Abstract: Objective To provide a basis for the model in this paper, we analyzed the characteristics of acute myocardial ischemia (AMI) models and relevant phenotypic indexes in the literature. Methods In the literature research, the time range was January 2001 to December 2021; “acute myocardial ischemia” and “animal experiments” were used as the subject search terms, and Web of Science, China Knowledge Network, Wanfang, and Weipu databases were searched to summarize the characteristics of AMI modeling and phenotypic indicators. In the animal experiments, 40 healthy 5- to 6-week-old SPF SD rats, both male and female, were randomly divided into four groups (sham male, sham female, coronary artery ligation (LAD) male, and LAD female), with 10 rats in each group. LAD group underwent ligation of the left anterior descending coronary artery ( LAD), Sham group underwent the same operation, but only threading without ligation. Powerlab was used to monitor electrocardiogram (ECG) changes, and HE staining was used to observe myocardial pathological changes. ELISA was used to detect serum cardiac enzymes (CK-MB, cTnI) and oxidative stress factors(MDA, SOD, Uch-L1) in the hippocampal CA1 region. The levels of apoptotic proteins (Caspase-3, PARP1, Cleaved Caspase-3, Cleaved PARP1) in the hippocampal CA1 region were detected by Western Blot. Results An analysis of 411 papers found that most studies selected SD or Wistar rats to prepare LAD models and concentrated on morphological and functional changes to the heart, while studies on heart-brain crosstalk were rare. Compared with the sham-operation groups, LAD male and female rats showed a significantly elevated ST segment on ECG, cardiac myocyte edema, disturbed myocardial fiber sorting, extensive inflammatory cell infiltration, and expression of serum CK-MB, cTnI, and Uch-L1. The expression of MDA, Cleaved Caspase-3/ Caspase-3, and cleaved PARP1/ PARP1 was increased and SOD was significantly decreased in the CA1 region of the rat hippocampus. Conclusions Acute myocardial ischemia can cause hippocampal oxidative stress and induce neuronal apoptosis, and cardiovascular disease is potentially associated with brain dysfunction.