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Clinical Use of Anabolics and Hormones
Clinical Use of Anabolics and Hormones
Anabolic steroid use can increase heart disease risk
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<blockquote data-quote="madman" data-source="post: 276919" data-attributes="member: 13851"><p>[URL unfurl="true"]https://physoc.onlinelibrary.wiley.com/doi/10.1113/JP284597[/URL]</p><p></p><p></p><p><strong>Reduce plakoglobin increases the risk of sodium current defects and artrial conduction abnormalities in response to androgenic anabolic steroids (2024)</strong></p><p><strong></strong></p><p><strong></strong></p><p><strong>Translational perspective</strong></p><p><strong></strong></p><p><strong><em>Our results show that atrial arrhythmias are an important clinical feature of arrhythmogenic right ventricular cardiomyopathy (ARVC) and confirm that males are more likely to show a full ARVC phenotype. <u>We demonstrate a previously unknown interaction between defective desmosomal gene expression and exposure to androgenic anabolic steroids (AAS) in atria</u>. This might explain, in part, the occurrence of atrial conduction slowing and arrhythmias (Akcakoyun et al., <a href="https://physoc.onlinelibrary.wiley.com/doi/10.1113/JP284597#tjp15920-bib-0003" target="_blank">2014</a>; Furlanello et al., <a href="https://physoc.onlinelibrary.wiley.com/doi/10.1113/JP284597#tjp15920-bib-0026" target="_blank">2007</a>; Nieschlag & Vorona, <a href="https://physoc.onlinelibrary.wiley.com/doi/10.1113/JP284597#tjp15920-bib-0062" target="_blank">2015</a>) in athletes using AAS to enhance their performance. <u>Based on our results, searching for desmosomal gene defects in known steroid users with atrial arrhythmias seems warranted</u>. <u>Such analyses might add to a better understanding of the cardiac damage observed in some of these patients</u>.</em></strong></p><p><strong><em></em></strong></p><p><strong><em><u>Our data, gained from well-controlled murine experiments, demonstrate that reduced expression of plakoglobin, as commonly observed in cardiac tissue of patients with pathogenic mutations in a variety of desmosomal genes</u> (Asimaki et al., <a href="https://physoc.onlinelibrary.wiley.com/doi/10.1113/JP284597#tjp15920-bib-0011" target="_blank">2009</a>),<u> renders atria more susceptible to AAS-induced pathology</u>. Prevention of atrial arrhythmias in arrhythmogenic cardiomyopathies is also of interest because they can give rise to inappropriate defibrillator shocks in affected patients (Camm et al., <a href="https://physoc.onlinelibrary.wiley.com/doi/10.1113/JP284597#tjp15920-bib-0020" target="_blank">2013</a>; Takehara et al., <a href="https://physoc.onlinelibrary.wiley.com/doi/10.1113/JP284597#tjp15920-bib-0083" target="_blank">2004</a>) and further compromise heart function.</em></strong></p><p></p><p><em><strong><u>We add exposure to AAS to the list of stimuli aggravating pro-arrhythmic phenotypes in carriers of desmosomal mutations and demonstrate that this affects atrial electrical function</u>. <u>Our data provide an explanation for the stronger phenotypic expression in male gene carriers with desmosomal mutations and the observed worse clinical outcome in ARVC patients with high physiological testosterone levels</u> (Akdis et al., <a href="https://physoc.onlinelibrary.wiley.com/doi/10.1113/JP284597#tjp15920-bib-0004" target="_blank">2017</a>; Antoniades et al., <a href="https://physoc.onlinelibrary.wiley.com/doi/10.1113/JP284597#tjp15920-bib-0008" target="_blank">2006</a>; Asimaki et al., <a href="https://physoc.onlinelibrary.wiley.com/doi/10.1113/JP284597#tjp15920-bib-0010" target="_blank">2007</a>; McKoy et al., <a href="https://physoc.onlinelibrary.wiley.com/doi/10.1113/JP284597#tjp15920-bib-0058" target="_blank">2000</a>; Protonotarios et al., <a href="https://physoc.onlinelibrary.wiley.com/doi/10.1113/JP284597#tjp15920-bib-0072" target="_blank">2001</a>).</strong></em></p></blockquote><p></p>
[QUOTE="madman, post: 276919, member: 13851"] [URL unfurl="true"]https://physoc.onlinelibrary.wiley.com/doi/10.1113/JP284597[/URL] [B]Reduce plakoglobin increases the risk of sodium current defects and artrial conduction abnormalities in response to androgenic anabolic steroids (2024) Translational perspective [I]Our results show that atrial arrhythmias are an important clinical feature of arrhythmogenic right ventricular cardiomyopathy (ARVC) and confirm that males are more likely to show a full ARVC phenotype. [U]We demonstrate a previously unknown interaction between defective desmosomal gene expression and exposure to androgenic anabolic steroids (AAS) in atria[/U]. This might explain, in part, the occurrence of atrial conduction slowing and arrhythmias (Akcakoyun et al., [URL='https://physoc.onlinelibrary.wiley.com/doi/10.1113/JP284597#tjp15920-bib-0003']2014[/URL]; Furlanello et al., [URL='https://physoc.onlinelibrary.wiley.com/doi/10.1113/JP284597#tjp15920-bib-0026']2007[/URL]; Nieschlag & Vorona, [URL='https://physoc.onlinelibrary.wiley.com/doi/10.1113/JP284597#tjp15920-bib-0062']2015[/URL]) in athletes using AAS to enhance their performance. [U]Based on our results, searching for desmosomal gene defects in known steroid users with atrial arrhythmias seems warranted[/U]. [U]Such analyses might add to a better understanding of the cardiac damage observed in some of these patients[/U]. [U]Our data, gained from well-controlled murine experiments, demonstrate that reduced expression of plakoglobin, as commonly observed in cardiac tissue of patients with pathogenic mutations in a variety of desmosomal genes[/U] (Asimaki et al., [URL='https://physoc.onlinelibrary.wiley.com/doi/10.1113/JP284597#tjp15920-bib-0011']2009[/URL]),[U] renders atria more susceptible to AAS-induced pathology[/U]. Prevention of atrial arrhythmias in arrhythmogenic cardiomyopathies is also of interest because they can give rise to inappropriate defibrillator shocks in affected patients (Camm et al., [URL='https://physoc.onlinelibrary.wiley.com/doi/10.1113/JP284597#tjp15920-bib-0020']2013[/URL]; Takehara et al., [URL='https://physoc.onlinelibrary.wiley.com/doi/10.1113/JP284597#tjp15920-bib-0083']2004[/URL]) and further compromise heart function.[/I][/B] [I][B][U]We add exposure to AAS to the list of stimuli aggravating pro-arrhythmic phenotypes in carriers of desmosomal mutations and demonstrate that this affects atrial electrical function[/U]. [U]Our data provide an explanation for the stronger phenotypic expression in male gene carriers with desmosomal mutations and the observed worse clinical outcome in ARVC patients with high physiological testosterone levels[/U] (Akdis et al., [URL='https://physoc.onlinelibrary.wiley.com/doi/10.1113/JP284597#tjp15920-bib-0004']2017[/URL]; Antoniades et al., [URL='https://physoc.onlinelibrary.wiley.com/doi/10.1113/JP284597#tjp15920-bib-0008']2006[/URL]; Asimaki et al., [URL='https://physoc.onlinelibrary.wiley.com/doi/10.1113/JP284597#tjp15920-bib-0010']2007[/URL]; McKoy et al., [URL='https://physoc.onlinelibrary.wiley.com/doi/10.1113/JP284597#tjp15920-bib-0058']2000[/URL]; Protonotarios et al., [URL='https://physoc.onlinelibrary.wiley.com/doi/10.1113/JP284597#tjp15920-bib-0072']2001[/URL]).[/B][/I] [/QUOTE]
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Clinical Use of Anabolics and Hormones
Clinical Use of Anabolics and Hormones
Anabolic steroid use can increase heart disease risk
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