Search

Background: Few experimental studies report effects of direct contusion on cardiac enzyme release. Cardiac troponins I (cTnI) and T (cTnT) have been shown 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 cTnT 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 mJ (n = 6), 200 mJ (n = 6). Coronary effluent samples for cTnI, cTnT, CK, and LD were collected at baseline, immediately after 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 (Elecsys) assays cross-react with cTnI and cTnT of the rabbit. The time-courses of cTnI, cTnT, CK, and LD were monophasic in form. After MC, all parameters rose significantly compared with baseline and with control group. The maximal 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 time 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 examination showed cellular disruption and after the more severe impact, the extent of pathologic changes was more extensive., Conclusion: After graded experimental MC, maximal cTnI concentration and area under cTnI curve increase with the power of impact kinetic energy. Levels of cTnI allow a much higher accuracy in detecting the extent of myocardial injury postMC in comparison with cTnT, CK, and LD in this experimental study. These results should be consistent with the more extensive cTnI release 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.

Current management of myocardial contusion is based on experience with ischemic heart disease, but the mechanism responsible for cardiac dysfunction may be quite different. The purpose of this study was to characterize the pathophysiology of myocardial contusion in a controlled animal model. Sprague-Dawley rat hearts were prepared on a standard Langendorff apparatus, and myocardial function (DP, + dP/dT, - dP/dT) measured via a left ventricular balloon. Bipolar atrial and ventricular leads were placed to define conduction changes. Coronary sinus effluent was sampled for pO2, pH, creatine phosphokinase (CPK), and lactic dehydrogenase (LDH). The hearts were freeze-clamped to measure phosphocreatine (PC) and adenosine triphosphate (ATP). Myocardial contusion was produced by a single blow with a weighted pendulum. Hearts were divided into control (n = 5), moderate impact--Group I (n = 5), and major impact--Group II (n = 5). Group I sustained a 25% decrease in function after an impact of 78 +/- 5 mJoules/gm, and Group II a 50% deficit after 87 +/- 7 mJoules/gm. Impact resulted in complete electrical arrest, followed by sequential ventricular, atrial, and AV nodal recovery; recovery time correlated directly with degree of injury. Coronary flow at 2 min postinjury was decreased (p less than 0.05) in Group I (12.8 +/- 0.8 ml/min) and Group II (11.5 +/- 1.3) compared to control (17.2 +/- 0.5), and returned to baseline levels at 20 min. LDH and CPK levels were twice as high in Group II as in Group I. The PC/ATP ratio in Group II increased from 1.63 at baseline to 2.54 (p less than 0.05) at 25 min, confirming ischemic reperfusion.(ABSTRACT TRUNCATED AT 250 WORDS)