A couple of getbiggers are referenced as case studies on humans.
2. VASCULAR EVENTS
Androgens have been discussed to predispose to thrombosis by effecting the structure and function of vascular tissues. Structurally, androgens decrease
elastin and increase collagen and other fibrous proteins in arterial vascular tissue and skin (20–23). Functionally, androgens have been linked with an
enhancement of vascular reactivity and with a decrease in aortic smooth muscle prostaglandin 12(24). Consistent with these findings has been the identifica-
tion of specific androgen receptors in the vascular tissues of several animal species(25). Further evidence implicates that androgens may affect platelet
function and there are data to support steroid-induced alterations in all stages of the coagulation cascade(9).
Recently, Tischer et al.(26) reported the case of a 32-year-old male body builder who died of cardiac arrest (CA) attributable to long-term abuse of
anabolic steroids. Coronary angiography and autopsy findings showed ectasia of the coronary arteries with hypertrophic intima and media. Such structural
changes of the coronary arteries together with the alterations of the lipid pro-files predispose users of anabolic steroids to the development of thrombosis.
3. MYOCARDIAL ALTERATIONS
3.1. Ventricular Hypertrophy and Fibrosis
Structural effects of AAS could be demonstrated both in studies on primary myocardial cell cultures(27)and in animal experiments (28–30). Addi-tionally, quantitative electron microscopy showed an enlargement of thesarcoplasmatic space and an imbalance of the mitochondrial–myofibrillar ratio.When the administration of anabolic steroids and training are combined, pathological alterations such as destruction of mitochondria and aberrant myofibrils, focal dehiscent intercalated discs, necrotic cells, mitochondrial disruption, and a decrease in myocyte capillary supply can be observed(31,32)
There is also evidence of an increased collagen production in experimental animals after steroid exposure(30).
Structural alterations to the heart have also been observed in humans.Luke et al.(12)reported the case of a previously healthy 21-year-old steroid-abusing weight lifter who died of CA. In addition to renal hypertrophy and hepatosplenomegaly, biventricular hypertrophy could be detected. The myocardium showed extensive fibrosis, small foci of necrosis, and myocytes with
contraction band necrosis. Additionally, cases with widespread patchy fibrosis(13,15), cardiomyopathy(33), and ventricular hypertrophy(34,35)have appeared in the literature. Myocardial fibrosis is thought to be caused by alack of blood supply in the hypertrophic myocardium(36). Melchert(37)sug-gested four hypothetical models of AAS-induced adverse cardiovascular effects: (a) an atherogenic model involving the effects of AAS on lipoprotein concentrations, (b) a thrombosis model involving the effects of AAS on clotting factors and platelets, (c) a vasospasm model involving the effects of AAS on the vascular nitric oxide system, and (d) a direct myocardial injury model involving the effects of AAS on individual myocardial cells. The existence of a concentric left ventricular (LV) hypertrophy in strength-trained athletes is still a topic of debate but is rejected according to a recent clinical study (38). In some highly trained athletes, the thickness of the LV wall may increase as a consequence of exercise training. In these athletes, the differential diagnosis between physiological and pathological hypertrophy may be difficult or impossible. On the basis of echocardiography data, the upper limit to which the thickness of the LV wall may be increased by training appears to be 16 mm. Therefore, athletes with a wall thickness of more than 16 mm are likely to have primary forms of pathological hypertrophy, such as hypertrophic cardiomyopathy, possibly associated with a long-term AAS abuse
(39,40) Guggenheim Et al (Getbig) recently reported that all of the above is irrelevant and just drink your milk, take your vitamins, do more cardio and you wont have anything to worry about.
3.2. Myocardial Infarction
Several case reports dealing with sudden cardiac death as a result of acute MI following steroid abuse have been published. The first documented MI in an athlete using anabolic steroids was that of a 22-year-old world-class weight lifter with no past or family history of cardiac diseases who claimed to have used the drugs for only 6 weeks (10). Angiography was normal, total choles-terol and LDL cholesterol were markedly elevated and HDL cholesterol depressed conversely. The proposed etiology in this case was coronary artery spasm combined with increased platelet aggregation, both secondary to ana-bolic steroid abuse.
A further case of fatal acute MI associated with depressed HDL and elevated LDL cholesterol was reported in a 29-year-old male body builder with secondary analphalipoproteinemia (41). A 23-year-old body builder presented with severe tight retrosternal chest pain. He had been using anabolic steroids for the past 5 years, at least 5 weeks previously. He was a nonsmoker with no family history of heart disease. His
electrocardiogram showed evidence of an acute lateral infarction, and despite treatment with streptokinase he subsequently developed signs of a full thickness infarct with a rise in cardiac enzyme activities (11).Ferenchick (42) described the case of a 22-year-old athlete who died of MI. Postmortem examination revealed occlusion of the left main and left-anterior descending coronary arteries by acute thrombosis.
A 37-year-old weight lifter suffered an MI after 7 years of steroid abuse. Cardiac catheterization 3 days after treatment with intravenous tissue plasmi-nogen activator showed a normal LV function and unremarkable coronary arteries (14) Huie (17) described the case of a 25-year-old male amateur weight trainer with no prior medical history who suffered from an acute MI. The patient
denied using illicit drugs except for anabolic steroids. To improve his strength, he took his first weekly 100-mg dose of nandrolone decanoate intramuscularly 16 weeks prior to his admission to hospital and continued this for 6 weeks. He stopped using it for the following 4 weeks, but then resumed the injections at the higher dose of 200 mg for another 6 weeks. His last injection took place 2 days prior to his admission to hospital. In this case, a coronary thrombosis was lysed with urokinase and a follow-up angiogram revealed only slight residual wall irregularities. The patient did well with cardiac rehabilitation and was discharged home 13 days after the MI took place. Although the specific cause of coronary thrombosis in this patient remains unknown, hematologic effects of this class of drugs and the subsequent impact on ischemic heart disease have to be considered
CASE REPORTS: LITERATURE REVIEW
Only a paucity of published autopsy cases of fatal steroid abuse including detailed description of postmortem findings is available so far. In 1990, Luke et al. presented the case of a previously healthy 21-year-
old weight lifter who collapsed during a bench press workout(12). He had taken AAS (testosterone and nandrolone) parenterally over a period of several months. Autopsy findings included marked LV and right ventricular hypertro-phy of the heart with extensive regional myocardial fibrosis. The coronary arteries exhibited no evidence of atherosclerosis. The cardiac valves were unremarkable. Microscopic examination of the heart revealed regional fibro-sis with principal involvement of the subepicardial and central LV and inter-ventricular septal areas but without evidence of inflammation. Additionally,
there were several tiny foci of acute myocardial fiber necrosis accompanied by sparse neutrophilic and round cell infiltrates. Occasionally, myocardial fibers exhibited contraction band formation. Furthermore, there was marked bilat-eral renal hypertrophy and hepatosplenomegaly. Gross inspection and micro-scopic examination of the other organs revealed no significant pathological
abnormalities aside from pulmonary edema. Two possible etiologies of the cardiac findings were discussed by the authors: (a) occult episode of viral or toxic myocarditis, and (b) rapid growth of the myocardium induced by the steroids thus leading to a deficiency in myocardial blood supply. Madea and Grellner (35) reported two cases of body builders who usedoral anabolic steroids (Dianabol ® , Oral-Turinabol® ) for more than 10 years.
One of them, a 28-year-old adipose male (weight 136 kg, height 178 cm) developed severe cardiovascular side effects such as atherosclerosis, recur-rent MI, and stroke as well as enlargement of all internal organs (organ weights: heart 800 g, liver 5719 g, both kidneys 910 g). Histological examination revealed disseminated interstitial as well as perivascular fibrosis and focal scars in the myocardium as well as signs of chronic congestion of the lungs, liver, and spleen. Furthermore, the authors observed sclerosis of the coronary arteries without significant occlusions. An acute cardiac failure as a result ofmassive biventricular hypertrophy (“cor bovinum”) was discussed as the actual cause of death. The other case dealt with a 40-year-old male who committed suicide by a gun shot to the head. The main pathological findings were ven-tricular hypertrophy (heart weight 470 g), acute myocardial necrosis adjacent to a myocardial scar, mild sclerosis of the coronary arteries, mild atheroscle-rosis, encephalomalcia in cerebellum and brain stem without any cerebroscle- rosis, and an old infarction in the right kidney. Recently, this author portrayed the case of a 23-year-old male body builder who had used anabolic steroids in combination with other performance enhancing drugs over a period of about 9 months and died of acute CA with- out previous symptoms (59) . After he had visited a dance hall, he went to bed.Six hours later he was found unconscious. Resuscitation attempts performed by an emergency physician were not successful. Table 1 lists the drugs that were were found in the apartment. In brief, gross autopsy findings were as follows: body weight 94 kg, height size 192 cm, male of athletic build, hyper-trophy of the heart (weight 500 g), dilatation of the right ventricle, focal indu-ration of the endocardium, soft and fragile liver parenchyma, cerebral edema, acute congestion of liver, spleen, and kidneys. Histologically, the myocar-dium showed enlargement and nuclear polymorphism of the LV muscle fibers. Additionally, disseminated focal necroses with loss of nuclear staining, inter- stitial fibrosis, and dehiscense of intercalated discs (Fig. 1A,B) were found. Capillary hyperemia, platelet aggregations and several fibrinous clots were found in the lungs, liver and kidneys (Figs. 2 and 3). Several small, cystic, blood-filled spaces were scattered throughout the liver parenchyma, partly lined by sinusoidal cells, and the hepatocytes showed nuclear fat-free vacu-oles. The various effects of these substances on cardiac function itself and on electrolyte concentrations that also influence the cardiac system were thought to explain death as a result of sudden myocardial dysfunction on the basis of AAS-associated alterations of the myocardium. This case report illustrates well the adverse effects of performance enhancing drugs on different organ systems. The case also reports that people die from smoking and drinking, and get run over every day, so therefore you might as well take gear anyway and completely fuck up your heart in the process too.
