AAS and Cardiovascular/Pulmonary Function

While many PED users have other risk factors for ASCVD, unfortunately because of their putative effects on thrombogenesis, high dose AAS may be all that's required for vascular occlusion.

To that end prophylactic ASA may be a reasonable means of lowering thrombogenic risk.
 

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While many PED users have other risk factors for ASCVD, unfortunately because of their putative effects on thrombogenesis, high dose AAS may be all that's required for vascular occlusion.

To that end prophylactic ASA may be a reasonable means of lowering thrombogenic risk.
In layman's terms you are saying aas can kill us if we ignore the risks.

Good to see you posting Dr Jim.
 
While many PED users have other risk factors for ASCVD, unfortunately because of their putative effects on thrombogenesis, high dose AAS may be all that's required for vascular occlusion.

To that end prophylactic ASA may be a reasonable means of lowering thrombogenic risk.
Downloaded and reading now.

"The thrombogenic effect of exogenous androgens is a consequence of them shifting the hemostatic balance towards a procoagulant state."


I have never even heard of this. Thank you for sharing. What is "prophylactic ASA" in your last sentence?
 
A more recent study showed that testosterone in concentrations not normally exerting any appreciably acute effects per se (0.75 μM, or 1.5 μM) is capable of potentiating cocaine’s effect on platelet function, in terms of enhancing TxB2 release (the stable metabolite of TxA2) and augmenting the aggregation response to arachidonate (150–200 μg/mL) and collagen (5 μg/mL for 0.75 μM testosterone, and 1–5 μg/mL for 1.5 μMtestosterone). The author concluded that testosterone may supplementarily increase thrombotic risk when concomitantly used with cocaine [162].


Ok, ok, so no cocaine on cycle. :p
 
Downloaded and reading now.

"The thrombogenic effect of exogenous androgens is a consequence of them shifting the hemostatic balance towards a procoagulant state."


I have never even heard of this. Thank you for sharing. What is "prophylactic ASA" in your last sentence?
Bc the literature is replete w case reports of YOUNG BB with vascular occlusion without prodromal symptoms its reasonable to suspect acute thrombosis due to platelet aggregation, rather than underlying ASCVD, as the inciting event.

If such is the case low dose Aspirin, such as 80mg QD, may be beneficial.
 
A more recent study showed that testosterone in concentrations not normally exerting any appreciably acute effects per se (0.75 μM, or 1.5 μM) is capable of potentiating cocaine’s effect on platelet function, in terms of enhancing TxB2 release (the stable metabolite of TxA2) and augmenting the aggregation response to arachidonate (150–200 μg/mL) and collagen (5 μg/mL for 0.75 μM testosterone, and 1–5 μg/mL for 1.5 μMtestosterone). The author concluded that testosterone may supplementarily increase thrombotic risk when concomitantly used with cocaine [162].


Ok, ok, so no cocaine on cycle. :p

Until I evaluated a 24yo competitive BB running high dose AAS, a 27 yo with a history of meth use was the youngest I’d seen with an AMI.
 
Although not conclusive based upon recent evidence it seems quite likely AAS (especially long term and high dose use) enhance platelet aggregation which further aggravates their deleterious effect on cardiac muscle.

For more info on the latter check out Peter Bonds excellent post on Meso.
 
Although not conclusive based upon recent evidence it seems quite likely AAS (especially long term and high dose use) enhance platelet aggregation which further aggravates their deleterious effect on cardiac muscle.

For more info on the latter check out Peter Bonds excellent post on Meso.
Will do. Thanks for following up in response to my questions.
 
In layman's terms you are saying aas can kill us if we ignore the risks.

Good to see you posting Dr Jim.

To that end based upon a plethora of case reports, ranging from rare (cerebral sinus thrombosis) to common (CVA’s) and recent data, the deleterious effects of AAS on cardiac function and as pro-coagualants should be recognized.

What’s most disconcerting: a number of those effected have little to no RF for ASCVD and implies AAS alone are thrombogenic, an adverse effect that may be mitigated by ASA.

Good to see you and a few other seasoned mates are still hanging around.
 
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View: https://www.youtube.com/watch?v=R1L0lLmw-b0


In this episode, I talk about why I take a statin even though I am in my 30s and have no major risk factors or short-term risk of cardiovascular disease, and why I believe everyone should do the same.

The main reason is this: cardiovascular disease is the number one cause of death in the United States. It remains a major cause of death and disability even in my demographic.

In one paper published in the Journal of the American Medical Association, one of the most important medical journals in the world, in 2012, men at age 45 who had risk factors that were all optimal (systolic and diastolic blood pressure less than 120 and 80 respectively, total cholesterol less than 180 mg/dL, no diabetes, and no tobacco smoking), still had a risk of having a cardiovascular event of 15% by age 80. Men with just one risk factor that was not optimal had a risk of a full 35% by age 85 (PMID 23117780).

Subclinical atherosclerosis, which affects quality of life, sexual, and physical functioning, is even more prevalent than these figures indicate. Why should anyone take any chances? Take a statin...
 

View: https://www.youtube.com/watch?v=R1L0lLmw-b0


In this episode, I talk about why I take a statin even though I am in my 30s and have no major risk factors or short-term risk of cardiovascular disease, and why I believe everyone should do the same.

The main reason is this: cardiovascular disease is the number one cause of death in the United States. It remains a major cause of death and disability even in my demographic.

In one paper published in the Journal of the American Medical Association, one of the most important medical journals in the world, in 2012, men at age 45 who had risk factors that were all optimal (systolic and diastolic blood pressure less than 120 and 80 respectively, total cholesterol less than 180 mg/dL, no diabetes, and no tobacco smoking), still had a risk of having a cardiovascular event of 15% by age 80. Men with just one risk factor that was not optimal had a risk of a full 35% by age 85 (PMID 23117780).

Subclinical atherosclerosis, which affects quality of life, sexual, and physical functioning, is even more prevalent than these figures indicate. Why should anyone take any chances? Take a statin...

I take 5mg ramipril from my cardiologist for lvh and mild lv dusfunction. My resting hr is also 90+ do you believe I should switch to telmisartan? Or can these two stack?
 
I take 5mg ramipril from my cardiologist for lvh and mild lv dusfunction. My resting hr is also 90+ do you believe I should switch to telmisartan? Or can these two stack?
both will not reduce your RHR. Maybe a betablocker of the newer generation like nebivolol would be better for you
and just to be sure:
when you say resting heart rate, this is your heart rate measured first thing in the monring still in bed or is it your "active" heart like (like when you work at a desk or something like that)
 
both will not reduce your RHR. Maybe a betablocker of the newer generation like nebivolol would be better for you
and just to be sure:
when you say resting heart rate, this is your heart rate measured first thing in the monring still in bed or is it your "active" heart like (like when you work at a desk or something like that)
Even just sitting throughout the day. At night time or in morning it’s maybe 75-85 but I’m also on tren and gh. My blood pressure on tren is around 140/80 I would like it a little lower and for kidney protection I’m wondering if telmisartan would be better
 
Depends. 5mg ramipril is not much so 80mg telmi will probably be more effective for BP. But they both wont lower our RHR. I would probably try Nebivolol if i were you with a night time HR of around 80.
 
Anabolic Steroids Use Is Associated with Impairments in Atrial and Ventricular Cardiac Structure and Performance in Athletes

Purpose: Despite potential severe cardiac side effects, anabolic androgenic steroids (AAS) are increasingly used by strength athletes. However, previous echocardiographic studies focused on the left ventricular (LV) strains but did not assess LV twist and untwist mechanics. Moreover, left atrial (LA) function has been often neglected, and its stiffness, an important determinant of LA reservoir function, has never been challenged. The aim of this study was to investigate the effects of AAS on LA and LV morphologies and functions in strength athletes.

Methods: Fifty subjects including 20 strength-trained young athletes age 32.0 ± 8.5 yr with a mean duration of AAS use of 4.7 ± 1.8 yr (users), 15 athletes with no history of AAS use (nonusers) and 15 sedentary controls underwent speckle tracking echocardiography to assess LA and LV morphology and function.

Results: Users showed higher LA reservoir dysfunction than nonusers (33.7% ± 10.9% vs 44.9% ± 9.9% respectively, P = 0.004) and higher LA stiffness (0.13 ± 0.05 vs 0.19 ± 0.08 A.U., respectively; P = 0.02), higher LV mass index and lower global and regional LV diastolic and systolic dysfunction (global longitudinal strain: -15.5% ± 3.2% vs -18.9% ± 1.8% respectively; P = 0.003), with a drop of LV twist-untwist mechanics (untwisting velocity: 61.5°·s-1 ± 20.2°·s-1 vs 73.7°·s-1 ± 16.1°·s-1 respectively, P = 0.04). There were significant correlations between LV mass and LV apical rotation (P = 0.003, r = 0.44) and diastolic longitudinal strain rate (P = 0.015, r = 0.33).

Conclusions: Our results showing significant LA and LV remodeling and dysfunctions in young AAS using athletes are alarming. Screening echocardiography based on speckle tracking echocardiography parameters for early diagnosis, as well as a stronger awareness in athletes and in physicians are warranted in this context.

Grandperrin A, Schuster I, Moronval P, Izem O, Rupp T, Obert P, Nottin S. Anabolic Steroids Use Is Associated with Impairments in Atrial and Ventricular Cardiac Structure and Performance in Athletes. Med Sci Sports Exerc. 2022 May 1;54(5):780-788. doi: 10.1249/MSS.0000000000002852. Epub 2021 Dec 30. PMID: 34974501. Anabolic Steroids Use Is Associated with Impairments in... : Medicine & Science in Sports & Exercise

 
Re: Steroids and heart disease

What about all the other people who
have/had heart problems but never used gear?

The pro bodybuilding lifestyle is not healthy, period

Eating huge amounts of food, cutting carbs to zero,
building more muscle than I am sure the human body
was ever built to carry, insulin use, PGF use, HGH use..

That's all I have right now ;)

Not saying gear is healthy, but gear was probably
a good thing compared to what else these guys did.

Mike used speed and smoked cigarettes ..

Did I just mention cigarettes? O NO! :confused:

Yeah, cigarettes seem to be taking a beating up here
with all these commercials. ...
Your toe falls off .. Must have been the
cigarettes not the diabetes ..
Heart attack? Must be the smokes, not the 5 big macs you eat every day for 20yrs ..
House went on fire?
Do you smoke? Yes .. It was the cigarettes, for sure.
Aren't you going to investigate? Nope, don't need to.
It was the smoking. :rolleyes:
We're taught in science that "correlation does not equal causation" then there's medical research where most of the time all they have is correlation so "hell yes" it probably equals causation. :-)
We all make choices in life. The most mundane human habits can cause us harm, but if an athlete dies young, it had to be the steroids. :-)

It's a bunch of rubbish. People die from all kinds of things for all kinds of reasons... be sensible, but take risks because life is really dull without them
 
Very good read I’ve been in TRT for about 6 years and just today had to have a cardio visit with more tests on the way yes have a lot of variables going on but overall good read anyhow
 

View: https://www.youtube.com/watch?v=R1L0lLmw-b0


In this episode, I talk about why I take a statin even though I am in my 30s and have no major risk factors or short-term risk of cardiovascular disease, and why I believe everyone should do the same.

The main reason is this: cardiovascular disease is the number one cause of death in the United States. It remains a major cause of death and disability even in my demographic.

In one paper published in the Journal of the American Medical Association, one of the most important medical journals in the world, in 2012, men at age 45 who had risk factors that were all optimal (systolic and diastolic blood pressure less than 120 and 80 respectively, total cholesterol less than 180 mg/dL, no diabetes, and no tobacco smoking), still had a risk of having a cardiovascular event of 15% by age 80. Men with just one risk factor that was not optimal had a risk of a full 35% by age 85 (PMID 23117780).

Subclinical atherosclerosis, which affects quality of life, sexual, and physical functioning, is even more prevalent than these figures indicate. Why should anyone take any chances? Take a statin...


Is the video still available? Also which statin do you take?
 
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