A cardiac troponin I study in a minimally invasive myocardial infarction canine model.

Cardiac troponin I (cTnI) is an important biomarker of acute myocardial infarction (MI) in animals and human beings. Nevertheless, no immunohistochemical study has been reported about the pattern of myocardial cTnI egression in a minimally invasive model. The present study intended to establish a minimally invasive model of MI and to evaluate the distribution of cTnI. Twelve Mongrel dogs were divided into 2 groups (n = 6): experimental and sham-operated group. Three incisions were made on the left thoracic wall, left anterior descending (LAD) of coronary artery was identified and titanium nips were clamped by video-assisted thoracoscopy surgery (VATS). Series of electrocardiograms (ECG) and biochemical analyses of blood samples - oxidatively modified proteins (OMP), creatine kinase (CK), and cTnI were performed. Furthermore, Masson's trichrome staining was used to observe the histopathology of cardiac myocytes, while immunohistochemistry was done to observe cTnI egression from myocardium. ECG showed elevated ST-segment, whereas OMP, CK and cTnI level increased remarkably and declined to baseline subsequently in the model group throughout study period. Masson's trichrome staining of model group showed a large amount of collagen deposition in the fibrotic area as compared to control group. In immunohistochemical staining, no loss of cTnI staining was observed in non-necrotic myocardium, meanwhile, a great loss was observed in necrotic myocardium. An exception was the myocardium of cardiac apex, where loss of cTnI was visible even in non-necrotic myocardium. All these results revealed that loss of cTnI occurs not only in the necrotic myocardium but also in so-called non-necrotic myocardium of minimally invasive MI model through VATS.