AAS and Cardiovascular/Pulmonary Function

[Michael Scally MD]

[Open Access] [Rats] Nandrolone Plus Moderate Exercise Increases the Susceptibility to Lethal Arrhythmias

Ghorbani Baravati H, Joukar S, Fathpour H, Kordestani Z. Nandrolone Plus Moderate Exercise Increases the Susceptibility to Lethal Arrhythmias. Res Cardiovasc Med. 2015;4(2):e26233. http://cardiovascmed.com/?page=article&article_id=26233

BACKGROUND: Until now, no experimental study has directly assessed the arrhythmogenesis of chronic consumption of anabolic androgenic steroids along with moderate-intensity endurance exercise.

OBJECTIVES: We evaluated the influence of integration of anabolic androgenic steroids along with moderate-intensity endurance exercise on susceptibility to lethal ventricular arrhythmias in rat.

MATERIALS AND METHODS: The animal groups were as follows: control group (CTL); exercise group (EX) which were under 6 weeks of treadmill exercise; nandrolone group (Nan) which received 5 mg/kg of nandrolone decanoate twice a week; vehicle group (Arach) which received Arachis oil (solvent of nandrolone); trained vehicle group (Arach + Ex); and trained nandrolone group (Nan + Ex).

One day after ending of the intervention period, arrhythmia was inducted by intravenous infusion of aconitine and ventricular arrhythmias were recorded. Then malondialdehyde (MDA) and glutathione peroxidase (GPX) of heart tissue were measured.

RESULTS: Nandrolone, exercise, and their combination were associated with heart hypertrophy. Exercise could prevent the incremental effect of nandrolone on MDA/GPX ratio.

Chronic administration of nandrolone with moderate-intensity endurance exercise had no significant effect on blood pressure, heart rate, and basal electrocardiographic parameters.

Combination of nandrolone and exercise significantly increased the incidence of ventricular fibrillation (VF) and reduced the VF latency (P < 0.05).

CONCLUSIONS: The findings suggest that chronic coadministration of nandrolone with moderate-intensity endurance exercise facilitates the VF occurrence in rat. Complementary studies are needed to elucidate the involved mechanisms of this abnormality.

 

[Michael Scally MD]

Bayat G, Javan M, Safari F, Khalili A, Shokri S, et al. Nandrolone decanoate negatively reverses the beneficial effects of exercise on cardiac muscle via sarcolemmal, but not mitochondrial KATP channel. Canadian Journal of Physiology and Pharmacology. http://www.nrcresearchpress.com/doi/abs/10.1139/cjpp-2015-0040

Background: ATP-sensitive potassium channels are supposed to have a substantial role in improvement of cardiac performance. This study was performed to evaluate whether nandrolone decanoate (ND) and/or exercise training could affect the expression of cardiac KATP channel subunits.

Methods: Thirty five male albino Wistar rats were randomly divided into 5 groups, including Sedentary Control (SC), Sedentary Vehicle (SV), Sedentary ND (SND), Exercise Control (EC), and Exercise-ND (E+ND). Exercise training was performed on a treadmill 5 times /week.

Nandrolone decanoate was injected (10 mg/kg/week, IM) to the rats in the SND and E+ND groups. Following cardiac isolation, the expression of both sarcolemmal and mitochondrial subunits of KATP channel was measured using western blot method.

Results: The expression of sarcolemmal but not mitochondrial subunits of KATP channel (kir6.2 and SUR2) of EC group was significantly higher compared to SC group while ND administration (SND group) did not show any change in their expression.

In the E+ND group, ND administration led to decrease the over-expression of sarcolemmal kir6.2 and SUR2 which previously induced by exercise. There was no significant association between the mitochondrial expression of either Kir6.2 or SUR2 proteins and administration of ND or exercise.

Conclusion: Supra-physiological dosage of ND negatively reverses the effects of exercise on the cardiac muscle expression of sarcolemmal, but not mitochondrial KATP channel subunits.

 

[Michael Scally MD]

AAS Hysteria At Its Finest! At 7+ feet, he was anything but normal. And, this was never checked out! Acromegalics gave heart concerns. Bur, much easier to jump to AAS.


Teen Bodybuilder Who Wants To Be The Next ‘The Rock' Dies After Heart Artery Exploded
http://www.techtimes.com/articles/8...the-rock-dies-after-heart-artery-exploded.htm

Andrej Gajdos was a 19-year-old bodybuilder in the United Kingdom (UK) who stood 7 feet and 2 inches and weighed about 280 pounds. The Slovakia-born teen aspired to become the next Dwayne 'The Rock' Johnson, whose shot to fame started with bodybuilding. Unfortunately, the dream ended with Gajdos' untimely death.

An average human heart is about 400 grams. Following an artery burst that killed Gajdos, his heart weighed 680 grams, coroners said. The fitness aficionado collapsed in front of Tesco, a seaside supermarket in Weston-super-Mare, Somerset, England. The heart's main artery - thoracic aorta - burst, killing Gajdos almost instantly.

Gajdos' weight training program was put under the spotlight. The teenager went to the gym twice a day. Doctors found traces of testosterone and anabolic steroids in his system. Anabolic steroid promotes muscle growth by mimicking testosterone. Gajdos' parents reported four types of steroids found in his apartment.

Avon Coroner's investigation found that Gajdos' organs were larger compared to an average person's. The added weight might have strained is heart muscles.

"He wasn't a normal man. It is extremely rare for a young person to have a torn aorta like that. I have only seen one other case in 15 years", said Dr. John Oxley who performed Gajdos' autopsy.

Oxley added that the steroids might have caused the heart's enlargement and increased the risk of thoracic break. Steroids might have played a part in Gajdos' death but Oxley didn't pinpoint the steroids as the exact cause. He suspected that the aspiring bodybuilder might have used the drugs for a substantial amount of time for his heart to get this big. The case is so rare it could also be a genetic disorder.

Doctors suspected Gajdos suffered from acromegaly, a case of excessive growth hormones, but never confirmed. A few years back, Gajdos was diagnosed with bronchiectasis or enlarged bronchi. Assistant coroner Dr. Peter Harrowing said genetics remains a possible cause of Gajdos' death. The thoracic rupture was a rare event and most likely caused by genetics.

"He was known and loved by many people", said Gajdos' grieving mother, Desana Krajcikova, who disclosed to the public that their family has reached the verdict they needed. "Burying your son isn't something anyone should ever have to do."

Gajdos started going to the gym at the age of 16. He started out as a skinny teenager but developed a liking to weightlifting. The combination of rigorous training, food consumption and steroids transformed him from a skinny kid to a lean powerhouse of muscles.

 

[Millard]

Acromegaly is serious. Why wouldn't his doctor follow up if acromegaly was suspected?

 

[Michael Scally MD]

Notwithstanding a diagnosis of gigantism, Size Matters.

[Open Access] Pfaffenberger S, Bartko P, Graf A, Pernicka E, Babayev J, et al. Size Matters! Impact of Age, Sex, Height, and Weight on the Normal Heart Size. Circulation: Cardiovascular Imaging. 2013;6(6):1073-9. http://circimaging.ahajournals.org/content/6/6/1073.full

Background—Therapeutic decisions in cardiology are determined frequently by cardiac chamber size. To decide whether cardiac dimensions are still in the normal range, reliable reference values are needed. However, published reference values mostly refer to historical cohorts using motion-mode measurements and have not been adjusted for sex or age.

The impact of body size was only vaguely addressed. The importance of such adjustments is illustrated by studies, which show that smaller individuals and women are at risk of delayed treatment and impaired outcome when currently used reference values are applied.

The aim of the present study was to assess the impact of body size, sex, and age on the normal heart size.

Methods and Results—We prospectively studied 622 individuals (52.7% women; 17–91 years; 143–200 cm; 32–240 kg) without cardiac disease by standard transthoracic echocardiography. Multivariable linear regression analyses of the impact of sex, age, height, and weight on cardiac chamber size were performed. By multivariable regression analysis (n=500), all 4 variables independently influenced cardiac chamber size.

The validity of cardiac dimensions predicted by the regression model was tested prospectively in a validation cohort (n=122). A calculator is proposed that estimates cardiac dimensions on the basis of the regression analysis.

Conclusions—Sex, height, weight, and age significantly affect the normal heart size. These parameters need to be considered when cutoff values indicating the need for treatment or even surgery are established.

 

[Dave202000]

A lot of those bb'ers have stayed on test cruise cycles and not come off...if you are prone to h2o retention u need to be wary as a diuretic should be used like Lasix also an AI as the increase in fluid volume systemic can cause WAYYYYYYY too much strain on the heart coupled with increase in LDL it is a recipe for disaster
My advice keep diet unbelievably clean
This means tuna plain egg whites and tons of garlic
I would advise against dirty bulk diets while on test or tren or whatever you fancy

 

[Michael Scally MD]

Lilly to Discontinue Development of Evacetrapib for High-Risk Atherosclerotic Cardiovascular Disease
https://investor.lilly.com/releasedetail.cfm?ReleaseID=936130

INDIANAPOLIS, Oct. 12, 2015 /PRNewswire/ -- Eli Lilly and Company (NYSE: LLY) and the ACCELERATE study's academic leadership have accepted the recommendation of the independent data monitoring committee to terminate the Phase 3 trial of the investigational medicine evacetrapib, due to insufficient efficacy. Lilly will discontinue development of evacetrapib for the treatment of high-risk atherosclerotic cardiovascular disease and will now conclude other studies in the program.

The independent data monitoring committee based its recommendation on data from periodic data reviews, which suggested there was a low probability the study would achieve its primary endpoint based on results to date. The study is not being stopped for safety findings. After further analysis, results of the study will be presented in scientific forums in the future.

Evacetrapib inhibits cholesterylester transfer protein (CETP), which transfers and thereby increases high-density lipoprotein and lowers low-density lipoprotein. http://jama.jamanetwork.com/article.aspx?articleid=1104630

 

[Michael Scally MD]

Stop with the HDL OCD.

Miller NE. CETP inhibitors and cardiovascular disease: Time to think again [version 1; referees: 2 approved] F1000Research 2014;3:124. http://f1000research.com/articles/3-124/v1

Inhibition of cholesteryl ester transfer protein (CETP) lowers plasma low-density lipoprotein cholesterol concentration and raises high-density lipoprotein (HDL) cholesterol, suggesting it might prevent cardiovascular disease (CVD).

From the outset, however, the concept has been controversial owing to uncertainty about its effects on HDL function and reverse cholesterol transport (RCT). Although there has long been good evidence that CETP inhibition reduces atherosclerosis in rabbits, the first information on CETP as a CVD risk factor in a prospectively followed cohort was not published until after the first Phase 3 trial of a CETP inhibitor had begun. The worrying finding that CVD incidence was related inversely to plasma CETP has since been reproduced in each of five further prospective cohort studies. Similar results were obtained in subjects on or off statin therapy, for first and second CVD events, and for mortality as well as CVD morbidity. Additionally, two recent studies have found alleles of the CETP gene that lower hepatic CETP secretion to be associated with an increased risk of myocardial infarction. Meanwhile, CETP gene transfer in mice was found to increase RCT from peripheral macrophages in vivo, and human plasma with high CETP activity was shown to have a greater capacity to remove cholesterol from cultured cells than plasma with low activity. This mounting evidence for a protective function of CETP has been given remarkably little attention, and indeed was not mentioned in several recent reviews. It appears to show that CETP inhibition does not test the HDL hypothesis as originally hoped, and raises a pressing ethical issue regarding two Phase 3 trials of inhibitors, involving more than forty thousand subjects, which are currently in progress. As the weight of evidence now clearly supports an adverse effect of CETP inhibition on CVD, an urgent review is needed to determine if these trials should be discontinued.


Hage MP, Azar ST. Treating low high-density lipoprotein cholesterol: what is the evidence? Therapeutic Advances in Endocrinology and Metabolism 2014;5(1):10-7. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3972998/

Epidemiological studies have shown an inverse association between high-density lipoprotein cholesterol (HDL-C) and cardiovascular disease (CVD) risk. However, genetic and interventional studies have failed to consistently support this relationship. There is an increasing body of evidence that the function of HDL, including its antiatherogenic properties and its reverse cholesterol transport activity, has a greater impact on CVD risk compared with levels of HDL alone. Targeting HDL has become a growing interest. Nevertheless, raising HDL pharmacologically has failed to show a considerable, if any, impact on cardiovascular outcome. Efforts should focus on improving HDL quality in addition to raising HDL levels when developing new therapies. Ongoing and future research will help determine the most safe and effective approach to improve cardiovascular outcome and establish the safety, efficacy and impact on atherosclerosis of the emerging HDL-raising therapies.


Voight BF, Peloso GM, Orho-Melander M, et al. Plasma HDL cholesterol and risk of myocardial infarction: a mendelian randomisation study. Lancet 2012;380(9841):572-80. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3419820/

Background - High plasma HDL cholesterol is associated with reduced risk of myocardial infarction, but whether this association is causal is unclear. Exploiting the fact that genotypes are randomly assigned at meiosis, are independent of non-genetic confounding, and are unmodified by disease processes, mendelian randomisation can be used to test the hypothesis that the association of a plasma biomarker with disease is causal.

Methods - We performed two mendelian randomisation analyses. First, we used as an instrument a single nucleotide polymorphism (SNP) in the endothelial lipase gene (LIPG Asn396Ser) and tested this SNP in 20 studies (20 913 myocardial infarction cases, 95 407 controls). Second, we used as an instrument a genetic score consisting of 14 common SNPs that exclusively associate with HDL cholesterol and tested this score in up to 12 482 cases of myocardial infarction and 41 331 controls. As a positive control, we also tested a genetic score of 13 common SNPs exclusively associated with LDL cholesterol.

Findings - Carriers of the LIPG 396Ser allele (2·6% frequency) had higher HDL cholesterol (0·14 mmol/L higher, p=8×10−13) but similar levels of other lipid and non-lipid risk factors for myocardial infarction compared with non-carriers. This difference in HDL cholesterol is expected to decrease risk of myocardial infarction by 13% (odds ratio [OR] 0·87, 95% CI 0·84–0·91). However, we noted that the 396Ser allele was not associated with risk of myocardial infarction (OR 0·99, 95% CI 0·88–1·11, p=0·85). From observational epidemiology, an increase of 1 SD in HDL cholesterol was associated with reduced risk of myocardial infarction (OR 0·62, 95% CI 0·58–0·66). However, a 1 SD increase in HDL cholesterol due to genetic score was not associated with risk of myocardial infarction (OR 0·93, 95% CI 0·68–1·26, p=0·63). For LDL cholesterol, the estimate from observational epidemiology (a 1 SD increase in LDL cholesterol associated with OR 1·54, 95% CI 1·45–1·63) was concordant with that from genetic score (OR 2·13, 95% CI 1·69–2·69, p=2×10−10).

Interpretation - Some genetic mechanisms that raise plasma HDL cholesterol do not seem to lower risk of myocardial infarction. These data challenge the concept that raising of plasma HDL cholesterol will uniformly translate into reductions in risk of myocardial infarction.

 

[Michael Scally MD]

For 30+y, physicians & public have been taught -> anything that raises HDL cholesterol must be good for you. We can firmly retire this idea. https://twitter.com/skathire/status/653572840185327617

 

[Dave202000]

For 30+y, physicians & public have been taught -> anything that raises HDL cholesterol must be good for you. We can firmly retire this idea. https://twitter.com/skathire/status/653572840185327617

right just like statins eradicate cholesterol and end up doing more harm than good….I hope u don't think I am a brainwashed HDL LDL robot if this is how it sounded my bad….actually Im leaning more toward genetic for incidence of MI or not besides LDL isn't the demon its been touted as

 

[Michael Scally MD]

Chmiel A, Mizia-Stec K, Wierzbicka-Chmiel J, et al. Low testosterone and sexual symptoms in men with acute coronary syndrome can be used to predict major adverse cardiovascular events during long-term follow-up. Andrology. http://onlinelibrary.wiley.com/doi/10.1111/andr.12103/abstract

Low total testosterone (TT) and sexual symptoms are common among men with coronary artery disease, however its impact on major adverse cardiovascular events (MACE) is still debatable.

We investigated whether low TT and coexisting sexual symptoms in men with acute coronary syndrome (ACS) can be used to predict the incidence of MACE.

In the prospective study 120 consecutive men (mean age 58 ± 9 years; diabetes 27%; current smokers 58%; left ventricular ejection fraction 50 ± 10%) with ACS were included. The group of men with the presence of three sexual symptoms (decreased frequency of morning erections, a lack of sexual thoughts and erectile dysfunction) and with TT serum concentration <3.2 ng/mL was distinguished.

All of the patients had their prognosis assessed according to the Global Registry of Acute Coronary Events (GRACE Score 2.0). Primary composite endpoint – MACE (recurrent ischaemia, non-fatal myocardial infarction, stroke and death) and secondary endpoint – in stent restenosis (ISR) were registered during the 18.3 month follow-up period.

The mean TT level in the entire group was 3.7 ± 0.5 ng/mL. Low TT was diagnosed in 63 (52.5%) men. Both low TT and sexual symptoms were diagnosed in 57 (47%) participants. During the follow-up, 29 (24.2%) participants experienced MACE, 20 (16.6%) men ISR.

In the Cox proportional hazards regression, high risk of death on the GRACE score (HR 3.16; 95% CI: 1.5–6.6; p = 0.002), the presence of low TT and sexual symptoms (HR 2.75; 95% CI: 1.26–6.04; p = 0.02) independently predicted an incidence of a MACE (p = 0.006).

For the secondary endpoint only low TT and sexual symptoms (HR 2.68; 95% CI: 1.03–6.94; p = 0.034) were independent covariates which predicted IRS.

Low TT which coexists with sexual symptoms in males with ACS can be used to predict MACE, especially IRS independently of classic cardiovascular risk factors.

 

[robert paulson]

[Open Access] [Rats] Nandrolone Plus Moderate Exercise Increases the Susceptibility to Lethal Arrhythmias

Ghorbani Baravati H, Joukar S, Fathpour H, Kordestani Z. Nandrolone Plus Moderate Exercise Increases the Susceptibility to Lethal Arrhythmias. Res Cardiovasc Med. 2015;4(2):e26233. http://cardiovascmed.com/?page=article&article_id=26233

BACKGROUND: Until now, no experimental study has directly assessed the arrhythmogenesis of chronic consumption of anabolic androgenic steroids along with moderate-intensity endurance exercise.

OBJECTIVES: We evaluated the influence of integration of anabolic androgenic steroids along with moderate-intensity endurance exercise on susceptibility to lethal ventricular arrhythmias in rat.

MATERIALS AND METHODS: The animal groups were as follows: control group (CTL); exercise group (EX) which were under 6 weeks of treadmill exercise; nandrolone group (Nan) which received 5 mg/kg of nandrolone decanoate twice a week; vehicle group (Arach) which received Arachis oil (solvent of nandrolone); trained vehicle group (Arach + Ex); and trained nandrolone group (Nan + Ex).

One day after ending of the intervention period, arrhythmia was inducted by intravenous infusion of aconitine and ventricular arrhythmias were recorded. Then malondialdehyde (MDA) and glutathione peroxidase (GPX) of heart tissue were measured.

RESULTS: Nandrolone, exercise, and their combination were associated with heart hypertrophy. Exercise could prevent the incremental effect of nandrolone on MDA/GPX ratio.

Chronic administration of nandrolone with moderate-intensity endurance exercise had no significant effect on blood pressure, heart rate, and basal electrocardiographic parameters.

Combination of nandrolone and exercise significantly increased the incidence of ventricular fibrillation (VF) and reduced the VF latency (P < 0.05).

CONCLUSIONS: The findings suggest that chronic coadministration of nandrolone with moderate-intensity endurance exercise facilitates the VF occurrence in rat. Complementary studies are needed to elucidate the involved mechanisms of this abnormality.

According to this note, a person is putting his life in jeopardy by using Nandrolone in conjunction with moderate-intensity exercise. What point were you trying to make by posting this? I presume that you suggest that this potential lethal result is not worrisome with testosterone compared to nandrolone?

 

[Storm79]

Re: Steroids and heart disease

https://thinksteroids.com/community/threads/134294658

Question mate

I injected 1 ml test e with 1ml deca (2ml) into left butt cheek and I forgot to aspirate , the oil went in fairly easy and after ward I've had this weird feeling in my head and neck for the last 5 days , head feels really heavy n stiff neck , but I didn't get any cough or other effects other than just head symptom ??? But the last day of two I've felt like something is pressing on my the inside of my rib cage it's very hard to describe ???

Do you think I need to go to the hospital ??? Or should I just keep taking one aspirin a day to help thin my blood out till it pass out my system ???

 

[Dave202000]

According to this note, a person is putting his life in jeopardy by using Nandrolone in conjunction with moderate-intensity exercise. What point were you trying to make by posting this? I presume that you suggest that this potential lethal result is not worrisome with testosterone compared to nandrolone?

He wasn't making any point all I see from this dude is some bullshit regurgitated studies that he copies and pastes pretty lame if u ask me

 

[Michael Scally MD]

do Nascimento AM, de Lima EM, Boechat G, et al. Testosterone induces apoptosis in cardiomyocytes by increasing proapoptotic signaling involving tumor necrosis factor-alpha and renin angiotensin system. Hum Exp Toxicol 2015;34(11):1139-47. http://het.sagepub.com/content/34/11/1139.abstract

Anabolic androgenic steroids lead to cardiac complications and have been shown to exhibit proapoptotic effects in cardiac cells; however, the mechanism involved in those effects is unclear.

The aim of this study was to assess whether apoptosis and the activation of caspase-3 (Casp-3) induced by testosterone in high concentrations involves increments in tumor necrosis factor-alpha (TNF-alpha) concentrations and angiotensin-converting enzyme (ACE) activity in cardiomyocytes (H9c2) cell cultures.

Cardiomyocytes were treated with testosterone (5 x 10(-6) mol/L), doxorubicin (9.2 x 10(-6) mol/L), testosterone + etanercept (Eta; 6.67 x 10(-5) mol/L), testosterone + losartan (Los; 10(-7) mol/L), and testosterone + AC-DEVD-CHO (10(-5) mol/L; Casp-3 inhibitor). Apoptosis was determined by flow cytometry and by the proteolytic activity of Casp-3.

We demonstrated that incubation of H9c2 cells for 48 h with testosterone causes the apoptotic death of 60-70% of the cells and co-treatments with Eta, Los, or AC-DEVD-CHO reduced this effect. Testosterone also induces apoptosis (concentration dependent) and increases the proteolytic activity of Casp-3, which were reduced by co-treatments. TNF-alpha and ACE activities were elevated by testosterone treatment, while co-treatment with Los and Eta reduced these effects.

We concluded that an interaction between testosterone, angiotensin II, and TNF-alpha induced apoptosis and Casp-3 activity in cultured cardiomyocytes, which contributed to the reduced viability of these cells induced by testosterone in toxic concentrations.

 

[Michael Scally MD]

Lima EM, Nascimento AM, Brasil GA, et al. Cardiopulmonary reflex, cardiac cytokines, and nandrolone decanoate: response to resistance training in rats. Can J Physiol Pharmacol 2015;93(11):985-91. http://www.nrcresearchpress.com/doi/abs/10.1139/cjpp-2015-0014

This study evaluated the effects of nandrolone associated with resistance training (RT) on cardiac cytokines, angiotensin-converting enzyme activity (ACEA), and the sensitivity of the Bezold-Jarisch reflex (BJR).

Male Wistar rats were divided into 3 groups:
CONT (received vehicle, no training);
EXERC (RT: after one week of water adaptation, rats were exercised by jumping into water twice a week for 4 weeks), and
ND+EXERC (received nandrolone decanoate 10 mg/kg, twice/week, i.m, associated with RT).

The BJR was analysed by measuring bradycardic and hypotensive responses elicited by serotonin administration. Myocyte hypertrophy and matrix collagen deposition were determined by morphometric analysis of H&E and picrosirius red-stained samples, respectively. TNF-alpha and ACEA were also studied.

RT promoted physiological myocyte hyrpertrophy but did not cause changes in the other parameters. The association of ND with RT increased myocyte hypertrophy, deposition of matrix type I collagen, TNF-alpha and ACEA; decreased IL-10, and impairment in the BJR were observed in ND+EXERC compared with CONT and EXERC.

ND is associated with alterations in cardiac structure and function as a result of the development of pathological cardiac hypertrophy (cardiac cytokine imbalance, elevation of ACEA) and cardiac injury, even when combined with resistance training.

 

[Dr JIM]

Retrospectively, this is an excellent example of what an evidence based thread should be. Kudos to you Dr Scally!

 

[Millard]

Retrospectively, this is an excellent example of what an evidence based thread should be. Kudos to you Dr Scally!

x2! It's the best thread anywhere on the internet for those seeking an expert curated lit review of most relevant and current research for AAS and cardiovascular function

 

[CensoredBoardsSuck]

Retrospectively, this is an excellent example of what an evidence based thread should be. Kudos to you Dr Scally!

x2! It's the best thread anywhere on the internet for those seeking an expert curated lit review of most relevant and current research for AAS and cardiovascular function

x3. I've been following this thread since I got here. I just wish the data painted a clearer picture. Until it does, we'll just have to keep following the thread.

 

[Dr JIM]

x3. I've been following this thread since I got here. I just wish the data painted a clearer picture. Until it does, we'll just have to keep following the thread.

Of course part of the problem is the retrospective nature of some the studies, with a considerable portion of the data being based upon "reliable" self reporting by AAS users.

Another problem is the considerable intra-observer variability of echocardiography, and therefore the reliability or limitations of echocardiographic data itself, especially in the absence of a baseline comparison

That being said, I've found this thread to be very informative with respect to what appears to be a relatively "new" adverse effect of AAS use, or more likely abuse, IMO.