Background:Atorvastatin (ATOR) used as a cholesterol-lowering drug. Ator is one of statins widely used, commercially available and increasingly used day by day.Few studies and limited data were existed on atorvastatin induced histological and ultrastructural changes in the cardiac muscle fibres. The present study was conducted to evaluate the potential toxicity of the human equivalent therapeutic doses of Atorvastatin on cardiac muscle fibres in induced hyperlipidemic adult male albino rats. Material and Methods: thirty adult male albino rats were used in this study, the rats used weighing (150±10) gm. Rats were divided into groups,Group one (5 rats), served as the control group (C) .Other twenty five rats were subjected to high fat diet (25% fat and 2% cholesterol) for 3 weeksand thenthey subdivided into three groups.Group two (five rats) was considered as a hyperlipidemic group (H).Group three, treated group one (T1) (ten rats) received atorvastatin(Ator 20mg) (1.5 mg / day / rat)for three weeks , by the end the third week five rats weresacrificed and other five rats were considered as the recovery group one (R1) , they received normal diet only for another three weeks. Group four , treated group two (T2) (ten rats) received Atorvastatin (Ator 20mg) (1.5 mg / day / rat)for other six weeks , by the end of the 6th week five rats weresacrificed and other five rats were considered as the recovery group two (R2) , they received only normal diet for another six weeks. At the end of each step of the experiment, rats were sacrificed and specimens of cardiac muscle fibres prepared by different methods for light and electron microscopic studies. Also blood sampling was obtained forthebiochemical study.Results: the histological data obtained from the different groups showed many changes, in hyperlipidemic group (H) indistinct and distorted striation and separation of cardiac muscle fibres , ,vesicular nuclei , presence of myofibroblasts with congested and dilated blood vessels, loss of some nuclei and condensation of nuclear chromatin with normal mitochondria were detected. Treated group one (T1) showed that cardiac muscle fibres restored their striation with separated and splitted myofibres and pyknotic nuclei, increased myofibrobasts ,lymphocytic infiltration ,congested blood vessels and mitochondrial vacuolation with disorganization of their cristae. In treated group two (T2) patchy loss of striation was observed with splitted cardiac muscle fibres ,pyknotic nuclei of cardiomyocytes, margination of nuclear chromatin ,congested blood vessels, lymphocytic infiltration, swelling of mitochondria with disorganization of their cristae. In recovery group one (R1) cardiac muscle fibres restored their striation. In recovery group two (R2) cardiac muscle fibres restored their normal architecture. The statistically evaluated data showed a significant difference in parentage of collagen and optical density of PAS + ve materials in the different groups when compared to the control group specially in T2.The laboratory evaluated data showedsignificant increase inlevels of cholesterol (C) , triglycerides (TG), low density lipoprotein- cholesterol (LDL-C), Very low density lipoprotein (vLDL), Atherogenic index(AI) and decrease in high density lipoprotein- cholesterol (HDL-C) between the control and the hyperlipidemic group. Administration of ATOR to the treated groups induce significant decrease inlevels of C, TG, LDL-C , (vLDL), (AI) and increase of HDL-C when compared with the hyperlipidemic group .Also there were significant decreasein levels of C, TG, LDL-C and increase of HDL-Cin recovery groups when compared with the hyperlipidemic group. Conclusion: administration of ATOR for long time led to adverse degenerative effects on structure of the cardiac muscle fibres, although it has a potent lowering effect on lipid profile in hyperlipidemia.