Posts Tagged ‘CK-MB Rapid Test’
At DIAGNOSTIC AUTOMATION Inc. (focusing on ELISA Kits) we take advantage of an influx of new technologies and information incorporating them into novel tests which enables us to offer innovative diagnostic tests every day. In addition to our 3 in 1 CARDIAC MARKERS TEST (cardiac elisa kits: Troponin I elisa kit, CK-MB elisa kit, myoglobin elisa kit)
Los Angeles-based Diagnostic Automation Inc. is pleased to offer three additional tests in forms of cardiac elisa kits (Cardiac Markers Rapid Tests) to customers around the world available in cassette format. These elisa kit tests are immunochromatography assays for the determination of three biochemical markers: C-reactive protein (CRP) ELISA kit, Lp(a) elisa kit, and Digoxin ELISA Kit, simultaneously in human serum or whole blood.
C-reactive protein (CRP): CPR is composed of five protein subunits, produced by the liver and found in blood that plays a key role in the innate immune response. The gene for this protein is on chromosome 1q21-q23. CRP is a marker for inflammation within the body and has been promoted as a screening test for coronary artery disease . Studies show that elevated levels of CRP are associated with a greater risk of psychological stress and clinical depression. Elevated levels of CRP may be indicative of elevated levels of certain cytokines, which can increase feelings of stress or depression. On the other hand, it is possible that depression or stress is a cause of elevated level of CRP. Irrespective of other factors, the study found that healthy people with CRP level above 3mg/liter had two to three fold increased risk of developing depression .
Model of C-reactive protein molecular structure 
Diagnostic applications: Role in cardiovascular disease
Strong evidence indicates that patients with elevated basal levels of CRP are at an increased risk of hypertension, heart diseases, and diabetes. C-reactive protein (CRP) is proposed as a screening test for predicting risk and guiding preventive approaches in cardiac diseases . Normal concentration in healthy human serum is usually lower than 10 mg/L, slightly increasing with aging. Higher levels are found in late pregnant women, mild inflammation and viral infections (10–40 mg/L), active inflammation, bacterial infection (40–200 mg/L), severe bacterial infections and burns (>200 mg/L). The half-life of CRP is constant, thus, CRP level is mainly determined by the rate of its production. A level above 2.4 mg/L has been associated with a doubled risk of a coronary event compared to levels below 1 mg/L. Inflammation can play an important role in atherosclerosis, the process in which fatty deposits build up in coronary arteries. Interest in CRP originated when studies found that patients with unstable angina or chest pain had high levels of this marker. Researchers found that CRP could be used to predict who would go on to have a heart attack. Moreover, in a meta-analysis of 20 studies involving 1,466 patients with coronary artery disease, CRP levels were found to be reduced after exercise interventions. Among those studies, higher CRP concentrations or poorer lipid profiles before beginning exercise were associated with greater reductions in CRP . Other studies have shown that CRP isn’t a predictor of heart attack risk in people without symptoms of heart disease.
(CRP) ELISA kit: At Diagnostic Automation using elisa kit, CRP level can be measured with a simple blood test . There are scientific evidences that by treating people with high CRP levels, their likelihood of developing a heart attack or stroke will decrease.
How can CRP values predict potential heart disease?
According to the American Heart Association (AHA) and the Center for Disease Control (CDC), the following guidelines are recommended for the assessment of cardiovascular risk in regards to CRP levels:
CRP is 1 milligram (mg) per liter or less , Low risk for cardiovascular disease
CRP is between 1 and 3 mg per liter, Moderate risk for cardiovascular disease
CRP greater than 3 mg per liter, High risk for cardiovascular disease
CRP level of greater than 10 mg per liter may be seen in an acute plaque rupture such as, a heart attack or stroke, provided there is no other explanation for the elevated level such as other inflammatory or infectious diseases
The CRP level can provide additional information about an individual’s cardiovascular risk in conjunction with other known cardiac risk factors, such as, diabetes mellitus, high blood pressure, high cholesterol, obesity, age, and smoking. Some experts recommend checking the serum CRP level routinely along with the cholesterol level. Ideally, for cardiac risk testing, it is advisable to use the average between 2 separate CRP levels drawn 2 weeks part. According to the American Heart Association checking the CRP level for the entire adult population is not recommended.
Lp(a): Lipoprotein (a), also called Lp(a) is a subclass of Lipoprotein consists of an LDL-like particle and the specific apolipoprotein(a) [apo(a)]. Lp(a) plasma concentrations are highly heritable and mainly controlled by the apolipoprotein(a) gene (LPA) positioned on human chromosome 6q26-27. The protein encoded by this gene is a serine proteinase that inhibits the activity of tissue-type plasminogen activator. Proteolytically cleaved portion of this protein results in fragments that attach to atherosclerotic lesions and promote thrombogenesis. Elevated plasma levels of this protein are linked to atherosclerosis .
A strong correlation between elevated level of Lp(a) and heart disease was confirmed by many studies which led to the consensus that Lp(a) is an important independent predictor of heart disease . Evidence from several studies suggest that elevated plasma Lp(a) increases the cardiac diseases risk associated with more traditional risk factors. The clinical use of Lp(a) measurement is to assess the risk of cardiovascular disease. We use a an elisa kit to measure this specific type of lipoprotein called lipoprotein-a, or Lp(a) in blood. Normal values are below 30 mg/dL (milligrams per deciliter). Normal value ranges may vary slightly among different laboratories. Higher than normal values of Lp(a) are associated with a high risk for atherosclerosis, stroke, and heart attack. Substantial increases are secondarily observed in nephrotic syndrome and end-stage renal disease, however environmental factors such as diet, and exercise do not have a major impact on the level of Lp(a). Although Lp(a) is considered a risk factor for heart disease, but the plasma Lp(a) determinations should be limited to either patients at high risk for the development of cardiac diseases or patients at borderline risk for the development of cardiac diseases in whom uncertainty may exist about how aggressively to treat modifiable risk factors such as elevated LDL and cholesterol . Multiple studies have shown that Aspirin and Niacin (Vitamin B3) in high doses, available by prescription known to significantly reduce the level of Lp(a) in some individual with high Lp(a) level
At Diagnostic Automation Lp(a) level can be measured with a simple blood test using Lp(a) ELISA kit with fast and accurate results in 120 minutes.
Model of Lipoprotein, Lp(a) molecular structure 
Digoxin: Digoxin is a cardiac glycoside which has different products with significant bioavailability and it is used to treat congestive heart failure, atrial fibrillation and paroxysmal atrial tachycardia . Many drugs interact with digoxin, often requiring an adjustment of the digoxin dose . Digoxin is cleared by the kidney and its clearance is low in premature neonates, increases in full term neonates, reaches a maximum in infants and decreases slowly during childhood and adulthood, with an apparent increase in susceptibility to toxicity with age [11, 12]. The circulating half-life is 1 to 1.6 days in patients with normal renal function. The myocardial concentrations of digoxin to serum levels remain relatively constant during normal renal function.
This distribution ratio of digoxin is approximately 29 to 1 between the heart and serum. Thus, monitoring digoxin therapy by measurement of serum levels is feasible from the pharmacological standpoint, since serum levels are related to tissue levels following post-absorption equilibration.
Recent study has shown that Digoxin has at least 2-compartment behavior. Its pharmacologic and clinical effects correlate not with serum digoxin concentrations but with those in the peripheral non-serum compartment. Digoxin improves the strength of myocardial contraction and results in the beneficial effects of increased cardiac output, decreased heart size, decreased venous pressure, and decreased blood volume.
Digoxin therapy also results in stabilized and slowed ventricular pulse rate. These therapeutic effects are produced through a network of direct and indirect interactions upon the myocardium, blood vessels, and the autonomic nervous system. Moreover, recent study show that Digoxin induces calcium uptake into cells by forming transmembrane calcium channels .
Digoxin is well absorbed after oral administration and is widely distributed to tissues, especially the heart, kidney, and liver. A number of factors can alter normal absorption, distribution, and bioavailability of the drug, including naturally occurring enteric bacteria in the bowel, presence of food in the gut, strenuous physical activity, ingestion of quinine or quinidine, and concomitant use of a wide range of drugs. Children generally require higher concentrations of digoxin.
After oral administration, there is an early rise in serum concentration. Equilibration of serum and tissue levels reaches at approximately 6 to 8 hours. For this reason, blood specimens for digoxin analysis should be drawn at least 6 to 8 hours after drug administration. Digoxin is excreted primarily in the urine. The average elimination half-life is 36 to 40 hours, but may be considerably prolonged in those with renal disease, causing digoxin accumulation and toxicity.
Symptoms of digoxin toxicity often mimic the cardiac arrhythmia’s for which the drug was originally prescribed for example, heart block and heart failure. Other typical symptoms of toxicity include gastrointestinal effects, including anorexia, nausea, vomiting, abdominal pain and diarrhea, and neuropsychologic symptoms, such as fatigue, malaise, dizziness, clouded or blurred vision, visual and auditory hallucination, paranoid ideation, and depression.
Model of Digoxin molecular structure 
A practical and sensitive method of digoxin quantitation in serum is by Digoxin ELISA kit which we offer at Diagnostic Automation. When digoxin is first prescribed, it takes about 1 or 2 weeks to stabilize in the blood and in the target organ which is heart. Digoxin first test should be done at around that time, in order to give an accurate reflection of the blood level and correct dosage of digoxin. Test performed before this period, may not show the correct levels in the blood.
The age or gender of the person being tested, health history, the method used for the test, and many other factors may affect when and how often a lab test is required. The therapeutic range is 0.8 to 2.0ng/mL for those being treated for heart failure and levels >4.0 ng/mL may be potentially life-threatening. This range for digoxin has been established over time. Once the dosage level is determined, digoxin levels are monitored routinely, at a frequency determined by the doctor, to verify correct dosage and if any changes occur in drug source, dosage, or other medications taken at the same time. Recent studies may help to improve patient selection for digoxin therapy, since Digoxin therapy may improve the prognosis of advanced heart failure patients with atrial fibrillation. However, no benefit of digoxin was demonstrated for patients in with sinus rhythm 
Routine measurement of serum digoxin concentration is probably not necessary in stable patients . Laboratory tests may be done for many reasons. Tests are performed for routine health screenings or if a disease or toxicity is suspected. Lab tests may be used to determine if a medical condition is improving or worsening. Lab tests may also be used to measure the success or failure of a medication or treatment plan. Moreover, Digoxin measurement is necessary in the following situations:
To check if a patient has reached steady state with a new digoxin dose
Following significant change in renal function
Following addition or discontinuation of a potentially interacting drug
Follow up on signs or symptoms consistent with digoxin toxicity
After introduction of any medication which may affect the levels of digoxin in the blood
After intestinal or stomach illness which also affect the absorption of digoxin
In patients with any kidney problems, which affect the secretion of digoxin
Patients with cancer or thyroid disease who have altered levels of digoxin in the blood
In patients undergoing therapy with high biotin doses (>5 mg/day), specimens should be drawn at least 8 hours after the last biotin administration. “Digoxin-like” immunoreactive factors may cause falsely-elevated values in some neonates and patients with advanced liver or renal disease.
1.Thompson D, Pepys MB, Wood SP. The physiological structure of human C-reactive protein and its complex with phosphocholine. Structure . 1999, 7 (2): 169–77
2. Clearfield MB . C-reactive protein: a new risk assessment tool for cardiovascular disease. The Journal of the American Osteopathic Association. 2005, 105 (9): 409–16.
3. Marie Kim Wium-Andersen, David Dynnes Ørsted, Sune Fallgaard Nielsen, MScEE, Børge Grønne Nordestgaard. Elevated C-Reactive Protein Levels, Psychological Distress, and Depression in 73 131 Individuals. JAMA Psychiatry. 2013;70(2):176-184.
4. Ridker PM. Clinical application of C-reactive protein for cardiovascular disease detection and prevention. Circulation. 2003;107: 363–369
5. Christopher J.K et al. Effect of six months’ exercise training on C-reactive protein levels in healthy elderly subjects. J Am Coll Cardiol. 2004;44(12):2411-2413.
6. Mahley RW, Weisgraber KH, Bersot TP. Disorders of lipid metabolism. In: Kronenberg HM, Melmed S, Polonsky KS, Larsen PR, eds. Williams Textbook of Endocrinology . 2008:chap 36, 11th ed. Philadelphia, Pa: Saunders Elsevier;
7. Nordestgaard BG, Chapman MJ, Ray K, et al. Lipoprotein(a) as a cardiovascular risk factor: current status. Eur Heart J. 2010;31:2844-2853.
8. Kamstrup PR, Tybjærg-Hansen A, Nordestgaard BG. “Lipoprotein(a) and risk of myocardial infarction–genetic epidemiologic evidence of causality”. Scand. J. Clin. Lab. Invest. 2011, 71 (2): 87–93.
9. Jortani SA, Voldew R Jr: Digoxin and its related endogenous factors. Crit Rev Clin Lab Sci 1997;34:225-274
10. Doherty, J.E. and Kane, J.J: Clinical Pharmacology of Digitalis Glycosides. ANN. REV. MED, 1975. 26: 159
11. Butler, V.P. Assays of Digitalis in blood. PROG. CARDOVASC. DIS., 1972. 14:571
12. Lewis RP. Clinical use of serum digoxin concentrations. Am J Cardiol 1992; 69:97G-107G
13. Kratz A, Ferraro M, Sluss PM, et al: Case records of the Massachusetts General Hospital: laboratory values. N Engl J Med 2004; 351(15):1549-1563
14. Arispe N, Diaz JC, Simakova O, Pollard HB. Heart failure drug digitoxin induces calcium uptake into cells by forming transmembrane calcium channels. Proc Natl Acad Sci U S A. 2008 19;105(7):2610-5
Our daily aim includes saving patients and helping people around the world by providing new and advanced diagnostic products. In one hand growing demand for highly effective and impactful medicines is being driven by an aging population and economic pressures. On the other hand the availability of genomic and proteomic tools and system biology approaches to identify novel biomarkers have permitted additional disease biomarkers to emerge. At DIAGNOSTIC AUTOMATION (focusing on ELISA Kits and rapid tests) standing at the leading edge of scientific innovations, we take advantage of an influx of new technologies and information incorporating them into novel tests which enables us to offer innovative diagnostic tests every day.
Despite the amazing scientific advances in the physical and biological sciences, the number of effective cardiovascular therapies and viable therapeutic targets remains surprisingly limited. The number of useful cardiovascular biomarkers is even fewer. To gain an insight into the disease processes in individual patients, their unique response to etiological risk factors, and their stages of disease progression, an array of diagnostic biomarkers are needed. We believe that most useful or specific diagnostic/prognostic/efficacy biomarkers eventually will be shown to have biological relevance to the disease. In our team we have a member who has experience in using systems biology tools such as microarray and proteomics in discovering novel biomarkers related to cardiovascular disease . The general principle employed involves the convergence of well-defined models, together with validation in clinical samples, to provide unique opportunities of early diagnosis. Three new patents for detection of early cardiovascular remodeling and heart failure using systems biology approach have been filed using this approach.
Cardiovascular diseases are the most prominent circulation disorders around the world. In 2008, there were an estimated 57 million global deaths, of which 30.5% were attributed to cardiovascular disease . This fraction is greater than combined deaths stemming from other diseases such as cancer, diabetes mellitus, nutritional/endocrine disorders, respiratory diseases, and digestive diseases. Moreover, Cardiovascular diseases (CVD) are the leading cause of morbidity and mortality in the United States. By 2030 approximately 116 million people in the United States (40.5 percent) will have some form of cardiovascular disease and the cost to treat them will triple . The social, economic, and human costs of cardiovascular disease continue to escalate as a result. However, death from cardiovascular diseases is preventable with accurate early-stage diagnosis and subsequent proper treatment. Correct diagnosis is dependent upon cardiac biomarkers. Cardiac biomarkers are proteins that are released into the blood following a myocardial infarction and are a valuable tool for assessing the pathogenesis and diagnosis of cardiovascular diseases. We believe that most useful or specific diagnostic biomarkers are the ones with biological relevance to the disease. To gain an insight into the disease processes in individual patients, their stages of disease progression, and to achieve an in-depth evaluation we have offer 6 different marker ELISA kits in our cardiac elisa kits in addition to our rapid tests. The integration of these tests will provide robust clinical phenotypes with high level of sensitivity and specificity which is pivotal for a successful diagnostic program. Used in conjunction with clinical information the rapid and accurate testing of cardiac markers is crucial especially in acute cases where every minute counts. Moreover, the insight from these tests will assist physician to make both an easier and more informed decision on their choice of medication to treat their patients more effectively in a timely manner.
Myocardial infarction (MI) or acute myocardial infarction (AMI),
Commonly known as a heart attack, results from the interruption of blood supply to a part of the heart, causing heart cells to die. WHO criteria formulated in 1979 has classically been used to diagnose MI; a patient is diagnosed with myocardial infarction if two (probable) or three (definite) of the following criteria are satisfied:
1. Clinical history of ischemic type chest pain lasting for more than 20 minutes
2. Changes in serial ECG tracings
3. Rise and fall of serum cardiac biomarkers such as creatine kinase-MB fraction and troponin.
The WHO criteria were refined in 2000 to give more prominence to cardiac biomarkers. According to the new guidelines, a cardiac troponin rise accompanied by either typical symptoms, pathological Q waves, ST elevation or depression, or coronary intervention is diagnostic of MI .
Presently, Muscle creatine kinase (CK) and brain subunits (CK-MB) and troponin T, are known as The standard biochemical metrics of myocardial injury. Therefore to achieve an in-depth evaluation we have combined 3 tests to have robust clinical phenotypes to provide adequate sensitivity or specificity. At DIAGNOSTIC AUTOMATION our integrated 3 in 1 cardiac rapid test includes Troponin I/Myoglobin/CK-MB both in human serum and in whole blood.
These 3 in 1 Cardiac Markers rapid tests are to be used as aids in the diagnosis of Acute Myocardial Infarction (AMI). In recent years, point-of-care 3 in 1cardiac rapid tests have emerged to play a vital role in the rapid diagnosis and treatment of acute chest pain patients. By combining three cardiac marker tests into one device, the test is able to identify multiple release profiles for improved sensitivity and thus, not only able to identify myocardial infarctions, but also to identify at-risk patients with a possible life-threatening cardiac event in the near future.
3 in 1CARDIAC MARKERS TEST
Los Angeles-based Diagnostic Automation is pleased to offer two Cardiac Markers Rapid Tests to customers around the world. Both 3 in 1 Cardiac Markers Rapid Tests are available in cassette format. These convenient 3-panel rapid tests are immunochromatography assays for the qualitative and quantitative determination of three biochemical markers (Troponin I, CK-MB, and Myoglobin) simultaneously in human serum or whole blood. The cardiac markers tests are point-of-care testing devices.
3 in 1 rapid test is for the qualitative assessment of cardiac Troponin I, CK-MB, and Myoglobin in human serum and whole blood.
HIGHLIGHTS OF 3 IN 1 CARDIAC MARKERS RAPID TESTS
These 3 in 1 Cardiac Markers rapid tests are to be used as aids in the diagnosis of Acute Myocardial Infarction (AMI). In recent years, point-of-care 3 in 1 cardiac elisa kits have emerged to play a vital role in the rapid diagnosis and treatment of acute chest pain patients. By combining three cardiac marker tests into one device, the test is able to identify multiple release profiles for improved sensitivity and thus, not only able to identify myocardial infarctions, but also to identify at-risk patients with a possible life-threatening cardiac event in the near future .
In addition to 3 in 1 rapid test at Diagnostic Automation, three ELISA kits are offered individually as well as:
1. Troponin I ELISA kit
1. Myoglobin ELISA kit
1. CK-MB ELISA kit
Here are brief description of each marker and its biological function:
1. Troponin is a complex of three regulatory proteins (troponin C, troponin I and troponin T) that is integral to muscle contraction in skeletal and cardiac muscle, but not smooth muscle.
Model of Troponin molecular structure 
For those more interested in the mechanism of contraction: Troponin is attached to Tropomyosin and lies within the groove between actin filaments in muscle tissue. In a relaxed muscle, Tropomyosin blocks the attachment site for the myosin cross-bridge, thus preventing contraction. When the muscle cell is stimulated to contract by an action potential, calcium channels open in the sarcoplasmic membrane and release calcium into the sarcoplasm. Some of this calcium attaches to troponin which causes it to change shape, exposing binding sites for myosin (active sites) on the actin filaments. Myosin binding to actin forms cross-bridges and contraction (cross bridge cycling) of the muscle begins. Both cardiac and skeletal muscles are controlled by changes in the intracellular calcium concentration. When calcium raises, the muscles contract, and when calcium falls, the muscles relax .
In medicine, Troponin levels can be used as a test for several different heart disorders, including myocardial infarction. From the 3 subunits of Troponin, Troponin-I is highly specific for cardiac muscle necrosis. Serum levels rise 3-6 hours after onset of chest pains, peak at 12–16 hours and return to baseline within 5–9 days.
The high specificity and sensitivity of this marker make it extremely useful to either take action against or rule out with confidence any risk of heart attack in patients presenting clinical symptoms such as chest pain, breathing difficulties or left arm pain.
Troponin I elisa kit is also offered at DIAGNOSTIC AUTOMATION
2. Myoglobin is Myoglobin is a heme (an iron- and oxygen-binding) protein found in skeletal and cardiac muscle that has attracted considerable interest as an early marker of MI. Its low molecular weight accounts for its early release profile: myoglobin typically rises 2-4 hours after onset of infarction, peaks at 6-12 hours, and returns to normal within 24-36 hours.
High concentrations of myoglobin in muscle cells allow organisms to hold their breaths longer. Diving mammals such as whales and seals have muscles with particularly high myoglobin abundance. Myoglobin is the primary oxygen-carrying pigment of muscle tissues which is responsible for making meat red. The color that meat takes is partly determined by the oxidation states of the iron atom in myoglobin and the oxygen species attached to it. When meat is in its raw state, the iron atom is in the +2 oxidation state, and is bound to a dioxygen molecule (O2). Cooked meat is brown because the iron atom is now in the +3 oxidation state, having lost an electron. Myoglobin is found in Type I muscle, Type II A and Type II B, but most consider myoglobin not to be found in smooth muscle.
Model of myoglobin molecular structure
Myoglobin is released from damaged muscle tissue, which has very high concentrations of myoglobin. The released myoglobin is filtered by the kidneys but is toxic to the renal tubular epithelium and so may cause acute renal failure. It is not the myoglobin itself that is toxic, but the portion that is dissociated from myoglobin in acidic environments (e.g., acidic urine).
Levels of myoglobin start to rise within 2-3 hours of MI or other muscle injury, reach their highest levels within 8-12 hours, and generally fall back to normal within one day. An increase in myoglobin is detectable sooner than troponin, but it is not as specific for heart damage and it will not stay elevated as long as troponin. Serial sampling of blood every 1-2 hours can increase the sensitivity and specificity; a rise of 25-40% over 1-2 hours is strongly suggestive of acute MI. If myoglobin does not increase within 12 hours following the onset of chest pain, a heart attack is very unlikely. Blood samples are drawn on admission and every 2-3 hours for up to 12 hours in those who come to the emergency room with a possible MI. An increase in blood myoglobin means that there has been very recent injury to the heart or skeletal muscle tissue. Additional tests, such as Troponin, are necessary to determine where the damage has occurred. Because myoglobin is also found in skeletal muscles, increased levels can occur in people who have accidents, seizures, surgery, or any muscle disease, such as muscular dystrophy. If myoglobin does not increase within 12 hours following the onset of chest pain, a heart attack is very unlikely.
Although a negative myoglobin result effectively rules out an MI, a positive result must be confirmed by testing for troponin. This is why at DIAGNOSTIC AUTOMATION we offer the 3 tests together as a cardiac elisa kits which increases both sensitivity and specificity of our diagnosis of AMI. By combining three cardiac marker tests into one device, the test is able to identify multiple release profiles for improved sensitivity and thus, not only able to identify myocardial infarctions, but also to identify at-risk patients with a possible life-threatening cardiac event in the near future. An increase in blood myoglobin means that there has been very recent injury to the heart or skeletal muscle tissue. Additional tests, such as Troponin, are necessary to determine where the damage has occurred. Because myoglobin is also found in skeletal muscles, increased levels can occur in people who have accidents, seizures, surgery, or any muscle disease, such as muscular dystrophy. Increased myoglobin levels can occur after muscle injections or strenuous exercise. Because the kidneys remove myoglobin from the blood, myoglobin levels may be high in people whose kidneys are failing. Heavy alcohol consumption and certain drugs can also cause muscle injury and increase myoglobin in blood .
Myoglobin levels are normally very low or not detectable in the urine. High levels of urine myoglobin indicate an increased risk for kidney damage and failure. Additional tests, (which we offer at DIAGNOSTIC AUTOMATION) as cardiac elisa kits, are done to monitor kidney function in these patients.
Myoglobin elisa kit is also offered at DIAGNOSTIC AUTOMATION .
3. Creatine Kinase–MB
Prior to the introduction of cardiac troponins, the biochemical marker of choice for the diagnosis of acute MI was the CK-MB isoenzyme. The criterion most commonly used for the diagnosis of acute MI was 2 serial elevations above the diagnostic cutoff level or a single result more than twice the upper limit of normal. Although CK-MB is more concentrated in the myocardium, it also exists in skeletal muscle and false-positive elevations occur in a number of clinical settings, including trauma, heavy exertion, and myopathy .
Model of CK-MB molecular structure 
CK-MB first appears 4-6 hours after symptom onset, peaks at 24 hours, and returns to normal in 48-72 hours. Its value in the early and late (>72 h) diagnosis of acute MI is limited. However, its release kinetics can assist in diagnosing subsequent infarction if levels rise after initially declining following acute MI.
The CK-MB isoenzyme exists as 2 isoforms: CK-MB1 and CK-MB2. Laboratory determination of CK-MB actually represents the simple sum of the isoforms CK-MB1 and CK-MB2. CK-MB2 is the tissue form and initially is released from the myocardium after MI. It is converted peripherally in serum to the CK-MB1 isoform rapidly after symptom onset. Normally, the tissue CK-MB1 isoform predominates; thus, the CK-MB2/CK-MB1 ratio is typically less than 1. A result is positive if the CK-MB2 is elevated and the ratio is greater than 1.7 [10 &11].
CK-MB ELISA Kit is also offered at DIAGNOSTIC AUTOMATION
Additional Cardiac Markers ELISA Kits offered at DIAGNOSTIC AUTOMATION :
1. Digoxin ELISA Kit
2. Lp(a) ELISA Kit
3. C-Reactive Protein (CRP) which is a Serum Rapid Test (Cassette) RapiCard™ InstaTest
Since these markers appear hours after the first symptoms, they are not fully sensitive to be used for an early detection of any heart problems. Moreover, because these markers remain high for up to two weeks, a positive test may not distinguish between an ongoing MI with the earlier one.
1. Arab S. et al. Cardiovascular proteomics: tools to develop novel biomarkers and potential applications. J Am Coll Cardiol. 2006 Nov 7;48(9):1733-41.
2. WHO. Cause-specific mortality, 2008. World Health Organization. Accessed on March, 2013. from:http://www.who.int/gho/mortality_burden_disease/global_burden_disease_DTH6_2008.xls
3. U.S. department of health and human resources Feb 2011. http://www.hhs.gov/news/press/2011pres/2011.html.
4. Alpert JS, et al. (2000). Myocardial infarction redefined—a consensus document of The Joint European Society of Cardiology/American College of Cardiology Committee for the redefinition of myocardial infarction. J Am Coll Cardiol 36 (3): 959–69. PMID 10987628 .
5. Rao SP, et al. (August 1999). Cardiac troponin I and cardiac enzymes after electrophysiologic studies, ablations, and defibrillator implantations. Am. J. Cardiol. 84 (4): 470, A9; PMID 10468091.
6. Nelson, D. L.; Cox, M. M. (2000). Lehninger Principles of Biochemistry (3rd ed.). New York: Worth Publishers. p. 206. ISBN 0-7167-6203-X
7. [Takano T (March 1977). Structure of myoglobin refined at 2.0 Å resolution. II. Structure of deoxymyoglobin from sperm whale. J. Mol. Biol. 110 (3): 569–84 ; PMID14871135.
8. [ Naka T, et al. (April 2005). Myoglobin clearance by super high-flux hemofiltration in a case of severe rhabdomyolysis: a case repor Crit Care 9 (2): R90–5; PMID 15774055.
9. Guzy PM (December 1977). Creatine phosphokinase-MB (CPK-MB) and the diagnosis of myocardial infarction. West. J. Med. 127 (6): 455–60; PMID 339548.
10. Puleo PR, et al. Use of a rapid assay of subforms of creatine kinase-MB to diagnose or rule out acute myocardial infarction. N Engl J Med. Sep 1 1994;331(9):561-6.
11. Newby LK, et al. Frequency and clinical implications of discordant creatine kinase-MB and troponin measurements in acute coronary syndromes. J Am Coll Cardiol. 2006;47(2):312-8.