ABSTRACT Introduction: Bisphenol A (BPA) is an environmental contaminant with a global use as a plasticizer. Daily BPA exposure begins early prenatally and continues throughout a person's life without exact limit or safety raising alarms concerning overall health. Objective: To explore potential cardiotoxicity of orally administered BPA in adult rat, and to assess the outcome of recovery period following BPA stoppage. Materials and Methods: Forty-eight adult male albino rats were allocated into four groups (12 each); control negative, control positive, BPA-treated and recovered. For eight weeks, rats in the 3rd group received daily BPA (50 mg/kg body weight, via oral gavage). In the recovery group, animals obtained BPA, for the same dose and duration similar to that in the 3rd group, then left to convalesce without BPA administration for 4 weeks. At the experimental end, blood was collected to estimate serum Creatine kinase-MB(CK-MB) level and heart specimens were handled for histology, immunohistochemistry, and quantitative morphometry study. Results: BPA persuaded several histological, immunohistochemical and biochemical alterations manifested as cardiac fiber disruption, vascular congestion, hemorrhage, RBCs extravasation, inflammatory cell infiltration and fibrosis. Cardiomyocytes displayed dark acidophilic sarcoplasm, pyknosis and perinuclear vacuolation. Also, the mean area % for collagen fiber deposition, glycogen content, Bcl-2-associated X protein, Nuclear factor kappa B (NF-κB) and Vimentin immune-expressions were significantly high. Furthermore, mast cell number/mm2, MDA and CK-MB levels were enhanced meanwhile SOD, GSH and CAT levels were declined. After 4-week recovery, cardiomyocytes and vascular changes exhibited marked improvement and all previous metrics were directed toward normal values, though most of them were still demonstrating low significant differences contrasted to controls. Conclusion: BPA induced cardiac structural and functional alterations via ROS generation, apoptosis, inflammation and fibrosis with considerable self-recovery following BPA cessation denoting transitory adverse impact. However, the particular mechanisms underlying cardiotoxicity or recovery still require further study.