Androgens can act directly on its receptors or via its dehydro metabolite. Its well determined that dehydrotestosterone is more potent than testosterone. Androgenic Anabolic Steroids (AAS) were developed to obtain a drug with its anabolic effect potentialized. Nandrolone decanoate (ND) is one of the most used AAS worldwide, mainly as drug of abuse to improve exercise performance and for aesthetic purposes. Dehydronadrolone (DHN) is less potent in acting on androgen receptor than ND itself. AAS has been implicated in cardiac side effects, such as cardiac hypertrophy, cytokine imbalance, and sudden cardiac death. But if ND or DHN are implicated remain to be evaluated. We investigated if the increase of the anabolic-to-androgenic ratio of the ND by the inhibition of the 5α-reductase improves the cardiac side effects of ND on heart, especially on cardiac hypertrophy and cytokine imbalance. Male Wistar rats were divided into 3 experimental groups: control animals receiving the vehicle (CONT; n=8; peanut oil, I.M., wekly; 0.9% saline; i.p., daily), animals receiving ND (DECA; n=8; 10 mg.Kg-1, twice a week, I.M.; 0.9% saline; i.p., daily), and animals receiving ND (DECAF; n=8; DN 10 mg.Kg-1, twice a week, I.M.) plus finasteride (100 µg.kg-1, i.p., daily), for four weeks. Surgical procedures were performed under sodium pentobarbital anesthesia (50mg.kg-1, intra-peritoneal, Crystal, Brazil). The experiments were performed in accordance with the ethical principles for animal experimentation by the Brazilian College of Animal Experimentation and were approved by our Institutional Ethics, Bioethics and Animal Welfare Committee (Protocol 68/2009). After the treatment period, animals were euthanized, the hearts were removed for morphometric analyzes, and determination of the cardiac pro-(TNF-α) and anti-inflammatory (IL-10) cytokines. Values are expressed as the mean ± S.E.M, compared with ANOVA using Tukey s post hoc test. Figure 1 shows that animals from DECA group present myocyte hypertrophy. Increasing the anabolic-to-androgenic ratio by finastride action, worsen all the morphometric parameters. Figure 2 presents the results of the cardiac cytokine evaluation. ND treatment increase TNF-α level while reduce the cardiac IL-10 content, indicating that ND determines cytokine embalance. Finasteride co-treatment with ND worsens the imbalance on cardiac cytokine elevating the pro-inflammatory cytokine and reducing the level of IL-10, when compared with the isolated ND treatment. In conclusion, increasing the anabolic-to-androgenic ratio of ND, by 5-α-reductase inhibitions worsen the side effects of ND on cardiac myocyte and cytokine balance, indicating that ND itself, not the DHN, is more important to determine these effects.