Creatine Kinase MB (CK-MB)


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Subject: Creatine Kinase MB (CK-MB)

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  • CK-MB is the myocardial fraction associated with MI and occurs in certain other states. MB can be used in estimation of infarct size. CK-MB, or CK-MB fraction, is an 84-kDa molecular weight enzyme that represents 40% of the CK present in myocardial tissue. As with total CK, CK-MB typically begins to rise 4–6 hours after the onset of infarction but is not elevated in all patients until about 12 hours. Elevations return to baseline within 36–48 hours, in contrast to elevations in serum troponin, which can persist for as long as 10–14 days. This means that CK-MB, unlike troponins, cannot be used for the late diagnosis of an acute MI but can be used to suggest infarct extension if levels rise again after declining. CK-MB generally comprises a lower fraction of total CK in skeletal muscle than in the heart. As a result, percentage criteria (4%) have been proposed to distinguish skeletal muscle damage from cardiac damage. However, these criteria are not recommended. They improve specificity but do so at the cost of sensitivity in patients who have both skeletal and cardiac injury.

  • Normal range:


  • CK-MB is a widely used early marker for myocardial injury.


Increased In

  • Necrosis or inflammation of cardiac muscle (CK index approximately 2.5%; in all other causes, CK index usually <2.5%):

    • AMI.

    • Cardiac contusion.

    • After thoracic/open heart surgery, values return to baseline in 24–48 hours. AMI is difficult to diagnose in the first 24 postoperative hours.

    • Resuscitation for cardiac arrest may increase CK and CK-MB in approximately 50% of patients, with peak at 24 hours, due to defibrillation (>400 J) and chest compression, but CK-MB/CK total ratio may not be increased, even with AMI.

    • Percutaneous transluminal coronary angioplasty.

    • Myocarditis.

    • Prolonged supraventricular tachycardia.

    • Cardiomyopathies (e.g., hypothyroid, alcohol).

    • Collagen diseases involving the myocardium.

    • Coronary angiography (transient).

  • Necrosis, inflammation, or acute atrophy of striated muscle:

    • Exercise myopathy; slight to significant increases in 14–100% of persons after extreme exercise (e.g., marathons); smaller increases in well-conditioned athletes

    • Skeletal muscle trauma with rhabdomyolysis, myoglobinuria

    • Skeletal muscle diseases (e.g., myositis, muscular dystrophies, polymyositis, collagen vascular diseases [especially SLE])

    • Familial hypokalemic periodic paralysis

    • Electrical and thermal burns and trauma (approximately 50% of patients; but not supported by LD-1 > LD-2)

    • Drugs (e.g., alcohol, cocaine, halothane [malignant hyperthermia], ipecac)

  • Endocrine disorders (e.g., hypoparathyroid, acromegaly, DKA; hypothyroidism—total CK four to eight times ULN in 60–80% of cases; becomes normal within 6 weeks of replacement therapy)

  • Some infections:

    • Viral (e.g., HIV, EBV, influenza, picornaviruses, coxsackievirus, echovirus, adenoviruses)

    • Bacterial (e.g., Staphylococcus, Streptococcus, Clostridium, Borrelia)

    • Rocky Mountain spotted fever

    • Fungal

    • Parasitic (e.g., trichinosis, toxoplasmosis, schistosomiasis, cysticercosis)

  • Others:

    • Malignant hyperthermia; hypothermia

    • Reye syndrome

    • Peripartum period for first day beginning within 30 minutes

    • Acute cholecystitis

    • Hyperthyroidism and chronic renal failure, which may cause persistent increase although the proportion of CK-MB remains low

    • Acute exacerbation of obstructive lung disease

    • Drugs (e.g., aspirin, tranquilizers)

    • Carbon monoxide poisoning

  • Some neoplasms:

    • For example, prostate, breast

    • Ninety percent of patients following cryotherapy for prostate carcinoma with peak at 16 hours to about five times ULN; similar increase in total CK

  • Percent activity distribution of CK isoenzymes in tissue

  • A CK-MB >15–20% should raise the possibility of an atypical macro CK-MB.

Not Increased In

  • Angina pectoris, exercise testing for CAD, or pericarditis. Elevation implies necrosis of cardiac muscle, even if a discrete infarct is not identified.

  • Following diagnostic cardiac catheterization or cardiac pacemaker unless myocardial injury is sustained during the procedure.

  • IM injections (total CK may be slightly increased).

  • Seizures (total CK may be markedly increased).

  • Brain infarction or injury (total CK may be increased).


  • The presence of CK-MB is not unequivocally specific for myocardium, because it is found in patients with muscular dystrophies, polymyositis, hypothermia and hyperthermia, uremia, DKA, and septic shock. Renal failure, tissue damage following surgery, and cardiac contusion may also cause an elevation of CK-MB.

  • Cardiac troponin is the preferred marker for the diagnosis of MI. CK-MB by mass assay is an acceptable alternative when cardiac troponin is not available.

Suggested Readings

Apple  FS, Preese  LM. Creatine kinase-MB: Detection of myocardial infarction and monitoring reperfusion. J Clin Immunoassay.  1994;17:24–29.
Gibler  WB, Lewis  LM, Erb  RE Early detection of acute myocardial infarction in patients presenting with chest pain and nondiagnostic ECGs: Serial CK-MB sampling in the emergency department. Ann Emerg Med.  1990;19(12):1359–1366.