CPK-MB test

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CPK-MB test
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Kinetics of cardiac markers in myocardial infarction with or without reperfusion treatment
Reference range 2 to 19.5 U/L (at 37 C in adults), [1]
some places 5 to 25 IU/L [2]
LOINC 49551-5, 51506-4, 2154-3, 13969-1, 32673-6, 38482-6

The CPK-MB test (creatine phosphokinase-MB), also known as CK-MB test, is a cardiac marker [3] used to assist diagnoses of an acute myocardial infarction, myocardial ischemia, or myocarditis. It measures the blood level of CK-MB (creatine kinase myocardial band), the bound combination of two variants (isoenzymes CKM and CKB) of the enzyme phosphocreatine kinase.[ citation needed ]

In some locations, the test has been superseded by the troponin test. However, recently, there have been improvements to the test that involve measuring the ratio of the CK-MB1 and CK-MB2 isoforms. [4]

The newer test detects different isoforms of the B subunit specific to the myocardium whereas the older test detected the presence of cardiac-related isoenzyme dimers.[ citation needed ]

Many cases of CK-MB levels exceeding the blood level of total CK have been reported, especially in newborns with cardiac malformations, especially ventricular septal defects. This reversal of ratios is in favor of pulmonary emboli or vasculitis. An autoimmune reaction creating a complex molecule of CK and IgG should be taken into consideration. [5]

See also

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<span class="mw-page-title-main">Phosphocreatine</span> Chemical compound

Phosphocreatine, also known as creatine phosphate (CP) or PCr (Pcr), is a phosphorylated form of creatine that serves as a rapidly mobilizable reserve of high-energy phosphates in skeletal muscle, myocardium and the brain to recycle adenosine triphosphate, the energy currency of the cell.

<span class="mw-page-title-main">Troponin</span> Protein complex

Troponin, or the troponin complex, is a complex of three regulatory proteins that are integral to muscle contraction in skeletal muscle and cardiac muscle, but not smooth muscle. Measurements of cardiac-specific troponins I and T are extensively used as diagnostic and prognostic indicators in the management of myocardial infarction and acute coronary syndrome. Blood troponin levels may be used as a diagnostic marker for stroke or other myocardial injury that is ongoing, although the sensitivity of this measurement is low.

<span class="mw-page-title-main">Creatine kinase</span> Class of enzymes

Creatine kinase (CK), also known as creatine phosphokinase (CPK) or phosphocreatine kinase, is an enzyme expressed by various tissues and cell types. CK catalyses the conversion of creatine and uses adenosine triphosphate (ATP) to create phosphocreatine (PCr) and adenosine diphosphate (ADP). This CK enzyme reaction is reversible and thus ATP can be generated from PCr and ADP.

In biochemistry, isozymes are enzymes that differ in amino acid sequence but catalyze the same chemical reaction. Isozymes usually have different kinetic parameters, or are regulated differently. They permit the fine-tuning of metabolism to meet the particular needs of a given tissue or developmental stage.

<span class="mw-page-title-main">Cardiac marker</span>

Cardiac markers are biomarkers measured to evaluate heart function. They can be useful in the early prediction or diagnosis of disease. Although they are often discussed in the context of myocardial infarction, other conditions can lead to an elevation in cardiac marker level.

<span class="mw-page-title-main">Unstable angina</span> Medical condition

Unstable angina is a type of angina pectoris that is irregular or more easily provoked. It is classified as a type of acute coronary syndrome (ACS).

<span class="mw-page-title-main">Acute pericarditis</span> Medical condition

Acute pericarditis is a type of pericarditis usually lasting less than 6 weeks. It is the most common condition affecting the pericardium.

<span class="mw-page-title-main">Troponin T</span> Protein family

Troponin T is a part of the troponin complex, which are proteins integral to the contraction of skeletal and heart muscles. They are expressed in skeletal and cardiac myocytes. Troponin T binds to tropomyosin and helps position it on actin, and together with the rest of the troponin complex, modulates contraction of striated muscle. The cardiac subtype of troponin T is especially useful in the laboratory diagnosis of heart attack because it is released into the blood-stream when damage to heart muscle occurs. It was discovered by the German physician Hugo A. Katus at the University of Heidelberg, who also developed the troponin T assay.

<span class="mw-page-title-main">Troponin I</span> Muscle protein

Troponin I is a cardiac and skeletal muscle protein family. It is a part of the troponin protein complex, where it binds to actin in thin myofilaments to hold the actin-tropomyosin complex in place. Troponin I prevents myosin from binding to actin in relaxed muscle. When calcium binds to the troponin C, it causes conformational changes which lead to dislocation of troponin I. Afterwards, tropomyosin leaves the binding site for myosin on actin leading to contraction of muscle. The letter I is given due to its inhibitory character. It is a useful marker in the laboratory diagnosis of heart attack. It occurs in different plasma concentration but the same circumstances as troponin T - either test can be performed for confirmation of cardiac muscle damage and laboratories usually offer one test or the other.

Glycogen phosphorylase isoenzyme BB is an isoenzyme of glycogen phosphorylase. This isoform of the enzyme exists in cardiac (heart) and brain tissue.

<span class="mw-page-title-main">TNNI3</span> Protein-coding gene in the species Homo sapiens

Troponin I, cardiac muscle is a protein that in humans is encoded by the TNNI3 gene. It is a tissue-specific subtype of troponin I, which in turn is a part of the troponin complex.

<span class="mw-page-title-main">CKMT2</span> Protein and coding gene in humans

Creatine kinase S-type, mitochondrial is an enzyme that in humans is encoded by the CKMT2 gene.

<span class="mw-page-title-main">Myocardial infarction</span> Interruption of blood supply to a part of the heart

A myocardial infarction (MI), commonly known as a heart attack, occurs when blood flow decreases or stops in the coronary artery of the heart, causing damage to the heart muscle. The most common symptom is chest pain or discomfort which may travel into the shoulder, arm, back, neck or jaw. Often it occurs in the center or left side of the chest and lasts for more than a few minutes. The discomfort may occasionally feel like heartburn. Other symptoms may include shortness of breath, nausea, feeling faint, a cold sweat or feeling tired. About 30% of people have atypical symptoms. Women more often present without chest pain and instead have neck pain, arm pain or feel tired. Among those over 75 years old, about 5% have had an MI with little or no history of symptoms. An MI may cause heart failure, an irregular heartbeat, cardiogenic shock or cardiac arrest.

<span class="mw-page-title-main">CKM (gene)</span> Protein and coding gene in humans

Creatine kinase, muscle also known as MCK is a creatine kinase that in humans is encoded by the MCK gene.

<span class="mw-page-title-main">Heart-type fatty acid binding protein</span> Protein-coding gene in the species Homo sapiens

Heart-type fatty acid binding protein (hFABP) also known as mammary-derived growth inhibitor is a protein that in humans is encoded by the FABP3 gene.

<span class="mw-page-title-main">Arterial embolism</span> Interruption of blood flow to an organ

Arterial embolism is a sudden interruption of blood flow to an organ or body part due to an embolus adhering to the wall of an artery blocking the flow of blood, the major type of embolus being a blood clot (thromboembolism). Sometimes, pulmonary embolism is classified as arterial embolism as well, in the sense that the clot follows the pulmonary artery carrying deoxygenated blood away from the heart. However, pulmonary embolism is generally classified as a form of venous embolism, because the embolus forms in veins. Arterial embolism is the major cause of infarction.

<span class="mw-page-title-main">Francis M. Fesmire</span> American emergency physician (1969–2014)

Francis Miller Fesmire was an American emergency physician and a nationally recognized expert in myocardial infarction. He authored numerous academic articles and assisted in the development of clinical guidelines on the standard of care in treating patients with suspected myocardial infarction by the American College of Emergency Physicians and the American Heart Association/American College of Cardiology. He performed numerous research investigations in chest pain patients, reporting the usefulness of continuous 12-lead ECG monitoring, two-hour delta cardiac marker testing, and nuclear cardiac stress testing in the emergency department. The culmination of his studies was The Erlanger Chest Pain Evaluation Protocol published in the Annals of Emergency Medicine in 2002. In 2011 he published a novel Nashville Skyline that received a 5 star review by ForeWord Reviews. His most recent research involved the risk stratification of chest pain patients in the emergency department.

A diagnosis of myocardial infarction is created by integrating the history of the presenting illness and physical examination with electrocardiogram findings and cardiac markers. A coronary angiogram allows visualization of narrowings or obstructions on the heart vessels, and therapeutic measures can follow immediately. At autopsy, a pathologist can diagnose a myocardial infarction based on anatomopathological findings.

Lee Limbird is a pharmacologist, Dean of the School of Natural Science, Mathematics and Business & Professor in the Department of Life and Physical Sciences at Fisk University, Nashville, Tennessee.

References

  1. "CREATINE KINASE – MB CK-MB LQ" (PDF).
  2. Cabaniss, C. Daniel (1990), Walker, H. Kenneth; Hall, W. Dallas; Hurst, J. Willis (eds.), "Creatine Kinase", Clinical Methods: The History, Physical, and Laboratory Examinations (3rd ed.), Boston: Butterworths, ISBN   978-0-409-90077-4, PMID   21250193 , retrieved 2022-04-18
  3. Guzy PM (December 1977). "Creatine phosphokinase-MB (CPK-MB) and the diagnosis of myocardial infarction". West. J. Med. 127 (6): 455–60. PMC   1237914 . PMID   339548.
  4. "Use of Cardiac Markers in the Emergency Department: - eMedicine" . Retrieved 2009-01-10.
  5. Boucek RJ Jr; Kasselberg AG; Boerth RC; Parrish MD; Graham TP Jr (July 1982). "Myocardial injury in infants with congenital heart disease: evaluation by creatine kinase MB isoenzyme analysis". Am J Cardiol. 50 (1): 129–35. doi:10.1016/0002-9149(82)90018-2. PMID   7090995.