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Postburn cardiac contractile function and biochemical markers of postburn cardiac injury
J W Horton1, N M Garcia, D J White
1Department of Surgery, University of Texas Southwestern Medical Center, Dallas 75235-9031, USA.
Insights
Severe burns cause cardiac dysfunction, detectable through cardiac troponin I (cTnI) levels, offering a specific marker for heart injury following thermal trauma.
Area of Science:
- Cardiovascular Research
- Burn Injury Pathophysiology
- Biochemical Markers of Cardiac Injury
Background:
- Assessing cardiac injury post-thermal trauma is challenging due to compensatory mechanisms.
- Creatine kinase (CK) and CKMB are used but lack cardiac specificity.
- Cardiac troponin I (cTnI) is a myocardium-specific marker detectable after cardiac injury.
Purpose of the Study:
- To evaluate cardiac contractile function at various postburn intervals.
- To correlate cardiac dysfunction with serum levels of CK, CKMB, and cTnI.
Main Methods:
- New Zealand white rabbits underwent scald burns (34% TBSA) or sham procedures.
- Cardiac function was assessed using Langendorff preparations.
- Serum CK, CKMB, and cTnI levels were measured at 2, 4, 6, and 24 hours post-burn.
Main Results:
- Burn rabbits exhibited cardiac dysfunction at all time points.
- Left ventricular systolic dysfunction correlated with increased cTnI and CK levels.
- CKMB levels did not correlate with burn-induced cardiac dysfunction.
Conclusions:
- Cardiac troponin I (cTnI) provides a specific biochemical indicator of cardiac injury after thermal trauma.
- cTnI measurements align with in vitro assessments of cardiac dysfunction.
- The cardiospecificity of cTnI overcomes limitations of CK and CKMB.
Background:
In vivo assessment of cardiac injury and contractile deficits after thermal injury remain difficult as neurohumoral compensatory mechanisms maintain cardiac output. While measurement of creatine kinase (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 systemic circulation within three to four hours after cardiac injury. The purpose of this study was to examine cardiac contractile function at several postburn intervals and to correlate the appearance of cardiac dysfunction with biochemical measures of cardiac injury (serum concentration of CK, CKMB, and cTnI).
Study Design:
New Zealand white rabbits were deeply anesthetized and a scald burn comprising 34 percent of the total body surface area (n = 36) or sham burn (n = 36) was accomplished using a template device. All burn rabbits were given lactated Ringer's solution (4 mL/kg/percent burn, Parkland formula). Blood samples were collected immediately prior to sacrifice in six animals from both burn and control groups, and animals were sacrificed either two, four, six or 24 hours after burn. Cardiac function was assessed in left ventricular preparations (Langendorff) and serum CK, CKMB, and cTnI levels were determined.
Results:
Cardiac dysfunction occurred at all times after burn as indicated by a lower peak systolic left ventricular pressure and +/- 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 systolic dysfunction after burn correlated with a progressive rise in cTnI and CK but not CKMB.
Conclusions:
The cardiospecificity of the cTnI eliminates concerns about tissue source associated with CK and CKMB and provides a biochemical measure of cardiac injury that is consistent with in vitro assessment of cardiac dysfunction.