Based on the successful establishment of acute and chronic RS models, we found that acute stress caused a compensatory increase in cardiac output, whereas chronic stress led to significantly reduced LVEF and ventricular wall thickening, accompanied by elevated levels of cTnI in serum and myocardium, along with pathological changes indicating myocardial ischemia and hypoxia, suggesting that chronic stress induces a critical transition from cardiac compensation to decompensation. Here, TNNI3 is linked to myocardial ischemia.