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Cardiac array

Product Method Size Catalog Price
Cardiac array B A T (evidence investigatorâ„¢) 54 Biochips EV3511 POA
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Intended Use

The Evidence Investigator Cardiac Plus array is to be used for the in-vitro simultaneous quantitative detection of multiple related immunoassays (in parallel) from a single patient sample. The Cardiac Plus Array consists of 6 assays: Troponin I, Myoglobin, Creatine Kinase-MB, Carbonic Anhydrase III, heart type Fatty Acid Binding Protein and Glycogen Phosphorylase BB. The Evidence Investigator Cardiac Plus Array is for research only and not for diagnostic purposes.

Clinical Significance

The biochemical, physiological and mechanical functioning of the heart can be affected by many different disorders.  The most common form of heart disease is coronary artery disease. This disease involves arteriosclerosis, stable and unstable angina, an acute myocardial infarction and can lead to cardiac death(1).

At different stages during a cardiac event markers are released which can be measured and therefore allow clinicians to make more accurate clinical decisions when diagnosing a patients heart condition and stage of disease progression.

Currently, diagnosis of myocardial injury involves determination of serum levels of different proteins and enzymes, which are markers of myocardial injury.

Principle

Biochip Array Technology is used to perform simultaneous quantitative detection of multiple analytes from a single patient sample. The core technology is the Randox Biochip, a solid-state device containing an array of discrete test regions containing immobilized antibodies specific to different markers. A sandwich chemiluminescent immunoassay is employed. Increased levels of these analytes in a specimen will lead to increased binding of antibody labeled with HRP and thus an increase in the chemiluminescent signal emitted.

The light signal generated from each of the test regions on the biochip is detected using digital imaging technology and compared to that from a stored calibration curve. From this the concentration is calculated.

Several different immunoassay based multi-analyte panels have been developed for use on Evidence Investigator. The Evidence Investigator Cardiac Plus Array quantitatively measures Myoglobin, Troponin I, Creatine Kinase MB , Carbonic Anhydrase III, Heart Type Fatty Acid Binding Protein and Glycogen Phosphorylase BB simultaneously.

REFERENCES

2. Wild, D. The Immunology Handbook, Nature Publishing Group, United Kingdom , pp 623-634.

Troponin I (cTnI) Assay

Intended Use

The Evidence Investigator Troponin I test has been designed for the quantitative measurement of cardiac Troponin I in human serum. This test is for research only, not for use in diagnostic purposes.

Clinical Significance

Cardiac Troponin I (cTnI), a myofibrillar protein with a molecular mass of 25 kDa, is part of a complex of proteins that regulates the contraction of the heart muscle. The troponin complex consists of actin, myosin and troponin. Troponin consists of three subunits; T, I and C. It is cTnI that functions in regulating the actinomyosin ATPase and so prevents muscle contraction in the absence of calcium. Only 2% of the cTnI is free in the cytosol, the rest is myofibrillar-bound. Troponin I exists in several isoforms but the cardiac isoform, cTnI, is specific to heart tissue. cTnI measurements are therefore completely specific for cardiac damage and so it is one of the common biochemical markers used in the clinical decision making to confirm or exclude a diagnosis of Acute Myocardial Infarction (AMI) (1, 2).

After an AMI, damage to the cardiac myocytes causes cTnI to leak out of these cardiac cells and enter into the circulation. cTnI rises 4-8h post-AMI, peaks between 14 and 36 h, and remains elevated for 3-7 days (4). Over the succeeding days after an AMI, there is degradation of the myofibrillar elements and a release of the ternary troponin complex. 

cTnI is a useful assay for determining the risk of patients with unstable angina. Clinical trials have shown that patients with unstable angina, therefore have suffered minor myocardial injury, and if they have an abnormal troponin level they have a higher incidence of cardiac death or acute myocardial infarction within the following four weeks than a group of patients with unstable angina who have normal troponin. By measuring cTnI it may also be an important marker for assessing whether patients should receive antithrombotic and anti-platelet drugs as those with a high cardiac troponin will benefit most from these therapies(3).

As mentioned this assay has a high clinical specificity for heart damage and is elevated after AMI. The measurement of elevated cTnI with normal levels of CK-MB in the serum indicates myocardial damage not detected by conventional markers (2).

Principle

The Evidence Investigator cardiac Troponin I Assay is a sandwich chemiluminescent immunoassay for the detection of cardiac Troponin I in serum. 

REFERENCES

1   Wild D. (ed), The Immunoassay Handbook, second edition, Nature Publishing Group, London, Basingstoke, New York, 2001

2   Collinson PO, Troponin T or Troponin I or CK-MB (or none), European Heart Journal, 1998; 19: (supplement N), N16-N24

3.  Wu AHB and Feng YJ, Biochemical differences between cTnT and cTnI and their clinical significance for diagnosis of acute coronary syndromes, European Heart Journal, 1998; 19: Supplement N, N25-N29

4.  Apple FS,  Cardiac Markers, Edited by Alan H B. Wu, Humana Press Inc., Totowa, New Jersey, 1998

Myoglobin (MYO) Assay

Intended Use

The Evidence Investigator Myoglobin test has been designed for the quantitative measurement of myoglobin in human serum specimens. This test is for research only, not for use in diagnostic purposes.

Clinical Significance

Myoglobin is a haeme protein with a low molecular weight of 17.8 kDa. It is located inside the muscle fibres of the heart and skeletal muscle(1). In the heart, the myoglobin delivers oxygen to the myocardium (the middle muscular layer of the heart wall) and it is Myoglobin that gives the myocardium its deep red color(2).

Myoglobin is released into the bloodstream after an Acute Myocardial Infarction (AMI) occurs and damages the cell membrane of the muscle cells. Elevated levels of Myoglobin can be detected between 2 and 6 hours after an infarction, earlier than most other biochemical markers, with levels peaking within 5 to 18 hours(1, 2).

Myoglobin has been found to be a more reliable marker and hence more useful than CK-MB or Troponin I or T for ruling out an AMI during the critical period when decisions are made regarding chest pain patients(1).

Simultaneous measurement of a skeletal muscle specific marker such as carbonic anhydrase III, heart type fatty acid binding protein or a cardiac specific marker such as troponin I as well as myoglobin has been suggested to be a good strategy for diagnosis(2).

Principle

The Evidence Investigator Myoglobin Assay is a sandwich chemiluminescent immunoassay for the detection of cardiac Myoglobin in serum. 

REFERENCES

1.  Tietz NW, Clinical Guide to Laboratory tests, second edition, WB Saunders Company 1990

2.  Wild D. (ed), The Immunoassay Handbook, second edition, Nature Publishing Group, London, Basingstoke, New York, 2001

Creatine Kinase –MB (CK-MB) Assay

Intended Use

The Evidence Investigator Creatine Kinase-MB test has been designed for the quantitative measurement of cardiac Creatine Kinase-MB (CK-MB) in human serum specimens. This test is for research only, not for use in diagnostic purposes.

Clinical Significance

Creatine Kinase is a dimeric protein composed of two enzymatically active M (muscle-type) and B (brain-type) subunits. It has three cytosolic isoenzymes and CK-MB is the isomeric form described here. CK-MB is found predominantly in cardiac muscle and makes up 30% of the total CK in cardiac muscle. However, it is not cardio-specific, a very small proportion - less than 1% of the total CK-MB is found in skeletal muscle.

Measurement of CK-MB instead of total CK enhances the specificity of the assay as it is more specific to cardiac damage. After an AMI, the level of CK-MB in the blood will increase within the first 4-6 hours after the onset of chest pain. The level of CK-MB will then peak at 18-24 hours and return to normal within 72 hours. The activity of CK-MB declines mono-exponentially, if there are no further events of ischemic injury(1).

Principle

The Evidence Investigator CK-MB Assay is a sandwich chemiluminescent immunoassay for the detection of cardiac CK-MB in serum. 

REFERENCES

2. Wild D. (ed), The Immunoassay Handbook, second edition, Nature Publishing Group, London, Basingstoke, New York, 2001

3. Tietz NW, Clinical Guide to Laboratory tests, second edition, WB Saunders Company, 1990

Carbonic Anhydrase III (CAIII) Assay

Intended Use

The Evidence Investigator CAIII test has been designed for the quantitative measurement of CAIII in human serum specimens. This test is for research only, not for use in diagnostic purposes.

Clinical Significance

Carbonic anhydrase III (CAIII), a 28kDa cytoplasmic protein, is found in high amounts in type I (slow-twitch) skeletal muscle but it is not present in heart muscle.

In patients who have had an AMI, the level of CAIII is normal and therefore measuring CAIII alone will not give any clinical advantage over myoglobin(1). However, it has been suggested by measuring myoglobin and CAIII this can differentiate between myocardial and skeletal muscle damage (2). For patients who are found to be positive for myoglobin and negative for CAIII this strongly indicates that the source of serum myoglobin is most likely to be cardiac in origin. These results are different than when the injury originates from skeletal muscles whereby although the level of myoglobin is high the level of CAIII is also high, indicating the damage may not be cardiac in origin. Therefore CAIII when measured with myoglobin will increase the specificity of the myoglobin assay for AMI (3,4).

Principle

The Evidence Investigator CAIII Assay is a sandwich chemiluminescent immunoassay for the detection of CAIII in serum. 

REFERENCES

Azzazy HME, Cummings PJ, Ambrozak DR and Christenson RH, Production and Characterization of Monoclonal Antibodies to Human Carbonic Anhydrase III, Hybridoma, 1998; 17(6): 553-558

2. Brogan GX, Vuori J, Friedman S, McCuskey CF,

Thode HC, Vaananen HK, Cooling DS and Bock JL, Improved Specificity of Myogobin Plus Carbonic Anhydrase Assay Versus that of Creatine Kinase-MB for Early Diagnosis of Acute Myocardial Infarction, Annals of Emergency Medicine, January 1996, 27(1), 22-27

 3. Wild D. (ed), The Immunoassay Handbook, second edition, Nature Publishing Group, London, Basingstoke, New York, 2001

4.  Väänänen HK, Syrjäla H. Rahkila P, Vuori J, Melamies LM, Myllylä V and Takala TES, Serum Carbonic Anhydrase III and Myoglobin Concentrations in Acute Myocardial Infarction, Clinical Chemistry, 1990; 36(4), 635-638

Glycogen Phosphorylase BB (GPBB) Assay

Intended Use

The Evidence Investigator GPBB test has been designed for the quantitative measurement of glycogen phosphorylase BB in human serum specimens. This test is for research only, not for use in diagnostic purposes.

Clinical Significance

In recent years, there has been an intensive search for markers to detect myocardial injury. Early identification and confirmation of acute myocardial infarction (AMI) is essential for making important decisions affecting treatment and also for general patient care(1).

Creatine Kinase MB (CK-MB), a biochemical marker of acute myocardial infarction (AMI) has been the accepted standard for many years but now its status is being challenged(2). Rabitzsch et al. (1995) have presented preliminary findings for the clinical utility of Glycogen Phosphorylase BB (GPBB) as a sensitive marker for acute ischemic coronary syndromes(1).

Glycogen Phosphorylase has three isoenzymic forms and the proportion of each varies between tissues. GPBB is found in the brain but it is also the principal isoform in the heart, while GPMM and GPLL predominate in skeletal muscle and the liver, respectively(3).  The physiological form of GP is a dimer, which is composed of two identical subunits. The molecular weight of GPBB as a monomer is approximately 94 kD.

GPBB is a key enzyme of glycogenolysis and its physical role is to provide the fuel for the energy supply for muscle contraction. In cardiomyocytes, GP is associated with glycogen and the sarcoplasmatic reticulum and forms a macromolecular complex. The degree of association of GP with this complex depends on the metabolic state of the myocardium. Mair (1998)(4) has explained the release of GPBB as requiring both a burst in glycogenolysis as well as an increase in plasma membrane permeability. Both of these events occur in the myocardium, when it is damaged by severe ischemia. Therefore, GPBB has been indicated as a promising analyte for the detection of ischemic myocardial damage (4 )

GPBB appears to be released early from injured myocardial cells reflecting the burst in glyconeolysis associated with myocardial ischemia and AMI and this is supported by a rapid increase in serum GPBB activity, which has been noted in patients with AMI. Rabitzsch et al (1995) results have indicated that GPBB may be one of the most sensitive markers in the early diagnosis of AMI. GPBB can be picked up within 4 hours of the onset of chest pain( 2, 5).

Principle

The Evidence Investigator GPBB Assay is a sandwich chemiluminescent immunoassay for the detection of GPBB in serum.

REFERENCES

6. Rabitzsch G, Mair J, Lechleitner P, Noll F, Hofmann U, Krause EG, et al. Immunoenzymetric assay of human glycogen phosphorylase isoenzyme BB in diagnosis of ischemic myocardial injury, Clinical Chemistry, 1995; 41(966): 251-64

7. Apple FS, Glycogen Phosphorylase BB and other cardiac proteins: Challenges to Creatine Kinase MB as the Marker for Detecting Myocardial injury, Clin Chem, 1995; 41/7: 963-965

8. Hofmann U, Rabitzsch G, Loster K, Handschack W, Noll F and Krause EG, Immuenzymometric assay for the heart specific glycogen phosphorylase BB in human serum using monoclonal antibodies, Biomed Biochim, Acta 48, 1989; 2/3: S132-S136

9. Mair, J. Glycogen phosphorylase isoenzyme BB to diagnose ischemic myocardial damage, Clinica Chimica, 1998;  Acta 272: 79-86

10. Rabitzsch G, Mair J, Lechleitner P, Noll F, Hofmann U, Krause EG, Dienstl F and Puschendorf B. Isoenzyme BB of glycogen phosphorylase b and myocardial infarction, Lancet, 1993; 341: 1032-1033

Heart Type Fatty-Acid Binding Protein (h-FABP) Assay

Intended Use

The Evidence Investigator h-FABP test has been designed for the quantitative measurement of h-FABP in human serum specimens. This test is for research only, not for use in diagnostic purposes.

Clinical Significance

Fatty Acid Binding Protein (FABP) is present in the cytoplasm of myocytes. It has an important role in lipid metabolism, binding long chain fatty acids and carrying them in the blood. The heart type isoenzyme of FABP is found in the heart and the skeletal muscles. Like myoglobin, FABP is a low molecular weight protein with a molecular weight of 14-15 kDa and it is also released within 3 - 6 hours after the onset of chest pain (1).

The release of proteins into plasma due to myocardial muscle damage are important diagnostic parameters to assist in myocardial infarction diagnosis. Like myoglobin, FABP is an early marker for Acute Myocardial Infarction (AMI) (2). h-FABP has been shown to aid in the diagnosis of AM I complementing Cardiac Troponin I as it is elevated at a much earlier timepoint. ((3,4))

Principle

The Evidence Investigator cardiac h-FABP Assay is a sandwich chemiluminescent immunoassay for the detection of h-FABP in serum. 

REFERENCES

1. Wild D. (ed), The Immunoassay Handbook, second edition, Nature Publishing Group, London, Basingstoke, New York, 2001

2.  Siegmann-Thoss C, Renneberg R, Glatz JFC, Spener F, Enzyme immunosensor for diagnosis of myocardial infarction, Sensors and Actuators B 30, 1996; 71-76

3.  Mc Cann CJ. etal. Novel Biomarkers in Early Diagnosis of Acute Myocardial Infarction compared with Cardiac Troponin T. Eur. Heart. J. 2008: 29; 2843-2850.

4.  Body R., Heart Fatty Acid Binding Protein for Rapid Diagnosis of Acute Myocardial Infarction in the Emergency Department. Emerg. Med. J. 2009: 26; 519-522.