AAS and Cardiovascular/Pulmonary Function

[Michael Scally MD]

Christopoulos G, DeSimone CV, Anavekar NS. 30-Year-Old Man with Outside-of-Hospital Cardiac Arrest. Mayo Clinic proceedings. Redirecting

A 30-year-old man was admitted to the cardiac intensive care unit after experiencing an out-of-hospital cardiac arrest. He was found unresponsive in bed and underwent 30 minutes of cardiopulmonary resuscitation, including 5 shocks for ventricular fibrillation before return of spontaneous circulation.

His medical history was notable for bipolar disorder, past suicidal ideation during adolescence, tobacco and alcohol abuse, and motor vehicle accidents resulting in cervical and thoracic spinal injuries. He had no prior cardiovascular history or symptoms before the cardiac arrest. There was no family history of premature coronary artery disease, cardiomyopathy, or sudden cardiac death.

His medications included supplements used to enhance athletic performance in bodybuilding, including anabolic steroids, creatine monohydrate, clenbuterol (a b2-agonist not approved by the US Food and Drug Administration [FDA]), taurine, saw palmetto, and amino acid supplements. He had used lithium in the past, but the last documented use was 3 years prior to presentation.

…

Anabolic steroid induced cardiomyopathy is a well-established entity in the literature. A number of case reports have linked anabolic steroids to ventricular hypertrophy, dilated cardiomyopathy, hypertension, atrial and ventricular arrhythmias, atherosclerotic disease, and myocardial infarction and sudden cardiac death.

Our case demonstrates that cardiomyopathy induced by anabolic steroids and performance-enhancing drugs should be considered in the differential diagnosis of ventricular arrhythmias in young patients without a personal or family history of organic heart disease. In addition, an elevated hemoglobin level of 19 g/dL, as seen in our patient, is not normal in a young, healthy man and should alert the clinician to further investigate for the driving etiology

 

[Michael Scally MD]

Chang S, Rasmussen JJ, Frandsen MN, et al. Procoagulant State in Current and Former Anabolic Androgenic Steroid Abusers. Thromb Haemost 2018;118:647-53. Thieme E-Journals - Thrombosis and Haemostasis / Abstract

Background - Anabolic androgenic steroid (AAS) abusers are considered at increased risk of cardiovascular morbidity and mortality. We hypothesized that current and former AAS abuse would induce a procoagulant shift in the haemostatic balance.

Methods - Men 18 to 50 years of age were included as current AAS abusers, former AAS abusers or controls. Morning blood samples were collected after overnight fasting. Thrombin generation (lag time, time to peak, peak height, and endogenous thrombin potential [ETP]) and coagulation factor II (prothrombin), VII and X, antithrombin, protein C, free protein S and tissue factor pathway inhibitor (TFPI) were assessed. Groups were compared by ANOVA or Kruskal–Wallis test and probabilities were corrected for multiple comparisons. Associations were evaluated using linear regression models.

Results - ETP was increased around 15% in current (n = 37) and former (n = 33) AAS abusers compared with controls (n = 30; p < 0.001). Prothrombin and factor X were increased ≥10% in AAS abusers and prothrombin was a predictor of ETP (p < 0.0005). Lag time and time to peak were increased 10 to 30% in current AAS abusers (p < 0.001) and associated with higher concentrations of TFPI, antithrombin, protein C and protein S (p < 0.0005; = 0.005). Multivariate linear regression, with all coagulation inhibitors as covariates, identified TFPI to be independently associated with lag time and time to peak (p < 0.0005).

Conclusion - Thrombin generation is augmented in current and former AAS abusers, reflecting a procoagulant state, with altered concentrations of coagulation proteins. Prospective studies are needed to clarify whether these findings translate into an increased thrombotic risk in AAS abusers potentially even after cessation.

 

[hurricane]

Christopoulos G, DeSimone CV, Anavekar NS. 30-Year-Old Man with Outside-of-Hospital Cardiac Arrest. Mayo Clinic proceedings. Redirecting

A 30-year-old man was admitted to the cardiac intensive care unit after experiencing an out-of-hospital cardiac arrest. He was found unresponsive in bed and underwent 30 minutes of cardiopulmonary resuscitation, including 5 shocks for ventricular fibrillation before return of spontaneous circulation.

His medical history was notable for bipolar disorder, past suicidal ideation during adolescence, tobacco and alcohol abuse, and motor vehicle accidents resulting in cervical and thoracic spinal injuries. He had no prior cardiovascular history or symptoms before the cardiac arrest. There was no family history of premature coronary artery disease, cardiomyopathy, or sudden cardiac death.

His medications included supplements used to enhance athletic performance in bodybuilding, including anabolic steroids, creatine monohydrate, clenbuterol (a b2-agonist not approved by the US Food and Drug Administration [FDA]), taurine, saw palmetto, and amino acid supplements. He had used lithium in the past, but the last documented use was 3 years prior to presentation.

…

Anabolic steroid induced cardiomyopathy is a well-established entity in the literature. A number of case reports have linked anabolic steroids to ventricular hypertrophy, dilated cardiomyopathy, hypertension, atrial and ventricular arrhythmias, atherosclerotic disease, and myocardial infarction and sudden cardiac death.

Our case demonstrates that cardiomyopathy induced by anabolic steroids and performance-enhancing drugs should be considered in the differential diagnosis of ventricular arrhythmias in young patients without a personal or family history of organic heart disease. In addition, an elevated hemoglobin level of 19 g/dL, as seen in our patient, is not normal in a young, healthy man and should alert the clinician to further investigate for the driving etiology

 

[Michael Scally MD]

Anabolic Androgenic Steroid Use as a Cause of Fulminant Heart Failure

A 39-year-old male weightlifter presented in fulminant heart failure. An echocardiogram revealed severe global biventricular failure. LV systolic function was estimated at 15%.

He was medically optimized and discharged in stable condition. The patient was asked to refrain from isometric resistance exercise. A follow-up 6-month echocardiogram showed evidence of partial recovery of systolic function with an LV ejection fraction of 39%.

His dilated cardiomyopathy was attributed to his use of both testosterone and boldenone in the 3-month period prior to his presentation.

Our case suggests that androgenic anabolic steroid use should be considered in the differential diagnosis of patients presenting with acute heart failure.

White M, Brennan E, Mi Ren KY, Shi M, Thakrar A. Anabolic Androgenic Steroid Use as a Cause of Fulminant Heart Failure. Canadian Journal of Cardiology. Anabolic Androgenic Steroid Use as a Cause of Fulminant Heart Failure

 

[Michael Scally MD]

Bianchi VE. Testosterone, myocardial function, and mortality. Heart Failure Reviews 2018. Testosterone, myocardial function, and mortality

The cardiovascular system is particularly sensitive to androgens, but some controversies exist regarding the effect of testosterone on the heart. While among anabolic abusers, cases of sudden cardiac death have been described, recently it was reported that low serum level of testosterone was correlated with increased risk of cardiovascular diseases (CVD) and mortality rate.

This review aims to evaluate the effect of testosterone on myocardial tissue function, coronary artery disease (CAD), and death. Low testosterone level is associated with increased incidence of CAD and mortality. Testosterone administration in hypogonadal elderly men and women has a positive effect on cardiovascular function and improved clinical outcomes and survival time.

Although at supraphysiologic doses, androgen may have a toxic effect, and at physiological levels, testosterone is safe and exerts a beneficial effect on myocardial function including mechanisms at cellular and mitochondrial level. The interaction with free testosterone and estradiol should be considered. Further studies are necessary to better understand the interaction mechanisms for an optimal androgen therapy in CVD.

 

[Michael Scally MD]

Bartlett J, Predazzi IM, Williams SM, et al. Is Isolated Low High-Density Lipoprotein Cholesterol a Cardiovascular Disease Risk Factor? Circulation: Cardiovascular Quality and Outcomes 2016;9:206. Is Isolated Low High-Density Lipoprotein Cholesterol a Cardiovascular Disease Risk Factor?

WHAT IS KNOWN
· High-density lipoprotein cholesterol (HDL-C) is inversely associated with cardiovascular risk (CVD). However, the extent to which HDL-C remains an independent CVD risk factor when other lipids are normal is unclear.


WHAT THE STUDY ADDS
· In the Framingham Offspring Study, HDL-C was not uniformly predictive of CVD risk.

· Triglycerides and low-density lipoprotein cholesterol were important modifiers of incident CVD at both ends of the HDL-C spectrum.

· Compared with isolated low HDL-C, the risk of CVD was 30% to 60% higher when low HDL-C was accompanied by higher levels of TG, low-density lipoprotein cholesterol, or both.

· High HDL-C was not associated with reduced CVD risk if accompanied by TG and low-density lipoprotein cholesterol <100 mg/dL.

Background—Although the inverse association between high-density lipoprotein cholesterol (HDL-C) and risk of cardiovascular disease (CVD) has been long established, it remains unclear whether low HDL-C remains a CVD risk factor when levels of low-density lipoprotein cholesterol (LDL-C) and triglycerides (TG) are not elevated. This is a timely issue because recent studies have questioned whether HDL-C is truly an independent predictor of CVD.

Methods and Results—3590 men and women from the Framingham Heart Study offspring cohort without known CVD were followed between 1987 and 2011. Low HDL-C (<40 mg/dL in men and <50 mg/dL in women) was defined as isolated if TG and LDL-C were both low (<100 mg/dL).

We also examined higher thresholds for TG (150 mg/dL) and LDL-C (130 mg/dL) and compared low versus high HDL-C phenotypes using logistic regression analysis to assess association with CVD.

Compared with isolated low HDL-C, CVD risks were higher when low HDL-C was accompanied by LDL-C ≥100 mg/dL and TG <100 mg/dL (odds ratio 1.3 [1.0, 1.6]), TG ≥100 mg/dL and LDL-C <100 mg/dL (odds ratio 1.3 [1.1, 1.5]), or TG and LDL-C ≥100 mg/dL (odds ratio 1.6, [1.2, 2.2]), after adjustment for covariates.

When low HDL-C was analyzed with higher thresholds for TG (≥150 mg/dL) and LDL-C (≥130 mg/dL), results were essentially the same. In contrast, compared with isolated low HDL-C, high HDL-C was associated with 20% to 40% lower CVD risk except when TG and LDL-C were elevated.

Conclusions—CVD risk as a function of HDL-C phenotypes is modulated by other components of the lipid panel.

 

[Michael Scally MD]

 

[hurricane]

Christopoulos G, DeSimone CV, Anavekar NS. 30-Year-Old Man with Outside-of-Hospital Cardiac Arrest. Mayo Clinic proceedings. Redirecting

A 30-year-old man was admitted to the cardiac intensive care unit after experiencing an out-of-hospital cardiac arrest. He was found unresponsive in bed and underwent 30 minutes of cardiopulmonary resuscitation, including 5 shocks for ventricular fibrillation before return of spontaneous circulation.

His medical history was notable for bipolar disorder, past suicidal ideation during adolescence, tobacco and alcohol abuse, and motor vehicle accidents resulting in cervical and thoracic spinal injuries. He had no prior cardiovascular history or symptoms before the cardiac arrest. There was no family history of premature coronary artery disease, cardiomyopathy, or sudden cardiac death.

His medications included supplements used to enhance athletic performance in bodybuilding, including anabolic steroids, creatine monohydrate, clenbuterol (a b2-agonist not approved by the US Food and Drug Administration [FDA]), taurine, saw palmetto, and amino acid supplements. He had used lithium in the past, but the last documented use was 3 years prior to presentation.

…

Anabolic steroid induced cardiomyopathy is a well-established entity in the literature. A number of case reports have linked anabolic steroids to ventricular hypertrophy, dilated cardiomyopathy, hypertension, atrial and ventricular arrhythmias, atherosclerotic disease, and myocardial infarction and sudden cardiac death.

Our case demonstrates that cardiomyopathy induced by anabolic steroids and performance-enhancing drugs should be considered in the differential diagnosis of ventricular arrhythmias in young patients without a personal or family history of organic heart disease. In addition, an elevated hemoglobin level of 19 g/dL, as seen in our patient, is not normal in a young, healthy man and should alert the clinician to further investigate for the driving etiology

Christ that case study sounds just like me!! Dilated cardiomyopathy has always inrigued me. They've never known how I got it. Plus I've always been told it's a condition that won't kill me but they're always concerned with my EF. I've stopped researching it. lol

 

[NorthMich]

I’m 56 and going to start low dose trt. I have normal BP and have been checked for left ventricular hypertrophy. My mother died at 62 from this, but had huge anxiety and unchecked BP as the cause.

 

[Michael Scally MD]

Mert KU, İlgüy S, Mert GÖ, Dural M, Iskenderov K. Noninvasive predictors of cardiac arrhythmias in bodybuilders. Revista Portuguesa de Cardiologia 2018. Noninvasive predictors of cardiac arrhythmias in bodybuilders - ScienceDirect

Introduction and Objective - Arrhythmias are often recorded in strength training athletes without cardiovascular abnormalities but may also be a sign of an underlying cardiovascular disease which carries a risk of sudden cardiac death (SCD). Nowadays, bodybuilding is a popular sport among adolescents and young adults.

There have been few studies of arrhythmias comparing bodybuilders with healthy controls and excluding anabolic steroid use. We aimed to assess the structural, functional and electrical characteristics of bodybuilders’ hearts compared with control subjects.

Methods - In this study, we assessed 35 male competitive bodybuilders and 35 healthy control subjects matched for age, gender, and body mass index. A detailed cardiovascular and systemic examination was performed at the beginning of the study to collect demographic data and anthropometric measures. Biochemical and hematologic, echocardiographic, 24-h Holter, and ECG measurements were obtained from all participants.

Results - Ventricular arrhythmias were encountered significantly more frequently in bodybuilders than in the control group. QT and QTc were not significantly different between groups. Tp-e interval, Tp-e/QT ratio, and Tp-e/QTc ratio were significantly greater in bodybuilders than in the control group (p<0.001 for all). There was a positive correlation between Tp-e interval, Tp-e/QT ratio, and Tp-e/QTc ratio and right ventricular (RV) diameter and arrhythmias.

Conclusion - Prolonged repolarization is common in athletes, although its predictive value is unclear. In this study, alterations in ventricular repolarization were positively correlated with RV dimensions. Therefore, we postulate that arrhythmias in strength athletes may be predicted by assessing the right ventricle echocardiographically and dispersions of repolarization on the ECG, and that SCD could be avoided in strength athletes by careful application of this information.

 

[hurricane]

Mert KU, İlgüy S, Mert GÖ, Dural M, Iskenderov K. Noninvasive predictors of cardiac arrhythmias in bodybuilders. Revista Portuguesa de Cardiologia 2018. Noninvasive predictors of cardiac arrhythmias in bodybuilders - ScienceDirect

Introduction and Objective - Arrhythmias are often recorded in strength training athletes without cardiovascular abnormalities but may also be a sign of an underlying cardiovascular disease which carries a risk of sudden cardiac death (SCD). Nowadays, bodybuilding is a popular sport among adolescents and young adults.

There have been few studies of arrhythmias comparing bodybuilders with healthy controls and excluding anabolic steroid use. We aimed to assess the structural, functional and electrical characteristics of bodybuilders’ hearts compared with control subjects.

Methods - In this study, we assessed 35 male competitive bodybuilders and 35 healthy control subjects matched for age, gender, and body mass index. A detailed cardiovascular and systemic examination was performed at the beginning of the study to collect demographic data and anthropometric measures. Biochemical and hematologic, echocardiographic, 24-h Holter, and ECG measurements were obtained from all participants.

Results - Ventricular arrhythmias were encountered significantly more frequently in bodybuilders than in the control group. QT and QTc were not significantly different between groups. Tp-e interval, Tp-e/QT ratio, and Tp-e/QTc ratio were significantly greater in bodybuilders than in the control group (p<0.001 for all). There was a positive correlation between Tp-e interval, Tp-e/QT ratio, and Tp-e/QTc ratio and right ventricular (RV) diameter and arrhythmias.

Conclusion - Prolonged repolarization is common in athletes, although its predictive value is unclear. In this study, alterations in ventricular repolarization were positively correlated with RV dimensions. Therefore, we postulate that arrhythmias in strength athletes may be predicted by assessing the right ventricle echocardiographically and dispersions of repolarization on the ECG, and that SCD could be avoided in strength athletes by careful application of this information.

It really makes me wonder just how safe weight training is. None of my docs have told me to stop though.
They just said don't go heavy and no pressing movements over my head(shoulder pressing type exercises). Very interesting and concerning study.

 

[Michael Scally MD]

Andrews MA, Magee CD, Combest TM, Allard RJ, Douglas KM. Physical Effects of Anabolic-androgenic Steroids in Healthy Exercising Adults: A Systematic Review and Meta-analysis. Curr Sports Med Rep 2018;17:232-41. https://journals.lww.com/acsm-csmr/fulltext/2018/07000/Physical_Effects_of_Anabolic_androgenic_Steroids.5.aspx

Many athletes use anabolic-androgenic steroids (AAS) for physical enhancement but the magnitude of these gains and associated adverse effects has not been rigorously quantified. MEDLINE, EMBASE, Cochrane, SPORTDiscus, and PsycINFO were searched to identify randomized placebo-controlled trials of AAS in healthy exercising adults that reported one of the following outcomes: muscular strength, body composition, cardiovascular endurance, or power.

Two authors appraised abstracts to identify studies for full-text retrieval; these were reviewed in duplicate to identify included studies. Study quality was assessed using the Cochrane method. Data were extracted in duplicate and pooled using the DerSimonian and Laird random effects model and to calculate the ratio of mean outcome improvement where possible.

Pooled standardized mean difference (SMD) in muscle strength between AAS and placebo was 0.27 (95% confidence interval, 0.07-0.47; I = 12.7%; 21 studies). Change in strength was 52% greater in the AAS group compared to placebo. The SMD for change in lean mass between AAS and placebo was 0.62 (95% confidence interval, 0.35-0.89; I = 26%; 14 studies).

Due to missing data, fat mass, cardiovascular endurance, power, and adverse effects were summarized qualitatively. Only 13 of 25 studies reported adverse effects including increased low density lipoprotein (LDL), decreased high density lipoprotein (HDL), irritability, and acne.

In healthy exercising adults, AAS use is associated with a small absolute increase in muscle strength and moderate increase in lean mass. However, the transparency and completeness of adverse effect reporting varied, most studies were of short duration, and doses studied may not reflect actual use by athletes.

 

[Michael Scally MD]

[OA] Cardiomyopathy Induced by Anabolic-Androgenic Steroid Abuse.

Bodybuilders use anabolic-androgenic steroids to increase muscle mass, but abuse of these hormones has been related to cardiomyopathy in the past.

A 60-year-old Caucasian male bodybuilder with medical history of male hypogonadism and on testosterone replacement therapy, allegedly preparing for a weightlifting competition and receiving stem cell infusions from his trainer, is transferred to the intensive care unit for worsening shortness of breath after failing treatment for community-acquired pneumonia.

Chest X-ray on transfer was suggestive of pulmonary oedema, and transthoracic echocardiography showed an ejection fraction of 25%–30%.

The patient was taken for cardiac catheterisation, which yielded non-ischaemic cardiomyopathy.

His testosterone levels were supratherapeutic. Anabolic-androgenic steroid abuse can be a cause of cardiomyopathy in patients who have no other risk factor for such disease.

Garner O, Iardino A, Ramirez A, Yakoby M. Cardiomyopathy induced by anabolic-androgenic steroid abuse. BMJ case reports 2018;2018. http://casereports.bmj.com/content/2018/bcr-2017-223891.full

 

[Michael Scally MD]

Testosterone to Estradiol Ratio Reflects Systemic and Plaque Inflammation and Predicts Future Cardiovascular Events

Aims - The effects of testosterone on cardiovascular disease (CVD) as reported in literature have been ambiguous. Recently, the interplay between testosterone and estradiol as assessed by testosterone/estradiol (T/E2) ratio was suggested to be better informative on the normal physiological balance.

Considering the role in CVD, we hypothesized that a low T/E2 ratio in men with CVD is associated with increased inflammation, a more unstable plaque and a worse cardiovascular outcome.

Methods and results - Testosterone and estradiol concentrations were determined in blood samples of 611 male carotid endarterectomy patients included in the Athero-Express Biobank Study.

T/E2 ratio was associated with baseline characteristics, atherosclerotic plaque specimens, inflammatory biomarkers and three-year follow-up information. Patients with low T/E2 ratio had more unfavorable inflammatory profiles compared to patients with high T/E2 as observed by higher levels of C-reactive protein (CRP) (2.81 μg/mL vs. 1.22 μg/mL (p < 0.001)) and higher leukocyte counts (8.98*109/L vs. 7.75*109/L (p = 0.001)) in blood.

In atherosclerotic plaques, a negative association between T/E2 ratio and number of neutrophils (B=-0.366(p = 0.012), plaque calcifications (OR: 0.816(p = 0.044)), interleukin-6 (IL-6) (B=-0.15 p = 0.009) and Il-6receptor (B=-0.13 p = 0.024) was found.

Furthermore, in multivariate Cox regression analysis, low T/E2 ratio was independently associated with an increased risk for major cardiovascular events (MACE) during three-year follow-up (HR 1.67(95%CI: 1.02-2.76) p = 0.043). In men with elevated body mass index, these effects were strongest.

Conclusions - In male patients with manifest atherosclerotic disease, low T/E2 ratio was associated with increased systemic inflammation, increased inflammatory plaque proteins and an increased risk of future major cardiovascular events as compared to men with normal T/E2 ratio.

These effects are strongest in men with elevated body mass index and are expected to be affected by aromatase activity in white fat tissues. Normalization of T/E2 ratio may be considered as target for the secondary prevention of CVD in men.

van Koeverden ID, de Bakker M, Haitjema S, et al. Testosterone to estradiol ratio reflects systemic and plaque inflammation and predicts future cardiovascular events in men with severe atherosclerosis. Cardiovascular Research 2018. Testosterone to estradiol ratio reflects systemic and plaque inflammation and predicts future cardiovascular events in men with severe atherosclerosis | Cardiovascular Research | Oxford Academic

 

[Michael Scally MD]

Oestradiol Level, Oestrogen Receptors, and Mortality in Elderly Men

Context - Although endogenous oestradiol, generally considered as the female hormone, has been little investigated in men, it could play a role in men's health, mortality in particular. The influence of oestrogen receptors (ER) genetic polymorphisms on this relationship has never been studied.

Design and Participants - The Three‐City cohort study included (1999‐2001) 3650 men ≥65 years who were followed for mortality over 12 years. At baseline, total oestradiol (tE2) was measured and ER genotyped in a random subsample of 472 men without hormonal treatment. Free oestradiol (fE2) was estimated using Vermeulen and Södergard algorithms.

Main Outcome - Mortality data were obtained from death certificates. We used inverse probability weighted Cox models to examine the association of oestradiol with all‐cause and cause‐specific mortality and its interaction with ER genetic polymorphisms.

Results - A total of 183 men died over the follow‐up (cardiovascular disease (CVD), n = 44; cancer, n = 57; other causes, n = 82). After adjustment, there was a quadratic relationship of all‐cause mortality with tE2 and fE2 (P‐quadratic = 0.04 and 0.05, respectively), with higher mortality for the top and bottom tertiles compared to the middle one.

These associations were stronger for CVD mortality (P‐quadratic = 0.01 and 0.02 for tE2 and fE2, respectively) and disappeared for cancer mortality. There was no evidence of an interaction of oestradiol with any ER polymorphisms on all‐cause mortality.

Conclusion - In elderly men, we showed a nonlinear association of tE2 and fE2 with all‐cause mortality. These quadratic relationships were stronger for CVD mortality and did not exist for cancer mortality. ER genetic polymorphisms did not modify this association.

Laouali N, Brailly-Tabard S, Helmer C, et al. Oestradiol level, oestrogen receptors, and mortality in elderly men: The three-city cohort study. Clinical Endocrinology 2018;0. https://doi.org/10.1111/cen.13797

 

[hurricane]

[OA] Cardiomyopathy Induced by Anabolic-Androgenic Steroid Abuse.

Bodybuilders use anabolic-androgenic steroids to increase muscle mass, but abuse of these hormones has been related to cardiomyopathy in the past.

A 60-year-old Caucasian male bodybuilder with medical history of male hypogonadism and on testosterone replacement therapy, allegedly preparing for a weightlifting competition and receiving stem cell infusions from his trainer, is transferred to the intensive care unit for worsening shortness of breath after failing treatment for community-acquired pneumonia.

Chest X-ray on transfer was suggestive of pulmonary oedema, and transthoracic echocardiography showed an ejection fraction of 25%–30%.

The patient was taken for cardiac catheterisation, which yielded non-ischaemic cardiomyopathy.

His testosterone levels were supratherapeutic. Anabolic-androgenic steroid abuse can be a cause of cardiomyopathy in patients who have no other risk factor for such disease.

Garner O, Iardino A, Ramirez A, Yakoby M. Cardiomyopathy induced by anabolic-androgenic steroid abuse. BMJ case reports 2018;2018. http://casereports.bmj.com/content/2018/bcr-2017-223891.full

I wonder what dose of "trt" he was really on. Don't know enough about stem cell research to comment on that.

 

[Michael Scally MD]

Melo Junior AF, Dalpiaz PLM, Sousa GJ, et al. Nandrolone alter left ventricular contractility and promotes remodelling involving calcium-handling proteins and renin-angiotensin system in male SHR. Life sciences 2018. Nandrolone alter left ventricular contractility and promotes remodelling involving calcium-handling proteins and renin-angiotensin system in male SHR - ScienceDirect

AIMS: Hypertension is a highly prevalent disease that has been correlated to severe organ damage and mortality. However, the role of androgens in hypertension is controversial. The aim of this study was to evaluate the cardiac effects of the nandrolone decanoate (NDL) in male SHR.

MAIN METHODS: At 12weeks of age, male SHR rats were separated into three groups: Control (CON), Nandrolone 10mg/kg twice weekly (NDL), and NDL plus Enalapril 10mg/kg/day (NDL-E) groups. The animals were treated for 4weeks. Haemodynamic parameters were acquired through ventricular catheter implantation. The left ventricle was stained with haematoxylin/eosin or picrosirius red. Western blot analysis of TNF-alpha, ACE, AT1R, beta1-AR, PLB, p-PLB(ser16) and SERCA2a was performed.

KEY FINDINGS: Nandrolone increased hypertension in SHR rats and enalapril reduced blood pressure to values below those of the control. NDL increased +dP/dtmax, -dP/dtmax and cardiac hypertrophy, which were prevented in the NDL-E group. Cardiac collagen deposition was increased in the NDL group, with this effect being attenuated by enalapril in NDL-E animals. TNF-alpha, ACE, AT1R and beta1-AR proteins were increased in the NDL, and enalapril decreased them, except for TNF-alpha. The ratio p-PLB(ser16)/PLB revealed an increase after nandrolone, which was prevented in the NDL-E group. The SERCA2a expression protein and SERCA2a/PLB were increased in NDL animals, which did not occur in the NDL-E group.

SIGNIFICANCE: Nandrolone has distinct effects on cardiac function and remodelling in male SHR, altering the hypertension development process in the heart through modulation of calcium handling proteins and the renin-angiotensin system.

 

[Michael Scally MD]

Kloner RA, Carson C, 3rd, Dobs A, Kopecky S, Mohler ER, 3rd. Testosterone and Cardiovascular Disease. J Am Coll Cardiol 2016;67(5):545-57. Elsevier: Article Locator

Testosterone (T) is the principal male sex hormone. As men age, T levels typically fall. Symptoms of low T include decreased libido, vasomotor instability, and decreased bone mineral density. Other symptoms may include depression, fatigue, erectile dysfunction, and reduced muscle strength/mass. Epidemiology studies show that low levels of T are associated with more atherosclerosis, coronary artery disease, and cardiovascular events. However, treating hypogonadism in the aging male has resulted in discrepant results in regard to its effect on cardiovascular events. Emerging studies suggest that T may have a future role in treating heart failure, angina, and myocardial ischemia. A large, prospective, long-term study of T replacement, with a primary endpoint of a composite of adverse cardiovascular events including myocardial infarction, stroke, and/or cardiovascular death, is needed. The Food and Drug Administration recently put additional restrictions on T replacement therapy labeling and called for additional studies to determine its cardiac safety.

Culic V. Testosterone and Cardiac Diastolic Function. J Am Coll Cardiol 2016;68:573-4. Testosterone and Cardiac Diastolic Function - ScienceDirect


Kloner RA, Carson C, 3rd, Dobs A, Kopecky S, Mohler ER, 3rd. Reply: Testosterone and Cardiac Diastolic Function. J Am Coll Cardiol 2016;68:574-5. Reply: Testosterone and Cardiac Diastolic Function - ScienceDirect

 

[Michael Scally MD]

Cardiovascular Impact of Testosterone Therapy for Hypogonadism

Introduction. Since 2010 some evidence supporting the possible increased cardiovascular (CV) risk related to testosterone treatment (TTh) has created much debate in the scientific community.

Based on these results, the US Food and Drug Administration agency has questioned TTh for aging men recognizing its value only for classical hypogonadism due to genetic or organic causes.

To better clarify this topic, we scrutinized and summarized, also by using meta-analytic methods, the data generated during the last seven years, as derived from the analysis of randomized controlled trials (RCTs) on TTh and CV risk.

Areas covered. Analysis included 31 RCTs published between 2010 and 2018. Retrieved trials included 2675 and 2308 patients in TTh and placebo groups, respectively. The analysis documented that TTh was not associated with an increased CV mortality or morbidity either when overall or major adverse CV events were considered.

Expert commentary. Despite present evidence it is important to recognize that the duration of the available trials is short (lower that 3 years) limiting final conclusions on this topic. In particular, the available information on possible long-term effects of TTh on CV risk is limited. Long-term safety studies are advisable to better clarify these points.

Rastrelli G, Dicuio M, Reismann Y, Sforza A, Maggi M, Corona G. Cardiovascular impact of testosterone therapy for hypogonadism. Expert Review of Cardiovascular Therapy 2018. https://www.tandfonline.com/doi/abs/10.1080/14779072.2018.1510314

 

[bob hughes]

Thank you doc for continuing to remind us that these substances must be treated with extreme respect and caution. Every time I read one of these case studies it reminds me of this. This is no joke.