interval, h Samples (Pts) Specificity, % 95% CI


(0 to <5) 443 (372) 94.6 (92.0-96.5)
(5 to <12) 372 (348) 93.8 (90.9-96.0)
(12 to <24) 368 (313) 94.0 (91.1-96.2)
>24 179 (118) 94.4 (90.0-97.3)


(0 to <5) 443 (372) 97.3 (95.3-98.6)
(5 to <12) 372 (348) 96.5 (94.1-98.1)
(12 to <24) 368 (313) 96.7 (94.4-98.3)
>24 179 (118) 95.5 (91.4-98.1)

(a) Pts, patients.

Table 3. Clinical sensitivities and specificities by hours from onset
of chest pain for cTnI measured on the AxSYM and Stratus analyzers.

Time Interval, h Samples (Pts) (a) Sensitivity, % 95% CI


(0 to <5) 25 (25) 36.0 (18.0-57.5)
(5 to <12) 39 (36) 79.5 (63.5-90.7)
(12 to <24) 79 (61) 77.2 (66.4-85.9)
(24 to <48) 89 (60) 91.0 (83.1-96.0)
(48 to <72) 46 (29) 93.5 (82.1-98.6)
>72 46 (21) 95.7 (85.2-99.5)


(0 to <5) 25 (25) 24.0 (9.4-45.1)
(5 to <12) 39 (36) 74.4 (57.9-87.0)
(12 to <24) 79 (61) 72.2 (60.9-81.7)
(24 to <48) 89 (60) 87.6 (79.0-93.7)
(48 to <72) 46 (29) 93.5 (82.1-98.6)
>72 46 (21) 87.0 (73.7-95.1)

Time Interval, h Samples (Pts) Specificity, % 95% CI


(0 to <5) 128 (121) 93.8 (88.1-97.3)
(5 to <12) 170 (164) 95.3 (90.9-97.9)
(12 to <24) 326 (242) 94.5 (91.4-96.7)
(24 to <48) 220 (157) 96.4 (93.0-98.4)
(48 to <72) 96 (63) 90.6 (82.9-95.6)
>72 133 (53) 91.0 (84.8-95.3)


(0 to <5) 128 (121) 99.2 (95.7-100.0)
(5 to <12) 170 (164) 97.6 (94.1-99.4)
(12 to <24) 326 (242) 97.5 (95.2-98.9)
(24 to <48) 220 (157) 97.3 (94.2-99.0)
(48 to <72) 96 (63) 97.9 (92.7-99.7)
>72 133 (53) 93.2 (87.5-96.9)

(a) Pts, patients.
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Title Annotation:Enzymes and Protein Markers
Author:Apple, Fred S.; Maturen, Andrew J.; Mullins, Richard E.; Painter, Pennell C.; Pessin-Minsley, Meliss
Publication:Clinical Chemistry
Date:Feb 1, 1999
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