Release kinetics of cardiac troponin I and cardiac troponin T in effluentsfrom isolated perfused rabbit hearts after graded experimental myocardial contusion

Background: Few experimental studies report effects of direct contusion on cardiac enzyme release. Cardiac troponins I(cTnI) and T (cTnT) have been sh own to be highly sensitive and specific markers of myocardial cell injury. This investigation was designed to determine and compare the acute effects of quantified magnitudes of blunt cardiac trauma upon release of cTnI and c TnT in comparison with creatine kinase (CK) and lactate dehydrogenase (LD), Methods: In 24 rabbit hearts prepared on a standard Langendorff apparatus, myocardial contusion (MC) was produced by a single blow with a ball falling from a predefined height, delivered directly to the surface of the heart. Hearts were divided into control (n = 6) and various quantified impacts: 75 mJoules (mJ) (n = 6), 100 mi (n = 6), 200 mJ (n = 6), Coronary effluent sa mples for cTnI, cTnT, CK, and LD were collected at baseline, immediately af ter MC and 5, 15, 30, 45, and 60 minutes after MC. At the end of experiment , histologic condition was evaluated. Results: The anti-cTnI and cTnT MAbs used in the cTnI (Access) and cTnT (El ecsys) assays cross-react with cTnI and cTnT of the rabbit. The time-course s of cTnI, cTnT, CK, and LD were monophasic in form, After MC, all paramete rs rose significantly compared with baseline and with control group. The ma ximal release occurred immediately after MC. The area under the cTnI curve and the maximal cTnI concentration were linked to the contusion energy when increased at 200 mJ, Maximal concentrations and areas under cTnT, CK, LD t ime activity curve were not linked to the contusion energy level and showed no between-energy group differences. The correlation found between maximal cTnI and maximal cTnT concentrations was 0.70 (p = 0.0001), Histologic exa mination showed cellular disruption and after the more severe impact, the e xtent of pathologic changes was more extensive. Conclusion: After graded experimental MC, maximal cTnI concentration and ar ea under cTnI curve increase with the power of impact kinetic energy. Level s of cTnI allow a much higher accuracy in detecting the extent of myocardia l injury postMC in comparison with cTnT, CK, and LD in this experimental st udy. These results should be consistent with the more extensive cTnI releas e with more severe impact in patients with blunt chest trauma. Furthermore, because specificity and time-course of release, both cTnI and cTnT should have a role in the diagnosis and evaluation of such patients.