Objective This study focused on the regulatory relationship between TNS1 and miR-574-5p in cardiac arrest and its clinical significance, and verified the therapeutic potential of targeted inhibition of miR-574-5p. Methods Oxygen-glucose deprivation/reoxygenation (OGD/R) cardiomyocyte models and mouse cardiac arrest/cardiopulmonary resuscitation (ACA/CPR) models were established. Quantitative real-time polymerase chain reaction (qRT-PCR) was used to detect the expression levels of miR-574-5p and TNS1; the targeting relationship between miR-574-5p and TNS1 was verified by dual-luciferase reporter gene assay; cell viability was detected by CCK-8 assay; apoptosis was measured by flow cytometry; the levels of cardiac injury marker cTnI and oxidative stress markers MDA and 4-HNE in serum were detected by enzyme-linked immunosorbent assay (ELISA); the hemodynamic monitoring system was used to evaluate the cardiac function indices dp/dtmin and dp/dtmax; echocardiography was performed to determine cardiac function parameters such as left ventricular ejection fraction (LVEF) and left ventricular fractional shortening (LVFS). Results OGD/R treatment significantly upregulated the expression of miR-574-5p and inhibited the expression of TNS1 in cardiomyocytes. Inhibition of miR-574-5p improved the survival rate of cardiomyocytes and alleviated oxidative stress injury. In the ACA/CPR model, the miR-574-5p antagonist group significantly improved cardiac function indices, reduced the levels of cardiac injury and oxidative stress markers, and reversed the upregulated miR-574-5p and downregulated TNS1 expression patterns in myocardial tissues. Conclusion This study confirmed that targeted inhibition of miR-574-5p can improve cardiac function by upregulating the expression of TNS1, providing a new therapeutic target for myocardial protection after cardiac arrest.