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<blockquote data-quote="tareload" data-source="post: 240525"><p>Excellent observation and thank you for sharing the data point. I am sure for those prone to heart arrhythmia / Post COVID complications the sleep issue with increasing T dose becomes critical as well. Thank you.</p><p></p><p>I will put together a plot of sleep quality vs T dose after I hit the wall again. Right now at 120 mg/week and slowly climbing. I like how the escitalopram controls my HR elevations during vivid dreams/nightmares and helps me get back to sleep quicker. So far it appears to be a supra T assist compound.</p><p></p><p>Data points so far at 80, 100, 120 mg/week.</p><p></p><p>BTW, for those who enjoy this sort of work:</p><p></p><p>Merry F'n Christmas.</p><p>[URL unfurl="true"]https://link.springer.com/article/10.1007/s00392-022-02129-5[/URL]</p><p></p><p></p><p></p><p><em>Through our autopsy-based approach, we identified five cases of lymphocytic (epi-)myocarditis in persons, who were unexpectedly found dead at home within the first week following mRNA-mediated anti-SARS-CoV-2 immunization. According to the Dallas criteria four samples were classified as definitive myocarditis. In the remaining case, comparable inflammatory infiltration of the epicardium, subepicardial fat and myocardium was found, but myocardial infiltration did not exceed the threshold of the Dallas criteria. All cases showed a consistent phenotype: (A) focal interstitial lymphocytic myocardial infiltration, in three cases accompanied by demonstrable microfocal myocyte destruction. (B) T-cell dominant infiltrate with CD4 positive T-cells outnumbering CD8 positive T-cells by far; (C) frequently associated with T-cell infiltration of epicardium and subepicardial fat tissue revealing a similar immune phenotype (CD4 > > CD8).</em></p><p><em></em></p><p><em>As well-known from myocardial infarction, it has to be considered that microscopically visible manifestation of myocardial damage under such acute conditions may lag behind function; this may relate to aspects of infiltrate composition, such as the relatively low macrophage content, or the histologically focal myocyte damage. Thus, functional effects may be much stronger than expected considering the histological picture. This is reflected by the fact that myocarditis is a major cause of sudden and unexpected death in infants, adolescents, and young adults with frequencies ranging from 1 to 14% among the young [<a href="https://link.springer.com/article/10.1007/s00392-022-02129-5#ref-CR18" target="_blank">18</a>,<a href="https://link.springer.com/article/10.1007/s00392-022-02129-5#ref-CR19" target="_blank">19</a>,<a href="https://link.springer.com/article/10.1007/s00392-022-02129-5#ref-CR20" target="_blank">20</a>,<a href="https://link.springer.com/article/10.1007/s00392-022-02129-5#ref-CR21" target="_blank">21</a>]. As outlined in the materials and methods section, evaluation of the likelihood of an AEFI reflects the temporal association and the autopsy findings (with exclusion of other reasons of sudden death), and negative molecular testing for potential infectious causes. Thus, case 5 with HHV6-DNA detected at low copy numbers was classified as possible. In general, a causal link between myocarditis and anti-SARS-CoV-2 vaccination is supported by several considerations: (A) a close temporal relation to vaccination; all cases were found dead within one week after vaccination, (B) absence of any other significant pre-existing heart disease, especially ischaemic heart disease or cardiomyopathy, (C) negative testing for potential myocarditis-causing infectious agents, (D) presence of a peculiar CD4 predominant T-cell infiltrate, suggesting an immune mediated mechanism. The latter criterion is supported by demonstration of a phenotypically identical T-cell infiltrate at the deltoidal injection site in one of the cases. It has to be emphasized, that a comparable (epi-)myocardial infiltration was neither found in any of the other 20 autopsies performed on bodies found dead within 20 days following an anti-SARS-CoV-2 vaccination nor in the age- and sex-matched cohorts from three independent periods from our autopsy-files.</em></p><p><em></em></p><p><em>Based on the autopsy findings and all available data, no other cause of death except (epi-)myocarditis was identified in any of the cases presented here. Hence, myocarditis has to be considered the likely cause of death. From a functional point of view, myocardial damage in our cases is not sufficient to postulate contractile failure as terminal cause of death; thus, arrhythmic failure, either by cardiac arrest or by ventricular fibrillation, has to be assumed as the mechanism leading to the patients’ death. Myocarditis-related acute cardiac arrest due to either asystoly or ventricular fibrillation is a well-established pathomechanism in other causes of acute myocarditis as well [<a href="https://link.springer.com/article/10.1007/s00392-022-02129-5#ref-CR22" target="_blank">22</a>, <a href="https://link.springer.com/article/10.1007/s00392-022-02129-5#ref-CR23" target="_blank">23</a>].</em></p><p></p><p></p><p>[ATTACH=full]27551[/ATTACH]</p></blockquote><p></p>
[QUOTE="tareload, post: 240525"] Excellent observation and thank you for sharing the data point. I am sure for those prone to heart arrhythmia / Post COVID complications the sleep issue with increasing T dose becomes critical as well. Thank you. I will put together a plot of sleep quality vs T dose after I hit the wall again. Right now at 120 mg/week and slowly climbing. I like how the escitalopram controls my HR elevations during vivid dreams/nightmares and helps me get back to sleep quicker. So far it appears to be a supra T assist compound. Data points so far at 80, 100, 120 mg/week. BTW, for those who enjoy this sort of work: Merry F'n Christmas. [URL unfurl="true"]https://link.springer.com/article/10.1007/s00392-022-02129-5[/URL] [I]Through our autopsy-based approach, we identified five cases of lymphocytic (epi-)myocarditis in persons, who were unexpectedly found dead at home within the first week following mRNA-mediated anti-SARS-CoV-2 immunization. According to the Dallas criteria four samples were classified as definitive myocarditis. In the remaining case, comparable inflammatory infiltration of the epicardium, subepicardial fat and myocardium was found, but myocardial infiltration did not exceed the threshold of the Dallas criteria. All cases showed a consistent phenotype: (A) focal interstitial lymphocytic myocardial infiltration, in three cases accompanied by demonstrable microfocal myocyte destruction. (B) T-cell dominant infiltrate with CD4 positive T-cells outnumbering CD8 positive T-cells by far; (C) frequently associated with T-cell infiltration of epicardium and subepicardial fat tissue revealing a similar immune phenotype (CD4 > > CD8). As well-known from myocardial infarction, it has to be considered that microscopically visible manifestation of myocardial damage under such acute conditions may lag behind function; this may relate to aspects of infiltrate composition, such as the relatively low macrophage content, or the histologically focal myocyte damage. Thus, functional effects may be much stronger than expected considering the histological picture. This is reflected by the fact that myocarditis is a major cause of sudden and unexpected death in infants, adolescents, and young adults with frequencies ranging from 1 to 14% among the young [[URL='https://link.springer.com/article/10.1007/s00392-022-02129-5#ref-CR18']18[/URL],[URL='https://link.springer.com/article/10.1007/s00392-022-02129-5#ref-CR19']19[/URL],[URL='https://link.springer.com/article/10.1007/s00392-022-02129-5#ref-CR20']20[/URL],[URL='https://link.springer.com/article/10.1007/s00392-022-02129-5#ref-CR21']21[/URL]]. As outlined in the materials and methods section, evaluation of the likelihood of an AEFI reflects the temporal association and the autopsy findings (with exclusion of other reasons of sudden death), and negative molecular testing for potential infectious causes. Thus, case 5 with HHV6-DNA detected at low copy numbers was classified as possible. In general, a causal link between myocarditis and anti-SARS-CoV-2 vaccination is supported by several considerations: (A) a close temporal relation to vaccination; all cases were found dead within one week after vaccination, (B) absence of any other significant pre-existing heart disease, especially ischaemic heart disease or cardiomyopathy, (C) negative testing for potential myocarditis-causing infectious agents, (D) presence of a peculiar CD4 predominant T-cell infiltrate, suggesting an immune mediated mechanism. The latter criterion is supported by demonstration of a phenotypically identical T-cell infiltrate at the deltoidal injection site in one of the cases. It has to be emphasized, that a comparable (epi-)myocardial infiltration was neither found in any of the other 20 autopsies performed on bodies found dead within 20 days following an anti-SARS-CoV-2 vaccination nor in the age- and sex-matched cohorts from three independent periods from our autopsy-files. Based on the autopsy findings and all available data, no other cause of death except (epi-)myocarditis was identified in any of the cases presented here. Hence, myocarditis has to be considered the likely cause of death. From a functional point of view, myocardial damage in our cases is not sufficient to postulate contractile failure as terminal cause of death; thus, arrhythmic failure, either by cardiac arrest or by ventricular fibrillation, has to be assumed as the mechanism leading to the patients’ death. Myocarditis-related acute cardiac arrest due to either asystoly or ventricular fibrillation is a well-established pathomechanism in other causes of acute myocarditis as well [[URL='https://link.springer.com/article/10.1007/s00392-022-02129-5#ref-CR22']22[/URL], [URL='https://link.springer.com/article/10.1007/s00392-022-02129-5#ref-CR23']23[/URL]].[/I] [ATTACH type="full"]27551[/ATTACH] [/QUOTE]
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