Clinical studies have demonstrated the predictive values of changes in electrocardiographic (ECG) parameters for the preexisting myocardial ischemic infarction. However, a simple and early predictor for the subsequent development of myocardial infarction during the ischemic phase is of significant value for the identification of ischemic patients at high risk. The present study was undertaken by using non-human primate model of myocardial ischemic infarction to fulfill this gap. Twenty male Rhesus monkeys at age of 2–3 years old were subjected to left anterior descending artery ligation. This ligation was performed at varying position along the artery so that it produced varying sizes of myocardial infarction at the late stage. The ECG recording was undertaken before the surgical procedure, at 2 h after the ligation, and 8 weeks after the surgery for each animal. The correlation of the changes in the ECG waves in the early or the late stage with the myocardial infarction size was analyzed. The R wave depression and the QT shortening in the early ischemic stage were found to have an inverse correlation with the myocardial infarction size. At the late stage, the R wave depression, the QT prolongation, the QRS score, and the ST segment elevation were all closely correlated with the developed infarction size. The poor R wave progression was identified at both the early ischemic and the late infarction stages. Therefore, the present study using non-human primate model of myocardial ischemic infarction identified the decreases in the R wave and the QT interval as early predictors of myocardial infarction. Validation of these parameters in clinical studies would greatly help identifying patients with myocardial ischemia at high risk for the subsequent development of myocardial infarction.

Evaluation of cardiac reserve under myocardial infarction in patients is important for prognosis. However, this evaluation is difficult to be done due to high risk for mortality in patients with severe myocardial infarction. The present study was undertaken using non-human primate model as a substitute for humans to investigate the relationship between cardiac reserve and myocardial infarct size. Rhesus monkeys of 2-3 years old (n = 27) were subjected to left anterior descending artery ligation to introduce acute myocardial infarction. By altering the ligation position along the artery, varying sizes of myocardial infarction were generated, from 20 to 58 % of the total myocardium mass. These subjects were divided into 4 groups based on the infarct size: below 25 %, between 25 and 35 %, between 35 and 45 %, and above 45 % of the total mass. Changes in cardiac contractility were determined by echocardiography along with the development of myocardial infarction, and by invasive hemodynamic measurement at the end of the experiment. Correlation analysis revealed that hearts with infarct sizes <25 % of the total mass fully responded to the increase in the load generated by heart rate escalation. Hearts with infarct sizes between 25 and 45 % responded the load increase with gradient decline in the maximum contractility. Hearts with infarct sizes more than 45 % failed to respond to the increase in the load. Therefore, we consider myocardial infarct size <25 % of the total mass as compensable injury, between 25 and 45 % as depleting injury, and more than 45 % as exhausted injury with regard to cardiac reserve. This would serve as a surrogate model for patients with myocardial infarction.

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