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      Anabolic Androgenic Steroid (AAS) Related Deaths: Autoptic, Histopathological and Toxicological Findings

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          Abstract

          Anabolic androgenic steroids (AASs) represent a large group of synthetic derivatives of testosterone, produced to maximize anabolic effects and minimize the androgenic ones. AAS can be administered orally, parenterally by intramuscular injection and transdermally. Androgens act by binding to the nuclear androgen receptor (AR) in the cytoplasm and then translocate into the nucleus. This binding results in sequential conformational changes of the receptor affecting the interaction between receptor and protein, and receptor and DNA.

          Skeletal muscle can be considered as the main target tissue for the anabolic effects of AAS, which are mediated by ARs which after exposure to AASs are up-regulated and their number increases with body building. Therefore, AASs determine an increase in muscle size as a consequence of a dose-dependent hypertrophy resulting in an increase of the cross-sectional areas of both type I and type II muscle fibers and myonuclear domains. Moreover, it has been reported that AASs can increase tolerance to exercise by making the muscles more capable to overload therefore shielding them from muscle fiber damage and improving the level of protein synthesis during recovery.

          Despite some therapeutic use of AASs, there is also wide abuse among athletes especially bodybuilders in order to improve their performances and to increase muscle growth and lean body mass, taking into account the significant anabolic effects of these drugs.

          The prolonged misuse and abuse of AASs can determine several adverse effects, some of which may be even fatal especially on the cardiovascular system because they may increase the risk of sudden cardiac death (SCD), myocardial infarction, altered serum lipoproteins, and cardiac hypertrophy.

          The aim of this review is to focus on deaths related to AAS abuse, trying to evaluate the autoptic, histopathological and toxicological findings in order to investigate the pathophysiological mechanism that underlines this type of death, which is still obscure in several aspects. The review of the literature allowed us to identify 19 fatal cases between 1990 and 2012, in which the autopsy excluded in all cases, extracardiac causes of death.

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          The athlete's heart. A meta-analysis of cardiac structure and function.

          Alexandra Van Keymeulen, Henriëtte E. van der Horst, Babette M Pluim … (2000)
          It has been postulated that depending on the type of exercise performed, 2 different morphological forms of athlete's heart may be distinguished: a strength-trained heart and an endurance-trained heart. Individual studies have not tested this hypothesis satisfactorily. The hypothesis of divergent cardiac adaptations in endurance-trained and strength-trained athletes was tested by applying meta-analytical techniques with the assumption of a random study effects model incorporating all published echocardiographic data on structure and function of male athletes engaged in purely dynamic (running) or static (weight lifting, power lifting, bodybuilding, throwing, wrestling) sports and combined dynamic and static sports (cycling and rowing). The analysis encompassed 59 studies and 1451 athletes. The overall mean relative left ventricular wall thickness of control subjects (0.36 mm) was significantly smaller than that of endurance-trained athletes (0.39 mm, P=0.001), combined endurance- and strength-trained athletes (0.40 mm, P=0.001), or strength-trained athletes (0.44 mm, P<0.001). There was a significant difference between the 3 groups of athletes and control subjects with respect to left ventricular internal diameter (P<0. 001), posterior wall thickness (P<0.001), and interventricular septum thickness (P<0.001). In addition, endurance-trained athletes and strength-trained athletes differed significantly with respect to mean relative wall thickness (0.39 versus 0.44, P=0.006) and interventricular septum thickness (10.5 versus 11.8 mm, P=0.005) and showed a trend toward a difference with respect to posterior wall thickness (10.3 versus 11.0 mm, P=0.078) and left ventricular internal diameter (53.7 versus 52.1 mm, P=0.055). With respect to cardiac function, there were no significant differences between athletes and control subjects in left ventricular ejection fraction, fractional shortening, and E/A ratio. Results of this meta-analysis regarding athlete's heart confirm the hypothesis of divergent cardiac adaptations in dynamic and static sports. Overall, athlete's heart demonstrated normal systolic and diastolic cardiac functions.
          Article 0 comments Cited 133 times – based on 0 reviews     Review now
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            Testosterone-induced increase in muscle size in healthy young men is associated with muscle fiber hypertrophy.

            Indrani Sinha-Hikim, Jorge N. Artaza, Linda J Woodhouse … (2002)
            Administration of replacement doses of testosterone to healthy hypogonadal men and supraphysiological doses to eugonadal men increases muscle size. To determine whether testosterone-induced increase in muscle size is due to muscle fiber hypertrophy, 61 healthy men, 18-35 yr of age, received monthly injections of a long-acting gonadotropin-releasing hormone (GnRH) agonist to suppress endogenous testosterone secretion and weekly injections of 25, 50, 125, 300, or 600 mg testosterone enanthate (TE) for 20 wk. Thigh muscle volume was measured by magnetic resonance imaging (MRI) scan, and muscle biopsies were obtained from vastus lateralis muscle in 39 men before and after 20 wk of combined treatment with GnRH agonist and testosterone. Administration of GnRH agonist plus TE resulted in mean nadir testosterone concentrations of 234, 289, 695, 1,344, and 2,435 ng/dl at the 25-, 50-, 125-, 300-, and 600-mg doses, respectively. Graded doses of testosterone administration were associated with testosterone dose and concentration-dependent increase in muscle volume measured by MRI (changes in vastus lateralis volume, -4, +7, +15, +32, and +48 ml at 25-, 50-, 125-, 300-, and 600-mg doses, respectively). Changes in cross-sectional areas of both type I and II fibers were dependent on testosterone dose and significantly correlated with total (r = 0.35, and 0.44, P < 0.0001 for type I and II fibers, respectively) and free (r = 0.34 and 0.35, P < 0.005) testosterone concentrations during treatment. The men receiving 300 and 600 mg of TE weekly experienced significant increases from baseline in areas of type I (baseline vs. 20 wk, 3,176 +/- 186 vs. 4,201 +/- 252 microm(2), P < 0.05 at 300-mg dose, and 3,347 +/- 253 vs. 4,984 +/- 374 microm(2), P = 0.006 at 600-mg dose) muscle fibers; the men in the 600-mg group also had significant increments in cross-sectional area of type II (4,060 +/- 401 vs. 5,526 +/- 544 microm(2), P = 0.03) fibers. The relative proportions of type I and type II fibers did not change significantly after treatment in any group. The myonuclear number per fiber increased significantly in men receiving the 300- and 600-mg doses of TE and was significantly correlated with testosterone concentration and muscle fiber cross-sectional area. In conclusion, the increases in muscle volume in healthy eugonadal men treated with graded doses of testosterone are associated with concentration-dependent increases in cross-sectional areas of both type I and type II muscle fibers and myonuclear number. We conclude that the testosterone induced increase in muscle volume is due to muscle fiber hypertrophy.
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              A defect in the Kv channel-interacting protein 2 (KChIP2) gene leads to a complete loss of I(to) and confers susceptibility to ventricular tachycardia.

              Michael Chu, Tú Nguyen-Dumont, Chin Lin … (2001)
              KChIP2, a gene encoding three auxiliary subunits of Kv4.2 and Kv4.3, is preferentially expressed in the adult heart, and its expression is downregulated in cardiac hypertrophy. Mice deficient for KChIP2 exhibit normal cardiac structure and function but display a prolonged elevation in the ST segment on the electrocardiogram. The KChIP2(-/-) mice are highly susceptible to the induction of cardiac arrhythmias. Single-cell analysis revealed a substrate for arrhythmogenesis, including a complete absence of transient outward potassium current, I(to), and a marked increase in action potential duration. These studies demonstrate that a defect in KChIP2 is sufficient to confer a marked genetic susceptibility to arrhythmias, establishing a novel genetic pathway for ventricular tachycardia via a loss of the transmural gradient of I(to).
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                Author and article information

                Journal
                Journal ID (nlm-ta): Curr Neuropharmacol
                Journal ID (iso-abbrev): Curr Neuropharmacol
                Journal ID (publisher-id): CN
                Title: Current Neuropharmacology
                Publisher: Bentham Science Publishers
                ISSN (Print): 1570-159X
                ISSN (Electronic): 1875-6190
                Publication date (Print): January 2015
                Publication date (Electronic): January 2015
                Volume: 13
                Issue: 1
                Pages: 146-159
                Affiliations
                [1 ] Department of Anatomical, Histological, Forensic and Orthopaedic Sciences, Sapienza University of Rome, Viale Regina Elena 336, 00161, Rome, Italy;
                [2 ]Neuromed, Istituto Mediterraneo Neurologico (IRCCS), Via Atinense 18, Pozzilli, 86077 Isernia, Italy
                [3 ]Section of Legal Medicine, Tor Vergata University of Rome
                Author notes
                [* ]Address correspondence to this author at the Department of Anatomical, Histological, Medico-legal and Orthopaedic Sciences, Sapienza University of Rome, Viale Regina Elena 336 (00185) Rome, IT; Tel: +39 06.49912622; E-mail: fra.busardo@ 123456libero.it
                Article
                Publisher ID: CN-13-146
                DOI: 10.2174/1570159X13666141210225414
                PMC ID: 4462039
                PubMed ID: 26074749
                SO-VID: 6dcbabc4-a353-4bc3-89ff-ce15b8319167
                Copyright © ©2015 Bentham Science Publishers
                License:

                This is an open access article licensed under the terms of the Creative Commons Attribution Non-Commercial License ( http://creativecommons.org/licenses/by-nc/3.0/) which permits unrestricted, non-commercial use, distribution and reproduction in any medium, provided the work is properly cited.

                History
                Date received : 26 July 2014
                Date revision received : 1 October 2014
                Date accepted : 25 October 2014
                Categories
                Subject: Article

                ScienceOpen disciplines: Pharmacology & Pharmaceutical medicine
                Keywords: anabolic androgenic steroids (aas),cardiovascular effects,sudden cardiac death,toxicity
                Data availability:
                ScienceOpen disciplines: Pharmacology & Pharmaceutical medicine
                Keywords: anabolic androgenic steroids (aas), cardiovascular effects, sudden cardiac death, toxicity

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