Cardiac marker

Cardiac marker
Diagnostics
LOINC 58260-1

Cardiac markers are biomarkers measured 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

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.
Creatine Kinase (CK-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) LDH 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 high sensitivity and specificity early after chest pain 7 hours

Glycogen phosphorylase isoenzyme BB (abbreviation: GPBB) is an isoenzyme of glycogen phosphorylase. Glycogen phosphorylase exists in 3 isoforms. One of these Isoforms is GP-BB. This isoform exists in heart and brain tissue. Because of the blood-brain barrier GP-BB can be seen as heart muscle specific. During the process of ischemia, GP-BB is converted into a soluble form and is released into the blood. This isoform of the enzyme exists in cardiac (heart) and brain tissue. GP-BB is one of the "new cardiac markers" which are discussed to improve early diagnosis in acute coronary syndrome. A rapid rise in blood levels can be seen in myocardial infarction and unstable angina. GP-BB elevated 1–3 hours after process of ischemia.

Recently, the intentional destruction of myocardium by alcohol septal ablation has led to the identification of additional potential markers.[5]

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.

However, in 2010, research at the Baylor College of Medicine revealed that, using diagnostic nanochips and a swab of the cheek, cardiac biomarker readings from saliva can, with the ECG readings, determine within minutes whether someone is likely to have had a heart attack.

See also

References

  1. ^ 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:10.1016/S0002-9149(99)00337-9. PMID 10468091. http://linkinghub.elsevier.com/retrieve/pii/S0002-9149(99)00337-9. 
  2. ^ 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 (4): 520–6. doi:10.1136/hrt.27.4.520. PMC 503341. PMID 14324110. http://heart.bmj.com/cgi/pmidlookup?view=long&pmid=14324110. 
  3. ^ "Use of Cardiac Markers in the Emergency Department: - eMedicine". http://emedicine.medscape.com/article/811905-overview. Retrieved 2009-01-06. 
  4. ^ 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. 
  5. ^ 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:10.1172/JCI35111. PMC 2525696. PMID 18769631. http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=2525696. 

Further reading

on GPBB

External links