AAS and Cardiovascular/Pulmonary Function

[hurricane]

This thread is freaking me out. I think I'm getting some psychosomatic chest pain.
If I'm keeping every cycle under a gram per week, typically in the 600-700 mg per week range in cycles lasting no more than 16 weeks, and I stick to my TRT dose the rest of the time, how concerned should I be?

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Impossible to say bro. I ran 6 cycles total and then the shit hit the fan. It may have had nothing to do with AAS use, or it may have contributed. Regardless of what caused it they now need to treat my symptoms. I can't ever cycle again and if I could go back I never would of. I'm not trying to scare you. Almost all will never have my issues. I just share it with Dr Jim and Dr Scally so they know how I'm doing. If it causes any of you to think about what your doing that's good but not my intention. I'm sure one of the Docs will chime in, but don't blow off chest pains IMO. Stay safe and listen to your body.

 

[Michael Scally MD]

Libby P. Triglycerides on the rise: should we swap seats on the seesaw? Eur Heart J 2015;36(13):774-6. Triglycerides on the rise: should we swap seats on the seesaw? | European Heart Journal

For decades, cardiovascular risk attributed to lipids beyond low-density lipoprotein (LDL) has focused appropriately on high-density lipoprotein (HDL). Indubitable observational data show a consistent inverse relationship between baseline HDL-C concentrations and cardiovascular risk. Yet, fidelity as a prospective risk marker does not guaranty that an analyte either lies in a causal pathway for disease, or that its therapeutic manipulation will yield clinical benefits. Indeed, multiple strategies to raise HDL levels therapeutically have thus far failed to forestall events in clinical trials [e.g. currently available fibrates, niacin, and the investigated cholesteryl ester transfer protein (CETP) inhibitors].


The high-density lipoprotein/triglyceride seesaw. High-density lipoprotein and triglycerides tend to vary inversely. Traditional thought has focused on the benefits of raising high-density lipoprotein and high-density lipoprotein as a protective factor for atherosclerosis. Triglycerides have received less attention as a causal risk factor as adjustment for high-density lipoprotein attenuates its association with risk. The new clinical and genetic data described in this commentary indicate that triglycerides and specifically the apolipoprotein constituent of many triglyceride-rich lipoproteins, apolipoprotein C3, may actually lie in the causal pathway for atherosclerosis. Thus, contrary to common belief, the current data suggest that we should focus more on triglyceride-rich lipoproteins as a target for cardiovascular risk reduction.

 

[Michael Scally MD]

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.thelancet.com/journals/lancet/article/PIIS0140-6736(12)60312-2/fulltext

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=8x10(-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=2x10(-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]

Do R, Willer CJ, Schmidt EM, et al. Common variants associated with plasma triglycerides and risk for coronary artery disease. Nat Genet 2013;45(11):1345-52. Common variants associated with plasma triglycerides and risk for coronary artery disease

Triglycerides are transported in plasma by specific triglyceride-rich lipoproteins; in epidemiological studies, increased triglyceride levels correlate with higher risk for coronary artery disease (CAD). However, it is unclear whether this association reflects causal processes. We used 185 common variants recently mapped for plasma lipids (P < 5 x 10(-8) for each) to examine the role of triglycerides in risk for CAD. First, we highlight loci associated with both low-density lipoprotein cholesterol (LDL-C) and triglyceride levels, and we show that the direction and magnitude of the associations with both traits are factors in determining CAD risk. Second, we consider loci with only a strong association with triglycerides and show that these loci are also associated with CAD. Finally, in a model accounting for effects on LDL-C and/or high-density lipoprotein cholesterol (HDL-C) levels, the strength of a polymorphism's effect on triglyceride levels is correlated with the magnitude of its effect on CAD risk. These results suggest that triglyceride-rich lipoproteins causally influence risk for CAD.

 

[hurricane]

Good articles Dr Scally.

 

[Michael Scally MD]

[Rats] Administration of Anabolic Steroid During Adolescence Induces Long-Term Cardiac Hypertrophy and Increases Susceptibility to Ischemia/Reperfusion Injury

Highlights

• Chronic administration of AAS during adolescence promoted persistent cardiac hypertrophy in adulthood.
• Cardiac hypertrophy was characterized by up-regulation in the βMHC expression, compatible with pathologic hypertrophy.
• Susceptibility to myocardial IR injury in adult life was significantly increased by AAS administration in adolescence.
• Molecular evidences support that down-regulation of catalase might have a pathophysiological role.

Chronic administration of anabolic androgenic steroids (AAS) in adult rats results in cardiac hypertrophy and increased susceptibility to myocardial ischemia/reperfusion (IR) injury. Molecular analyses demonstrated that hyperactivation of type 1 angiotensin II (AT1) receptor mediates cardiac hypertrophy induced by AAS and also induces down-regulation of myocardial ATP-sensitive potassium channel (KATP), resulting in loss of exercise-induced cardioprotection. Exposure to AAS during adolescence promoted long-term cardiovascular dysfunctions, such as dysautonomia.

We tested the hypothesis that chronic AAS exposure in the pre/pubertal phase increases the susceptibility to myocardial ischemia/reperfusion (IR) injury in adult rats. Male Wistar rats (26day old) were treated with vehicle (Control, n=12) or testosterone propionate (TP) (AAS, 5mgkg-1 n=12) 5 times/week during 5 weeks. At the end of AAS exposure, rats underwent 23days of washout period and were submitted to euthanasia.

Langendorff-perfused hearts were submitted to IR injury and evaluated for mechanical dysfunctions and infarct size. Molecular analysis was performed by mRNA levels of alpha-myosin heavy chain (MHC), betaMHC and brain-derived natriuretic peptide (BNP), ryanodine receptor (RyR2) and sarcoplasmic reticulum calcium ATPase 2a (SERCA2a) by quantitative RT-PCR (qRT-PCR).

The expression of AT1 receptor and KATP channel subunits (Kir6.1 and SURa) was analyzed by qRT-PCR and Western Blot. NADPH oxidase (Nox)-related reactive oxygen species generation was assessed by spectrofluorimetry. The expression of antioxidant enzymes was measured by qRT-PCR in order to address a potential role of redox unbalance.

AAS exposure promoted long-term cardiac hypertrophy characterized by increased expression of betaMHC and betaMHC/alphaMHC ratio. Baseline derivative of pressure (dP/dt) was impaired by AAS exposure. Postischemic recovery of mechanical properties was impaired (decreased left ventricle [LV] developed pressure and maximal dP/dt; increased LV end-diastolic pressure and minimal dP/dt) and infarct size was larger in the AAS group. Catalase mRNA expression was significantly decreased in the AAS group.

In conclusion, chronic administration of AAS during adolescence promoted long-term pathological cardiac hypertrophy and persistent increase in the susceptibility to myocardial IR injury possible due to disturbances on catalase expression.

Cruz Seara FA, Barbosa RA, Oliveira DF, et al. Administration of anabolic steroid during adolescence induces long-term cardiac hypertrophy and increases susceptibility to ischemia/reperfusion injury in adult Wistar rats. J Steroid Biochem Mol Biol. https://www.sciencedirect.com/science/article/pii/S0960076017300122

 

[hurricane]

[Rats] Administration of Anabolic Steroid During Adolescence Induces Long-Term Cardiac Hypertrophy and Increases Susceptibility to Ischemia/Reperfusion Injury

Highlights

• Chronic administration of AAS during adolescence promoted persistent cardiac hypertrophy in adulthood.
• Cardiac hypertrophy was characterized by up-regulation in the βMHC expression, compatible with pathologic hypertrophy.
• Susceptibility to myocardial IR injury in adult life was significantly increased by AAS administration in adolescence.
• Molecular evidences support that down-regulation of catalase might have a pathophysiological role.

Chronic administration of anabolic androgenic steroids (AAS) in adult rats results in cardiac hypertrophy and increased susceptibility to myocardial ischemia/reperfusion (IR) injury. Molecular analyses demonstrated that hyperactivation of type 1 angiotensin II (AT1) receptor mediates cardiac hypertrophy induced by AAS and also induces down-regulation of myocardial ATP-sensitive potassium channel (KATP), resulting in loss of exercise-induced cardioprotection. Exposure to AAS during adolescence promoted long-term cardiovascular dysfunctions, such as dysautonomia.

We tested the hypothesis that chronic AAS exposure in the pre/pubertal phase increases the susceptibility to myocardial ischemia/reperfusion (IR) injury in adult rats. Male Wistar rats (26day old) were treated with vehicle (Control, n=12) or testosterone propionate (TP) (AAS, 5mgkg-1 n=12) 5 times/week during 5 weeks. At the end of AAS exposure, rats underwent 23days of washout period and were submitted to euthanasia.

Langendorff-perfused hearts were submitted to IR injury and evaluated for mechanical dysfunctions and infarct size. Molecular analysis was performed by mRNA levels of alpha-myosin heavy chain (MHC), betaMHC and brain-derived natriuretic peptide (BNP), ryanodine receptor (RyR2) and sarcoplasmic reticulum calcium ATPase 2a (SERCA2a) by quantitative RT-PCR (qRT-PCR).

The expression of AT1 receptor and KATP channel subunits (Kir6.1 and SURa) was analyzed by qRT-PCR and Western Blot. NADPH oxidase (Nox)-related reactive oxygen species generation was assessed by spectrofluorimetry. The expression of antioxidant enzymes was measured by qRT-PCR in order to address a potential role of redox unbalance.

AAS exposure promoted long-term cardiac hypertrophy characterized by increased expression of betaMHC and betaMHC/alphaMHC ratio. Baseline derivative of pressure (dP/dt) was impaired by AAS exposure. Postischemic recovery of mechanical properties was impaired (decreased left ventricle [LV] developed pressure and maximal dP/dt; increased LV end-diastolic pressure and minimal dP/dt) and infarct size was larger in the AAS group. Catalase mRNA expression was significantly decreased in the AAS group.

In conclusion, chronic administration of AAS during adolescence promoted long-term pathological cardiac hypertrophy and persistent increase in the susceptibility to myocardial IR injury possible due to disturbances on catalase expression.

Cruz Seara FA, Barbosa RA, Oliveira DF, et al. Administration of anabolic steroid during adolescence induces long-term cardiac hypertrophy and increases susceptibility to ischemia/reperfusion injury in adult Wistar rats. J Steroid Biochem Mol Biol. https://www.sciencedirect.com/science/article/pii/S0960076017300122

Great article. Hopefully some of the younger members will read it.

 

[MarinePhinFan]

Dr. Scally, do you believe that the heart failure and LV hypertrophy are mainly due to HBP from the AAS?

I currently work in a cath/ep lab and commonly see these things. I am not a cardiologist or EP, but I work hand in hand with them. I'd say other than cocaine abuse, HBP is the number one cause that I see in regards to these 2 problems. Again, I'm just going off of my anecdotal evidence and I wanted to hear your opinion.

 

[Michael Scally MD]

[OA] [Death] Large In-transient Left Ventricular Thrombus due to Anabolic Steroid-induced Cardiomyopathy

The presence of small or moderate size thrombosis is not uncommon in left ventricle (LV) as results of basic co-moribund disease, but huge LV thrombosis that protrudes to aortic valve in the LV outflow tract (LVOT) tract is an exceptionally rare phenomenon.

We report a 34-year-old bodybuilder athlete with cardiomyopathy and massive LV thrombosis.

The thrombosis extended to LVOT and protruded through the aortic valve in systole and posed a high risk of systemic emboli.

The patient underwent open heart surgery, and the clot was removed.

The operation was complicated by low cardiac output syndrome that managed by intra-aortic balloon pump and high dose of inotropic drugs and hemodialysis.

The patient died on the 15th day after surgery with multiorgan failures.

Sabzi F, Faraji R. Large In-transient Left Ventricular Thrombus due to Anabolic Steroid-induced Cardiomyopathy. Indian J Crit Care Med 2017;21(1):51-4. http://www.ijccm.org/article.asp?issn=0972-5229;year=2017;volume=21;issue=1;spage=51;epage=54;aulast=Sabzi

 

[hurricane]

[OA] [Death] Large In-transient Left Ventricular Thrombus due to Anabolic Steroid-induced Cardiomyopathy

The presence of small or moderate size thrombosis is not uncommon in left ventricle (LV) as results of basic co-moribund disease, but huge LV thrombosis that protrudes to aortic valve in the LV outflow tract (LVOT) tract is an exceptionally rare phenomenon.

We report a 34-year-old bodybuilder athlete with cardiomyopathy and massive LV thrombosis.

The thrombosis extended to LVOT and protruded through the aortic valve in systole and posed a high risk of systemic emboli.

The patient underwent open heart surgery, and the clot was removed.

The operation was complicated by low cardiac output syndrome that managed by intra-aortic balloon pump and high dose of inotropic drugs and hemodialysis.

The patient died on the 15th day after surgery with multiorgan failures.

Sabzi F, Faraji R. Large In-transient Left Ventricular Thrombus due to Anabolic Steroid-induced Cardiomyopathy. Indian J Crit Care Med 2017;21(1):51-4. http://www.ijccm.org/article.asp?issn=0972-5229;year=2017;volume=21;issue=1;spage=51;epage=54;aulast=Sabzi

Incredible article. This should be a must read for everyone on this forum. My first diagnosis was dialated cardiomyopathy with a EF of 15-20%. With medication that improved dramatically to 40-45%. But within a year of my diagnosis I had my wife dial 911 because I couldn't breathe and passed out. I was admitted again to Yale and Dr Marieb found a PE. Scariest day of my life. I thought I was dead. Went on warfarin and switched over to xarelto when it came out. The PE was scarier then any other heart issue or surgery I've had. I worry so much about the members on this forum who don't even know what RBC or hematocrit even mean. Very good article that really hits home.

 

[Michael Scally MD]

@hurricane

Are you using AAS?

 

[hurricane]

@hurricane

Are you using AAS?

No Dr Scally. After my ablation for a fib and atrial flutter, and the insertion of a pacemaker thanks to sick sinus syndrome that was causing bradycardia I decided to stop rolling the dice with my health. But like a idiot I did use even about 6 months after my PE. And then this past October is when I had my other surgeries and I am now off AAS and will remain off. I currently take coreg, ivabradine, and xarelto. And probably will for life. Initially when first diagnosed I was using around a 1,000mg of test with a ton of ephedrine. My EP out of Yale Dr Marieb was more suspect of the ephedrine use over the AAS. Although he's stated that AAS use "probably" didn't help my condition. So now I try to be someone who helps these young kids realize what their doing. If only I had read the article you just posted earlier in life. What you do here is incredible. I truly believe that article should be a must read for every member. I can only yell so much at them. The urge to use will always be there, but my children and wife are more important then AAS. Thanks for everything you do for this site. I wish you well and am always willing to discuss my cardiac issues if it helps even one individual stay safe.

 

[MarinePhinFan]

No Dr Scally. After my ablation for a fib and atrial flutter, and the insertion of a pacemaker thanks to sick sinus syndrome that was causing bradycardia I decided to stop rolling the dice with my health. But like a idiot I did use even about 6 months after my PE. And then this past October is when I had my other surgeries and I am now off AAS and will remain off. I currently take coreg, ivabradine, and xarelto. And probably will for life. Initially when first diagnosed I was using around a 1,000mg of test with a ton of ephedrine. My EP out of Yale Dr Marieb was more suspect of the ephedrine use over the AAS. Although he's stated that AAS use "probably" didn't help my condition. So now I try to be someone who helps these young kids realize what their doing. If only I had read the article you just posted earlier in life. What you do here is incredible. I truly believe that article should be a must read for every member. I can only yell so much at them. The urge to use will always be there, but my children and wife are more important then AAS. Thanks for everything you do for this site. I wish you well and am always willing to discuss my cardiac issues if it helps even one individual stay safe.

So the EP thinks that the test may be a factor in your arrhythmia? Wow...

I've done very few cycles. And I've never done anything other than Test (max 500mg/week) and PCT's. I thought I was being "safe". I wonder if there are any studies out there about test causing these types of things?

 

[hurricane]

So the EP thinks that the test may be a factor in your arrhythmia? Wow...

I've done very few cycles. And I've never done anything other than Test (max 500mg/week) and PCT's. I thought I was being "safe". I wonder if there are any studies out there about test causing these types of things?

I would have to believe there are studies out there that possibly draw a correlation between the two. Again, there is no definitive way to prove AAS was the cause of these issues. Except for the fact I was a very healthy USAF commando with excellent cardiac health. Genetics and underlying conditions also may have contributed once AAS use was introduced to my body. But like my EP has stated. It would be great if we knew what caused it, but we would still treat the symptoms the same way. Cycle smartly and stay safe.

 

[MarinePhinFan]

I would have to believe there are studies out there that possibly draw a correlation between the two. Again, there is no definitive way to prove AAS was the cause of these issues. Except for the fact I was a very healthy USAF commando with excellent cardiac health. Genetics and underlying conditions also may have contributed once AAS use was introduced to my body. But like my EP has stated. It would be great if we knew what caused it, but we would still treat the symptoms the same way. Cycle smartly and stay safe.

Probably. I have read many studies that show low test could cause heart problems, but since I'm not a cardiologist or EP, I haven't really looked into test and the effects on the heart too much. In fact, and due to those studies I mentioned, I thought I was potentially helping my heart by keeping my test levels high. lol

 

[hurricane]

Probably. I have read many studies that show low test could cause heart problems, but since I'm not a cardiologist or EP, I haven't really looked into test and the effects on the heart too much. In fact, and due to those studies I mentioned, I thought I was potentially helping my heart by keeping my test levels high. lol

Remember. Keeping them high is one thing. Keeping your test supra physiologically is another thing. Just be safe and you should be fine.

 

[JRA]

Great thread with very informative, medical articles to get one into deep contemplation. I am very curious (which has been mentioned) about genetics. We need a study on 3 brothers/triplets. Have 1 on heavy AAS, 1 on medium AAS, and 1 on no AAS. Of course, they would have to eat the same and exercise the same, and have the same girlfriend. .. Genetics, to me, seems very important. Eg, my grandfather smoked cig's for 65 years, and died naturally at 94. My father, smoked and drank heavily for 30 years uptill 60 y.o.), and is going strong at 95 (pacemaker at 90). My mother was diagnosed with non-smokers lung cancer and given 3 months to get her affairs in order, and lived an additional 7 years. I am 62 y.o., and have been bb/olympic lifting naturally since I was 15. Just started my first test 200mg weekly for 3 months now. Blood tests were very good but I did have high estradiol at 53, so am taking .25 dex eod. Anyways, thanks everyone.

 

[hurricane]

Great thread with very informative, medical articles to get one into deep contemplation. I am very curious (which has been mentioned) about genetics. We need a study on 3 brothers/triplets. Have 1 on heavy AAS, 1 on medium AAS, and 1 on no AAS. Of course, they would have to eat the same and exercise the same, and have the same girlfriend. .. Genetics, to me, seems very important. Eg, my grandfather smoked cig's for 65 years, and died naturally at 94. My father, smoked and drank heavily for 30 years uptill 60 y.o.), and is going strong at 95 (pacemaker at 90). My mother was diagnosed with non-smokers lung cancer and given 3 months to get her affairs in order, and lived an additional 7 years. I am 62 y.o., and have been bb/olympic lifting naturally since I was 15. Just started my first test 200mg weekly for 3 months now. Blood tests were very good but I did have high estradiol at 53, so am taking .25 dex eod. Anyways, thanks everyone.

I have 2 younger brothers. My middle brother has zero health issues. My youngest brother(35)has heart issues and lupus plus the same blood clotting disorder as myself. My middle brother has never touched AAS. My younger brother and myself have. Coincidence?? We both see the same EP and he's convinced genetics are a huge factor in our similar conditions. While AAS use may not have caused our issues, he's quite certain they exacerbated the situation. That's a very small sample size and is in no way can anything be concluded with just myself and my brother. But interesting enough for further studies to be done.

 

[Michael Scally MD]

[Old view: HDL a causal risk factor; Emerging view: HDL a biomarker for impaired clearance of TG-rich lipoproteins.]

Khera AV, Kathiresan S. Genetics of coronary artery disease: discovery, biology and clinical translation. Nat Rev Genet;advance online publication. Genetics of coronary artery disease: discovery, biology and clinical translation : Nature Reviews Genetics : Nature Research

Coronary artery disease is the leading global cause of mortality. Long recognized to be heritable, recent advances have started to unravel the genetic architecture of the disease. Common variant association studies have linked approximately 60 genetic loci to coronary risk.

Large-scale gene sequencing efforts and functional studies have facilitated a better understanding of causal risk factors, elucidated underlying biology and informed the development of new therapeutics.

Moving forwards, genetic testing could enable precision medicine approaches by identifying subgroups of patients at increased risk of coronary artery disease or those with a specific driving pathophysiology in whom a therapeutic or preventive approach would be most useful.

 

[hurricane]

[Old view: HDL a causal risk factor; Emerging view: HDL a biomarker for impaired clearance of TG-rich lipoproteins.]

Khera AV, Kathiresan S. Genetics of coronary artery disease: discovery, biology and clinical translation. Nat Rev Genet;advance online publication. Genetics of coronary artery disease: discovery, biology and clinical translation : Nature Reviews Genetics : Nature Research

Coronary artery disease is the leading global cause of mortality. Long recognized to be heritable, recent advances have started to unravel the genetic architecture of the disease. Common variant association studies have linked approximately 60 genetic loci to coronary risk.

Large-scale gene sequencing efforts and functional studies have facilitated a better understanding of causal risk factors, elucidated underlying biology and informed the development of new therapeutics.

Moving forwards, genetic testing could enable precision medicine approaches by identifying subgroups of patients at increased risk of coronary artery disease or those with a specific driving pathophysiology in whom a therapeutic or preventive approach would be most useful.

Another great article! My daughter was referred to CT Children's Medical Center because of a murmur her pediatrician heard. They performed an echo and everything looked fine. Were going to do genetic testing on her and my son to see if their carrying any markers. Son is 16, my daughter is 8. I can tell you this @Michael Scally MD I will never be able to forgive myself if I passed any of this to my children. Really great article and thanks again for all you do in keeping us informed.