Evaluation of trauma-induced secondary cardiac injury with myocardial radionuclide imaging

Objectives: Based on the early detection of cardiac dysfunction in vitro and normal cardiac function in vivo after the original discovery of non-fatal mechanical trauma. To evaluate secondary cardiac injury due to trauma with ^99mTc-MIBI and ¹⁸F-FDG myocardial imaging, in order to provide a probe to early warning and intervention of the occurrence of trauma-induced secondary cardiac injury.

Methods: The healthy Wistar rats were randomly divided into control, trauma and auto-macrophage agonist trauma group. Cardiac function per rat were evaluated at 1h, 6h, 12h and 24h after trauma. The autophagy marker proteins LC3-II, Beclin-1 and mitochondrial membrane potential of myocardial tissue and myocytes were measured at 24h after trauma. ROI was delineated at the heart (H) and superior mediastinal region(M) for each ^99mTc-MIBI image and the ratio of H/M was calculated, ¹⁸F-FDG PET myocardial imaging was performed before and after trauma, respectively.

Results: Compared with the normal control group, (1) The expression of LC3-II and beclin1 protein decreased at 1h after trauma and reached the lowest level at 6h after trauma, then gradually recovered, and returned to normal level at 24h after trauma (P > 0. 05). (2) The mitochondrial membrane potential decreased and the H/M ratio decreased by ^99mTc-MIBI myocardial imaging in rats 6h after trauma (P < 0.05). No abnormal changes were observed in ¹⁸F-FDG myocardial glucose metabolism imaging. However, 7d after trauma, myocardial ¹⁸F-FDG imaging showed that the glucose metabolism in anterior wall of myocardium was higher than that in other ventricular walls, and the H/M was decreased by myocardial ^99mTc-MIBI imaging. The local radioactivity value (count / g) of the anterior wall was lower than that of the normal control group. (3) The myocardial autophagy level and ^99mTc-MIBI myocardial imaging were significantly improved at 6h after trauma with autophagy agonist (PARA), before trauma (P < 0.05).

Conclusions: The decrease of mitochondrial membrane potential in myocardial tissue after mechanical trauma may lead to trauma-induced secondary cardiac injury by inducing autophagy. Early mitochondrial dysfunction after mechanical trauma and myocardial ischemic 7d later. ^99mTc-MIBI myocardial imaging can be used as one of the early warning indicators of posttraumatic delayed cardiac injury.