Discussion
Our case highlights an interesting presentation of a dilated cardiomyopathy with acute decompensated heart failure one year after cessation of anabolic steroids in a patient who had performed intensive physical training, and showed no improvement of the ejection fraction after cessation of the abuse and initiation of conventional heart failure therapy. In literature there are several reports documenting AAS-induced cardiotoxicity and in particular DCM [1-13] (Table 1) although few of them indicate irreversible effects on cardiac muscle performance [1,6,8,13] Table. We believe that what can happen in irreversible myocytes damage like in ours patient or even in fatal cases [14,15], is a more profound damage to the myocytes that can be caused by the synergism of AAS, possibly at high dosage and for a prolonged span of time with other factors that enhance the AAS damage, first of all strenuous exercise training. We will examine first the AAS general toxic effect mechanisms on cardiac myocytes and then the AAS synergism with strenous exercise and with other potential myocites damaging factors like the growth hormone (GH).
Regarding the general AAS cardiac toxic effect AASs can have numerous cardiovascular side effects and they have a proven direct cardiotoxicity [16]. The mechanisms underlying this cardiotoxici-ty are still not properly understood, but some studies suggest that the adverse effects of AASs on cardiac muscle can be direct: in rat cardiomyocytes, AASs induce apoptotic cell death in a dose-de-pendent manner [17]. The apoptotic process may be triggered by a membrane receptor -second messenger cascades that increase polyamines which are known to mediate uncontrolled transmem-brane Ca++ flux and also by increasing intracellular Ca++ via Ca++ in-flux and Ca++ mobilization from the sarcoplasmatic reticulum [17]. The uncontrolled increase of Ca++ affects apoptotic mitochondrial membrane permeability and triggers the release of apoptogenic factors including caspase-9 from damaged mitochondria [17]. This mechanism was confirmed by an in-vitro study on the cardiomyo-cytes ultrastructure of rodents after AASs exposure demonstrating mitochondria and myofibrils aberrations similar to those observed in the early stages of human heart failure [18].