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(Stroke. 2002;33:286.)
© 2002 American Heart Association, Inc.

Research Reports

Creatine Kinase-MB Elevation After Stroke Is Not Cardiac in Origin

Comparison With Troponin T Levels

Hakan Ay, MD; Ethem Murat Arsava, MD Okay Sariba, MD

From the Department of Neurology, Hacettepe University Hospital, Ankara, Turkey.

Correspondence to Hakan Ay, MD, Hacettepe University Hospitals, Department of Neurology, Sihhiye 06100, Ankara-Turkey. E-mail ayhmgh{at}hotmail.com

Abstract

Background and Purpose— Creatine kinase-MB (CK-MB) increases in some patients with stroke, with no clear evidence of an acute coronary syndrome. Its elevations have been suggested to represent a biological marker for stroke-related myocardial injury. Troponin T has superior sensitivity and specificity to CK-MB in revealing minor myocardial injury. Therefore, we studied troponin T levels after stroke to determine whether troponin T increases in parallel to CK-MB.

Methods— We made daily measurements of CK-MB, myoglobin, total creatine kinase (total CK), and troponin T levels up to day 5 in 32 patients with large hemispheric infarction and with no history of coronary heart disease. The daily enzyme levels were compared with those of a control group of 22 patients with neurological diseases other than stroke.

Results— Serum CK-MB, myoglobin, and total CK levels were elevated above the cutoff value in 11, 26, and 20 patients with stroke, respectively. These enzyme levels gradually increased within the first 3 days and declined afterward. Troponin T did not exceed the reference range in any patients. One patient had elevated myoglobin and 3 had elevated total CK in the control group. The difference between groups was significant for CK-MB, myoglobin, and total CK at various time points.

Conclusions— Troponin T, a more specific biochemical marker of myocardial injury, does not increase after stroke. Normal troponin T along with elevated CK-MB signifies that CK-MB is not the biological marker for myocytolysis. CK-MB elevations in stroke patients are likely to be noncardiac in origin.

Key Words: creatine kinase-MB • myocardial infarction • stroke, ischemic • troponin T

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