Cardiac marker
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Cardiac markers are tests used to evaluate heart function. They are often discussed in the context of myocardial infarction, but other conditions can lead to an elevation in cardiac marker level.
Most of the early markers identified were enzymes, and as a result, the term "cardiac enzymes" is sometimes used. However, not all of the markers currently used are enzymes. For example, in formal usage, troponin would not be listed as a cardiac enzyme.[1]
Contents |
[edit] Types
Types include:
| Test | Sensitivity and specificity | Approximate peak | Description |
|---|---|---|---|
| Troponin test | The most sensitive and specific test for myocardial damage. Because it has increased specificity compared with CK-MB, troponin is a superior marker for myocardial injury. | 12 hours | Troponin is released during MI from the cytosolic pool of the myocytes. Its subsequent release is prolonged with degradation of actin and myosin filaments. Differential diagnosis of troponin elevation includes acute infarction, severe pulmonary embolism causing acute right heart overload, heart failure, myocarditis. Troponins can also calculate infarct size but the peak must be measured in the 3rd day. released in 2–4 hours and persists for up to 7 days. |
| CPK-MB test | It is relatively specific when skeletal muscle damage is not present. | 10–24 hours | CK-MB resides in the cytosol and facilitates high energy phosphates into and out of mitochondria. It is distributed in a large number of tissues even in the skeletal muscle. Since it has a short duration, it cannot be used for late diagnosis of acute MI but can be used to suggest infarct extension if levels rise again. This is usually back to normal within 2–3 days. |
| Lactate dehydrogenase (LDH) | LH is not as specific as troponin. | 72 hours | Lactate dehydrogenase catalyses the conversion of pyruvate to lactate. LDH-1 isozyme is normally found in the heart muscle and LDH-2 is found predominately in blood serum. A high LDH-1 level to LDH-2 suggest MI. LDH levels are also high in tissue breakdown or hemolysis. It can mean cancer, meningitis, encephalitis, or HIV. this usually back to normal 10–14 days. |
| Aspartate transaminase (AST) | This was the first used.[2] It is not specific for heart damage, and it is also one of the liver function tests. | ||
| Myoglobin (Mb) | low specificity for myocardial infarction | 2 hours | Myoglobin is used less than the other markers. Myoglobin is the primary oxygen-carrying pigment of muscle tissue. It is high when muscle tissue is damaged but it lacks specificity. It has the advantage of responding very rapidly,[3] rising and falling earlier than CK-MB or troponin. It also has been used in assessing reperfusion after thrombolysis.[4] |
| Ischemia-modified albumin (IMA) | low specificity | IMA can be detected via the albumin cobalt binding (ACB) test, a limited available FDA approved assay. Myocardial ischemia alters the N-terminus of albumin reducing the ability of cobalt to bind to albumin. IMA measures ischemia in the blood vessels and thus returns results in minutes rather than traditional markers of necrosis that take hours. ACB test has low specificity therefore generating high number of false positives and must be used in conjunction with typical acute approaches such as ECG and physical exam. Additional studies are required. | |
| Pro-brain natriuretic peptide | This is increased in patients with heart failure. It has been approved as a marker for acute congestive heart failure. Pt with < 80 have a much higher rate of symptom free survival within a year. Generally, pt with CHF will have > 100. | ||
| Glycogen phosphorylase isoenzyme BB |
Recently, the intentional destruction of myocardium by alcohol septal ablation has led to the identification of additional potential markers.[5]
[edit] Limitations
Depending on the marker, it can take between 2 to 24 hours for the level to increase in the blood. Additionally, determining the levels of cardiac markers in the laboratory - like many other lab measurements - takes substantial time. Cardiac markers are therefore not useful in diagnosing a myocardial infarction in the acute phase. The clinical presentation and results from an ECG are more appropriate in the acute situation.
[edit] See also
- Myocardial markers in myocardial infarction
- Reference ranges for blood tests#Cardiac tests
[edit] References
- ^ Rao SP, Miller S, Rosenbaum R, Lakier JB (August 1999). "Cardiac troponin I and cardiac enzymes after electrophysiologic studies, ablations, and defibrillator implantations". Am. J. Cardiol. 84 (4): 470, A9. doi:. PMID 10468091. http://linkinghub.elsevier.com/retrieve/pii/S0002-9149(99)00337-9.
- ^ NISSEN NI, RANLOV P, WEIS-FOGH J (July 1965). "EVALUATION OF FOUR DIFFERENT SERUM ENZYMES IN THE DIAGNOSIS OF ACUTE MYOCARDIAL INFARCTION". Br Heart J 27: 520–6. doi:. PMID 14324110. PMC: 503341. http://heart.bmj.com/cgi/pmidlookup?view=long&pmid=14324110.
- ^ "Use of Cardiac Markers in the Emergency Department: - eMedicine". http://emedicine.medscape.com/article/811905-overview. Retrieved on 2009-01-06.
- ^ Christenson RH, Ohman EM, Topol EJ, et al. (September 1997). "Assessment of coronary reperfusion after thrombolysis with a model combining myoglobin, creatine kinase-MB, and clinical variables. TAMI-7 Study Group. Thrombolysis and Angioplasty in Myocardial Infarction-7". Circulation 96 (6): 1776–82. PMID 9323061. http://circ.ahajournals.org/cgi/pmidlookup?view=long&pmid=9323061.
- ^ Lewis GD, Wei R, Liu E, et al. (October 2008). "Metabolite profiling of blood from individuals undergoing planned myocardial infarction reveals early markers of myocardial injury". J. Clin. Invest. 118 (10): 3503–12. doi:. PMID 18769631.
[edit] Further reading
- Ross G, Bever F, Uddin Z, Devireddy L, Gardin J (2004). "Common scenarios to clarify the interpretation of cardiac markers". J Am Osteopath Assoc 104 (4): 165–76. PMID 15127984.Full text
[edit] External links
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