Types of Cardiac Markers
Types of Cardiac Markers
TroponinTroponin C, I, and T are proteins that form the thin filaments of muscle fibres. They modulate the movement of contractile proteins in muscle tissue. The test for troponin may be regarded as the most sensitive and specific test for myocardial damage.
Cardiac-derived troponins are TnI (cTnI) and TnT (cTnT). They are generally first detectable 2 to 4 hours after the onset of acute MI (commonly known as a heart attack) and peak at 10 to 24 hours. The long persistence of levels (>1 to 2 days) is why the troponin assessment is regarded as a test of choice.
A number of other conditions that can cause elevated Troponin levels are:
- Acute infarction
- Severe pulmonary embolism causing acute right heart overload
- Heart failure
- Myocarditis
- Quantitative (measures amounts) immunoassays
- Qualitative (positive or negative) cTnI test
The enzyme Creatine kinase is responsible for transferring a phosphate group from ATP to creatine. Creatine kinase is composed of M and/or B subunits and forms: CK-MM, CK-MB, and CK-BB isoenzymes. CK-MB may be regarded as a sensitive and specific marker for myocardial infarction. Its value changes in 3 to 4 hours after an MI, peaks in 10-24 hours. The normal value is restored within 72 hours. Because of this short duration it cannot be used for late diagnosis of acute MI.
It is however important to note that CK-MB levels also rises in conditions like:
- Skeletal muscle damage (such as in muscular dystrophy or a crush injury)
- Renal failure
Another utility of CK-MB is to access the success of a thrombolytic therapy. Different molecular forms of MB are found in the circulation. By checking the prevalent form of MB in the blood, one can say if the thrombolysis (breaking up and dissolving blood clots ) has succeeded.
Myoblobin
The protein myoglobin is found in both skeletal and myocardial muscle. It is released rapidly following a tissue injury. Levels may be elevated as early as one hour after myocardial injury. It has to be noted that skeletal muscle trauma can also cause this effect.
If a person shows the acute symptoms but the myoglobin level does not rise within 3 to 4 hours, then it unlikely to be an MI. A number of methods are available for its measurement. In spite of a rapid rise, myoglobin is a less used cardiac marker because of its low specificity.
Lactate dehydrogenase (LDH)
Lactate dehydrogenase (LDH) is not as specific as troponin. LDH has two isoenzymes: LDH-1 and LDH-2. LDH-1 isozyme is ordinarily found in the heart muscle and LDH-2 is found mostly in blood serum. A high LDH-1 level to LDH-2 suggests MI. Tissue breakdown or haemolysis can also lead to elevated LDH levels.
C-reactive protein (CRP)
C-reactive protein (CRP) is a protein found in serum or plasma at elevated levels as a result of inflammatory processes. CRP is increased several hundred-fold during acute or chronic inflammation. Recent studies suggest that CRP levels are useful in predicting the risk for a thrombotic event (such as a blood clot causing MI).
Homocysteine
Homocysteine is an amino acid. The American Heart Association says that very high levels of homocysteine in the blood is related to a higher risk of coronary heart disease, stroke, and peripheral vascular disease; and that it may also have an effect on atherosclerosis.
Others:
- Apart from the above mentioned cardiac markers, the following ones also exist:
- Aspartate transaminase (AST): More commonly used in Liver function tests (LFT).
- Ischemia-modified albumin (IMA): Use is not widespread. Further studies are required.
- Pro-brain natriuretic peptide: It is Increased in patients with heart failure. It may be used as a marker for acute congestive heart failure
- Glycogen phosphorylase isoenzyme BB: A new cardiac marker supposed to improve early diagnosis in acute coronary syndrome.
References:
- Cecil Medicine, 23rd Ed. Harrison's PRINCIPLES OF INTERNAL MEDICINE, 17TH Edition
- Cardiovasc Pathol. 2007 Nov-Dec;16(6):329-35. Epub 2007 Jun 20.
- INTERNATIONAL JOURNAL OF CLINICAL & LABORATORY RESEARCH Volume 29, Number 2, 56-63, DOI: 10.1007/s005990050064
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