Cardiac troponin I and myocardial contusion in the rabbit

Patients with cardiac contusion have a high risk of cardiac complications during emergency anesthesia. Despite the progress in cardiac imaging, a biologic marker of myocardial damage such as cardiac troponin I remains useful and has been proposed in clinical practice. The relationship among histologic injury, left-ventricular function, and release of cardiac enzymes and cardiac troponin I has been investigated after a controlled myocardial contusion in a rabbit model.

A global trauma (two levels of energy: 250 and 350 mJ) was produced on an isolated preparation of rabbit's heart, of which the temperature, perfusion flow, beating rate, and left-ventricular volume were kept constant. Left-ventricular pressure and its first derivative as a function of time were measured during a 60-min period after the blow; a timed collection of the effluent was made to assess creatine kinase, lactate dehydrogenase, and cardiac troponin I. At the end of the period, an anatomic score of the contusion was calculated by histologic examination of the hearts.

Compared with a control group, the two levels of cardiac trauma resulted in a proportional anatomic injury significantly correlated with left-ventricular dysfunction (Delta%dP/dtmax = -16 +/- 12 and -36 +/- 20% at 3 min, mean +/- SD). Transient releases in cardiac markers after the lesser amount of trauma contrasted with a prolonged and biphasic release of cardiac troponin I after the greater amount. Peak cardiac troponin I level was correlated with anatomic injury (rho = 0.596, P= 0.001) and negatively correlated with left-ventricular dysfunction (r = -0.375, P= 0.04).

Cardiac troponin I is a marker of anatomic and functional consequences of experimental cardiac trauma and may be a predictive indicator of early posttraumatic cardiac complications during the postoperative period.