POSTBURN CARDIAC CONTRACTILE FUNCTION AND BIOCHEMICAL MARKERS OF POSTBURN CARDIAC INJURY

BACKGROUND: In vivo assessment of cardiac injury and contractile defic its after thermal injury remain difficult as neurohumoral compensatory mechanisms maintain cardiac output. While measurement of creatine kin ase (CK) and the isoenzyme of creatine kinase (CKMB) have been used as clinical indicators of cardiac injury, these biochemical markers are not completely specific for cardiac muscle, Cardiac protein troponin I (cTnI) is unique to the myocardium but can be detected in the systemi c circulation within three to four hours after cardiac injury. The pur pose of this study was to examine cardiac contractile function at seve ral postburn intervals and to correlate the appearance of cardiac dysf unction with biochemical measures of cardiac injury (serum concentrati on of CK, CKMB, and cTnI). STUDY DESIGN: New Zealand white rabbits wer e deeply anesthetized and a scald burn comprising 34 percent of the to tal body surface area (n=36) or sham burn (n=36) was accomplished usin g a template device. All burn rabbits were given lactated Ringer's sol ution (4 mL/kg/percent burn, Parkland formula). Blood samples were col lected immediately prior to sacrifice in six animals from both burn an d control groups, and animals were sacrificed either two, four, six or 24 hours after burn. Cardiac function was assessed in left ventricula r preparations (Langendorff) and serum CK, CKMB, and cTnI levels were determined. RESULTS: Cardiac dysfunction occurred at all times after b urn as indicated by a lower peak systolic left ventricular pressure an d +/- dP/dt maximum compared with time-matched shams and the shift of left ventricular function curves plotted for burn groups downward and to the right of those calculated for shams, p<0.05. Left ventricular s ystolic dysfunction after burn correlated with a progressive rise in c TnI and CK but not CKMB. CONCLUSIONS: The cardiospecificity of the cTn I eliminates concerns about tissue source associated with CK and CKMB and provides a biochemical measure of cardiac injury that is consisten t with in vitro assessment of cardiac dysfunction.