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Annals of Clinical & Laboratory Science 35:66-72 (2005)
© 2005 Association of Clinical Scientists

Albumin Cobalt Binding Assay to Rule Out Acute Coronary Syndrome

Jude M. Abadie1, Cary L. Blassingame2 and Daniel D. Bankson1,2
1 Department of Laboratory Medicine, University of Washington Medical Center, and 2 Pathology and Laboratory Medicine Service, Veterans Affairs Puget Sound Health Care System, Seattle, Washington

Address correspondence to Jude M. Abadie, Department of Laboratory Medicine (NW 120), University of Washington Medical Center, Seattle, WA 98105, USA: tel 206 598 5974; fax 206 598 6189; e-mail judeabadie{at}medscape.com.


   Abstract
Top
 Abstract
Introduction
 Materials and Methods
 Results
 Discussion
 Acknowledgements
 References
 
The purpose of this study was to validate the Albumin Cobalt Binding (ACB®) assay at the Seattle Veterans Affairs (VA) Hospital to determine if it would provide an earlier rule-out of acute coronary syndrome (ACS) in patients, compared to current use of cardiac injury markers. This study compares the distribution of ischemia modified albumin (IMA) values of our patient population to those provided by the kit manufacturer. IMA values were determined photometrically on a Roche Modular Analytical System on 200 subjects: 69 subjects not experiencing chest pain (normals), 78 subjects presenting to the emergency room (ER) with chest pain whose initial and subsequent troponin results were negative (non-converters), and 53 subjects presenting to the ER with chest pain whose initial troponin result was negative but subsequent troponin results were positive (converters). Based on the relationships between IMA values in the initial samples from the non-converters and converters, we constructed a ROC curve to identify an optimum IMA rule-out value. The IMA values (mean ± SD) for the normals, non-converters, and converters were 89 ± 7.1, 100 ± 13.9, and 126 ± 14.1 U/ml, respectively, and each mean was statistically different from the means of the other groups. The ROC curve comparing converters and non-converters showed an area of 0.89 (p <0.001) compared to the line of identity. An IMA cut-off of 97 U/ml gives a 98% sensitivity and 45% specificity and may be the best decision point to differentiate between these groups in our population. Nine of 78 non-converters were classified as having unstable angina. In conclusion, the ACB assay has a strong negative predictive value and sensitivity in our population for predicting the troponin results at 6 to 24 hr post-presentation. Because ACB results may be facility- and instrument-dependent, each facility should conduct an independent ROC analysis to determine the optimal IMA rule-out level. The ACB assay, when used in conjunction with cardiac injury markers and assessment of unstable angina, holds promise in reducing inappropriate low-risk hospital admissions and improving the clinical management of patients with chest pain.

(received 9 December 2004; accepted 15 December 2004)

Keywords: ischemia modified albumin, cobalt binding assay, acute coronary syndrome


   Introduction
Top
 Abstract
 Introduction
Materials and Methods
 Results
 Discussion
 Acknowledgements
 References
 
In the USA, about eight million annual emergency room (ER) visits are attributed to acute chest pain [1]. This presents a tremendous challenge to ER physicians, demanding an accurate and efficient clinical evaluation, triage, and subsequent management and care for these patients. Acute coronary syndrome (ACS), defined as an imbalance between the supply and demand for myocardial oxygen, is currently a diagnosis based on a continuum of clinical conditions including unstable angina, non-Q-wave and Q-wave AMI, patient history, and other risk factors. ACS accompanying ischemic heart disease represents about 1.4 million of these visits [2]. Furthermore, up to 70,000 of these patients are inappropriately discharged, which can lead to numerous malpractice claims [3].

Several studies reported that between 2 and 8% of patients with acute myocardial infarction (AMI) are inappropriately discharged to home [3–6]. This is attributed to the fact that 1 of 20 patients with AMI is an atypical presenter [7–9]. In general, patients with AMI who are discharged to home experience twice the death rate (25%) compared to those who are admitted to the hospital [10–11]. Failure to diagnose and subsequently treat AMI is responsible for the greatest total dollar loss for malpractice claims against ER physicians [12–14].

More than 700,000 chest pain presenters are hospitalized for evaluation with concurrent testing and subsequently discharged with a diagnosis other than ACS [1,15]. In a preliminary cost-avoidance study conducted by Ischemia Technologies, Inc., at the Harborview Medical Center (HMC) of the University of Washington (UW) Health Care System, it was determined that $2,893 was saved with every patient discharged to home for follow-up on the basis of a negative Ischemia Modified Albumin (IMA) value (chest pain of non-specific origin) (unpublished data from Donna Edmonds, November 2004; Ischemia Technologies, Denver, CO; www.ischemia.com). This cost-avoidance study considered the costs of diagnostic studies on an out-patient basis when appropriate. The figures reflect a need to improve the management of chest pain presenters in these patients. If extrapolated to include all US hospitals, this preliminary study suggests significant savings if IMA could rule-out ACS in 100% of the non-ACS chest pain presenters.

Traditional clinical measurements such as 12-lead ECG monitoring, imaging studies, and evaluation of necrosis markers have failed to become a true "gold standard" in diagnosing or ruling out myocardial ischemia [16–17]. Measuring IMA levels using the Albumin Cobalt Binding (ACB) assay has been approved only as a rule-out marker for cardiac ischemia. Perhaps the strongest prognostic function of IMA as a marker of ischemia lies in its ability to rule out ACS in patients whose chest pain does not suggest an imminent myocardial infarction. The failure of conventional diagnostic tests to identify ACS patients who are at risk for AMI indicates the need for a highly sensitive marker.

Unlike injury markers such as CK-MB, myoglobin, and troponin, IMA is believed to be a marker of cardiac ischemia. The IMA level rises within minutes after the onset of ischemia and remains elevated for several hours after the cessation of the ischemic event [18]. IMA rises in the presence of ischemia and not as a result of necrosis. During ACS, prolonged ischemia leads to necrosis and subsequently (several hours later) to elevated injury markers such as CK-MB, myoglobin, and troponin. Patients with reversible ischemia, who may be experiencing unstable angina, generally have elevated IMA level, but may not have elevated injury markers [19]. This study suggested that IMA levels may often return to normal levels when injury markers first become elevated. Elevated IMA levels are associated with cirrhosis and lung cancer, but not with GI cancer, brain ischemia, end-stage renal disease, or viral infection.

The US Veterans Administration (VA) hospital system has initiated a nation-wide action plan to improve cardiac care outcomes [20]. A study of the VA cardiac care program, commissioned by the Department of Veterans Affairs, demonstrated that VA patients who experience an AMI have a higher mortality than their Medicare veteran and non-veteran cohorts. The study also stated that AMI is the most common diagnosis in the VA system [21]. Perhaps the implementation of ischemia markers, like the ACB assay, will prove to be a key component of the action plan to improve the VA cardiac care program by providing a rule out test for chest pain presenters who are not experiencing ACS. The current lack of a sensitive marker hinders appropriate discharge of non-ACS patients, resulting in numerous expenses and patient mismanagement [22–23]. The expenses include increased length of hospital stay and unnecessary, costly laboratory tests to assess cardiac injury markers, especially in teaching facilities [24].

In this study we performed IMA testing on samples collected at the Harborview Medical Center (HMC), a Level 1 trauma center of the University of Washington Health System. We measured IMA values for our typical population and determined an optimal rule-out value for ACS. We envision that the outcomes of this ACB study may help to improve cardiac care programs nation-wide by decreasing spending, improving patient management, and decreasing mortality.


   Materials and Methods
Top
 Abstract
 Introduction
 Materials and Methods
Results
 Discussion
 Acknowledgements
 References
 
Patient samples for this study were collected from Harborview Medical Center (HMC), and normal control samples were collected from volunteers at the Seattle division of the Puget Sound Health Care System VA. HMC is a level 1 northwest regional trauma center. All procedures were in accordance with the ethical standards established by the UW Institutional Review Board.

IMA was determined by the ACB assay using kits provided by Ischemia Technologies, Inc., (Denver, CO) and analyzed with the Roche/Hitachi modular analytical system (Roche Diagnostics, Indianapolis, IN). The ACB assay uses dithiothreitol (DTT) as a colorimetric indicator to measure cobalt that is not bound to the N-terminus of serum albumin. The absorbance is measured by spectrophotometry at 550 nm and the results are reported as U/ml.

The ACB assay is based on the concept that myocardial ischemia creates an environment that alters the N-terminal structure of albumin. This is manifested by decreased exogenous Co(II) binding [25]. However, the biochemical mechanism that leads to altered Co(II) to albumin during ischemia is not understood. IMA concentrations can be determined by addition of a known amount of Co(II) to a specimen and measuring the unbound Co(II) by colorimetirc assay using DTT. There is an inverse relationship between the amount of ACB and color intensity.

Method validation and clinical decision points were evaluated using criteria proposed by Ischemia Technologies, Inc. Cardiac troponin I results were determined via microparticle enzyme immunoassay on an AxSYM analyzer (Abbott Laboratories, Abbott Park, IL). For this study, troponin I values <0.5 ng/ ml were considered negative for ischemia, and values >5.0 ng/ml were considered positive.

A total of 200 prospectively enrolled subjects were divided into 3 groups. The first group was composed of 69 volunteers (mean age, 49 yr) with no history of heart disease, chest pain, or any other ischemic disease. These subjects served as the normal control group. The second group was composed of 78 subjects who were seen at the HMC ER with chest pain and whose initial and subsequent troponin results were all negative (mean age, 66 yr). Patients in this group, identified as "non-converters," were subsequently discharged with a diagnosis other than MI. The patients’ charts were reviewed to determine if any non-converters could be identified as experiencing unstable angina (UA) at the time of presentation. The third group consisted of 53 subjects who were seen at the HMC ER with chest pain and whose initial troponin result was negative, but subsequent troponin results were positive (mean age 64 yr). Patients in this group, identified as "converters," were diagnosed as ACS and/or MI.

The ACB assays were performed to determine IMA results from the first drawn troponin sample in the non-converters and the converters. All of the first-drawn samples in both groups were negative for troponin I. Patients presenting with an elevated first-draw troponin were excluded in this study. In addition, none of the patients had cirrhosis or lung cancer.

Blood samples were collected in red-top Vacutainer tubes (Becton, Dickinson and Co, New Brunswick, NJ) in the absence of anticoagulants; serum was separated by centrifugation. The sera from all first-draw negative troponin samples reported by the laboratory were immediately frozen at –20°C. All patient samples were later reviewed and assigned as either non-converters or converters. IMA values are unaffected when the serum samples are frozen within 1 hr after blood collection and then assayed within 1 hr after thawing [19,25].

Statistical analyses employed a statistical package for Microsoft Excel (Analyse-it version 1.68 (Oxon, UK)). Parametric and non-parametric measures among the 3 groups were compared by box-whisker plots. Receiver operator characteristic (ROC) curve analysis was used to show, for each possible decision threshold, the percentage of abnormal subjects correctly diagnosed (ie, true positives) versus the percentage of normal subjects incorrectly diagnosed as abnormal (ie, false positives).


   Results
Top
 Abstract
 Introduction
 Materials and Methods
 Results
Discussion
 Acknowledgements
 References
 
The clinical characteristics of the 3 study groups are presented in Fig. 1Go. There were 69 subjects identified as "normals" whose average age was 49 yr and average IMA value was 89 U/ml. This population comprised individuals not experiencing chest pain at the time of blood draw and without a history of chest pain or an ischemic process. Seventy-eight of the 200 subjects were identified as non-converters. The average age of this group was 66 yr, and the average IMA was 100 U/ml. This group included 9 subjects who were later identified as experiencing unstable angina at the time of sample collection. The average age of these nine individuals was 68 yr, and their average IMA was 112 U/mL (range = 101 to 126 U/ml). The third group, containing 53 subjects, was identified as the converters. Their mean age was 64 yr, and they had an average IMA of 126 U/ ml. IMA values for both abnormal populations were significantly different from each other and from the normal group (p <0.0001).



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  		Fig. 1. Comparison of 3 study groups (normals, non-converters, converters). The dotted arrows indicate that 9 of the 78 subjects in the non-converters group had unstable angina and likely belong in the converters group. Values are mean ± SD.

 
The ROC curve evaluating the group of non-converters compared to the group of converters is shown in Fig. 2Go. The area under the curve is 0.89. A cutoff of 97 U/mL appears to be optimal for distinction between these 2 populations, giving 98% sensitivity and 45% specificity.



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  		Fig. 2. ROC curve for non-converters vs converters, with the unstable angina group in the originally assigned non-converters group.

 
Fig. 3Go shows the ROC curve generated when 9 unstable angina patients from the group of non-converters were moved to the group of converters. The area under this curve was 0.91, and a cutoff of 96 U/mL gives 98% sensitivity and 48% specificity. ROC curves were also generated for comparing the normals to non-converters and normals to converters (data not shown). These curves were generated without transferring the 9 unstable angina patients to the converters group. The ROC curve comparing the normal population to the converters shows an area of 0.99, and an IMA cutoff of 85 U/ml gives 100% sensitivity and 38% specificity. Using the 97 U/ml cutoff, which is just above the lowest value in the converters group, gives a sensitivity of 98% and a specificity of 91%. The ROC curve comparing the normal population to the non-converters shows an area of 0.77, indicating a less striking distinction between these two populations. Using an 85 U/ml cutoff appears to be the best distinguishing point, giving an 86% sensitivity and 38% specificity.



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  		Fig. 3. ROC curve for non-converters vs converters, with the unstable angina patients reassigned to the converters group.

 

   Discussion
Top
 Abstract
 Introduction
 Materials and Methods
 Results
 Discussion
Acknowledgements
 References
 
Perhaps this study can serve as a guide to correct current problems in chest pain management in many different facilities. For example, the new VA organizational plan, entitled "Capital Asset Realignment for Enhanced Services," will require remediation at many levels if the overhauling goals of the program are to succeed. The present study suggests that the ACB assay could become a key component in improving the cardiac care program throughout the VA system and may be extrapolated to improve chest pain management throughout the USA. Part of the problem of assessing ACS patients in the ER is that an abnormal ECG rarely follows transient myocardial ischemia [26]. The ER ECG readings are generally normal in about 50% of patients who present with ACS [27]. Furthermore, cardiac injury markers may identify only post-ischemic events, indicating recent irreversible damaged myocardium due to an acute MI.

In this study, the significantly higher IMA value in the converters is likely attributed to an ischemic state that subsequently manifests in myocardial events leading to a positive troponin result shortly after presentation. The mean value of 126 U/ml for this group suggests that these patients were ischemic at presentation. While the mean value for the converters was significantly higher than that of the non-converters, the non-converters were different from the normals. To compare these groups and possibly correct for some of this difference, we retrospectively identified 9 of the 78 non-converters as experiencing unstable angina at the time of presentation. These 9 subjects were moved to the group of converters. The resulting changes in means did not alter the level of significance. However, the ROC curve comparing the non-converters to converters became a slightly stronger distinguisher.

This study suggests that 96 U/ml may be the IMA cutoff value that our facility should use for clinical practice. An IMA value of 96 U/ml was the lowest value in our converters group and appeared to be the optimal decision point when analyzing the ROC curve, comparing the non-converters to the converters (with the 9 unstable angina patients).

Our apparent cut-off value of 96 U/ml is higher than the 85 U/ml value that was recommended by the manufacturer, Ischemia Technologies, Inc. (IMA ACB Test packet insert). However, as shown by Ischemia Technologies, the 85 U/ml cut-off value generates nearly a 100% sensitivity when comparing the normals to both the non-converters and the converters. We consider it essential to make the appropriate population comparisons when choosing a decision point. Discrepancies in the cut-off value may reflect differences in our patient selection and population. Specifically, the selection of these patients was designed so that (a) they are the highest risk patients and possibly those experiencing the greatest degree of ischemia, (b) their ischemia may have been irreversible and progressed to necrosis, and (c) IMA levels may have been at their peak because their troponin result was negative at presentation and subsequently became positive. In addition to these factors, left ventricular hypertrophy was reported to contribute to slightly elevated IMA levels [28]. Perhaps identification of these individuals might further facilitate a cut-off point selection.

As previously stated, a potential benefit that the ACB assay offers is monetary savings by decreasing the length of hospital stay and reducing costs of subsequent monitoring. More important than saving money, the ACB assay may hold promise in decreasing mortality by possibly suggesting subsequent positive troponin results in chest pain presenters. While the assay’s immediate future functions are as a rule-out test, there is interest that elevated IMA levels might serve a more primary role in predicting an AMI [20]. The usefulness and cost effectiveness of ACB assays should be independently determined at each facility that considers offering this test. Because of short reagent stability, it is important for each laboratory to assess its testing volume. The test may be best suited for a high-volume trauma hospital. In the future, a more stabilized reagent system may make it feasible for smaller facilities to offer the ACB assay.

While the specific molecular alterations and events that induce albumin modification have been only partially elucidated [29–33], the high sensitivity of the ACB assay as an ACS rule-out marker has been repeatedly demonstrated [19–20,30]. Perhaps better understanding of how myocardial ischemic and reperfusion events produce changes at the subcellular level will be necessary in order to develop a true ACS rule-out gold standard. Future studies of ACB testing in relation to improved cardiac care programs should include patient follow-up and risk stratification.


   Acknowledgements
Top
 Abstract
 Introduction
 Materials and Methods
 Results
 Discussion
 Acknowledgements
References
 
We thank Mr. Michael Ka and all of the technicians at Harborview Medical Center and the Seattle VA hospitals for assistance in sample collection. We thank Drs. Hossein Sadrzadeh and Pete Rainey for discussions during the preparation of this manuscript. We thank Ischemia Technologies, Inc., for help in conducting this study.


   References
Top
 Abstract
 Introduction
 Materials and Methods
 Results
 Discussion
 Acknowledgements
 References
 

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