Creatine Kinase (CK), MB and Total

Serum

3 mL

0.6 mL (Note: This volume does not allow for repeat testing.)

Red-top tube or gel-barrier tube

CK is most commonly elevated in acute myocardial infarction (AMI) in which it has its greatest usefulness. Collection of specimen at onset of symptoms to establish baseline values is needed. A patient at onset of acute myocardial infarction (AMI) will have normal results, but some patients reach medical attention at or beyond CK peak. To support the diagnosis of AMI, three CK isoenzyme determinations have classically been recommended, one on admission, a second 12 hours after admission, a third 24 hours after admission. Another at 48 hours may be needed. CK-MB usually peaks between 15 and 20 hours after the onset of a myocardial infarction. Pappas summarizes current literature regarding timing as follows. In non-Q wave, incomplete occlusion, nontransmural MI, CK-MB peaks on the average 15 hours from onset. In Q wave (complete occlusion) (transmural) infarction, CK-MB average peak is 17 to 20 hours after onset of symptoms. He emphasizes the importance of a sample for CK-MB drawn 16 hours after onset.¹ When increased CK-MB values have returned to normal, CK isoenzyme determinations are usually no longer required.

MB is the myocardial fraction associated with MI and occurs in certain other states. MB can be used in estimation of infarct size. MB increases have been reported with entities which cause damage to the myocardium, such as myocarditis, some instances of cardiomyopathy, and with extensive rhabdomyolysis, Duchenne muscular dystrophy, malignant hyperthermia, polymyositis, dermatomyositis, mixed connective tissue disease, myoglobinemia, Rocky Mountain spotted fever, Reye syndrome, and rarely in rheumatoid arthritis with high titer RF.² CK-MB does not generally abruptly rise and fall in such nonacute MI settings, as it does in acute myocardial infarct (AMI).

Triglycerides >300 mg/dL will cause >20% loss of CK-MB activity. Exercise, intramuscular injections, myxedema, grand mal seizures, prior trauma or surgery and acute MI very early or late lead to the combination of increased total CK but usually normal CK-MB. Increased CK-MB has been described in marathon runners without MI.³ CK isoenzyme analysis is not usually practical when the total CK is very low, although in elderly people with low muscle mass, the use of sensitive mass concentration assays may be useful. A single CK isoenzyme examination may be misleading. One should look for a pattern in serial CK isoenzyme analyses and seek confirmation with the isoenzymes of LD (LDH), ideally beginning with onset to establish the baseline. LD isoenzyme 1:2 flip is most consistently found about two days after onset of acute infarction of myocardium. The diagnosis of myocardial injury should not be based solely on MB isoenzyme, but rather should be supported by clinical findings, ECG, and often other laboratory parameters (ie, confirmation by LD isoenzymes).¹

CK total: kinetic, 340 nm spectrophotometric; CK-MB: immunochemiluminometric assay (ICMA)

See tables.

CK-MB is usually not elevated in exercise (total CK elevated); myxedema (total CK elevated in about half of cases); injections into muscle (total CK elevated); strokes, CVA, and other brain disorders in which total CK may be increased; pericarditis; pneumonias or other lung diseases; pulmonary embolus; seizures (CK may be very high but no great MB increase, if any). Although CK-MB is not usually increased in angina, some CK-MB elevations are recognized in angina patients, depending partly on laboratory methodology.