Had a Heart Attack today at age ~30. Be safe guys.

[RockyP]

After 18 months of treatment, the EVAPORATE trial showed a significant decrease in total noncalcified plaque and total plaque volume with icosapent ethyl, compared to an increase in the placebo group. (I believe this was in conjunction with a statin)

Results from EVAPORATE Trial Suggest that Cardioprotective Benefits of Eicosapentaenoic Acid (EPA) are Related to Plaque Reduction and Stabilization - American College of Cardiology

www.acc.org

“Proven to induce plaque stabilization…”

Made my day with this brother.

 

[RockyP]

@RockyP
Reduction of remnant lipoproteins
In addition to triglyceride values, great attention has recently been paid to remnant lipoproteins (RLP-C), recognized as highly atherogenic. In fact, these particles contain up to four times the concentration of cholesterol compared to LDL, thus potentially resulting much more atherogenic. Indeed, in the ANCHOR and MARINE studies, IPE therapy was shown to result in a reduction in RLP-C of up to 30% compared to placebo (by—25.8%, P = 0.0001 and—29.8%, P = 0.004, respectively), being able to partially explain the beneficial effects of this therapy that go beyond the reduction of triglyceride values.

Stabilizing effect on atheromatous plaque
The EVAPORATE study provides important mechanistic information regarding the therapeutic effect that IPE exerts on the characteristics of vulnerable atheromatous plaques, from growth reduction to the induction of true plaque regression. In particular, it was also observed that the total volumetric progression rates of fibroadipose component plaques were −34% in the IPE group compared to a progression of 32% in the placebo group (P = 0.0002). Furthermore, this reduction in plaque volume progression was not accompanied by a significant reduction in LDL cholesterol and triglycerides from baseline10. It is interesting to note how, compared to the data existing in the literature regarding the effects of statins on the volume of coronary plaques, the data emerging from the EVAPORATE study are surprising, since the effect of IPE would appear to be more effective than an intensive therapy with statins on the stabilization and regression of atheromatous plaque.11,12

https://academic.oup.com/eurheartjsupp/article/25/Supplement_B/B37/7135765

You can’t see it but I’m reaching out for a hug. Come on in for the real thing brother! Thanks again.

 

[Ghoul]

Soft plaque can be detected via cleerly CCTA.

I could've phrased that better.

I don't mean it's undetectable in the sense of technology, rather that dangerous levels of plaque accumulation go undetected. With a zero CAC score, and no symptoms, a clinician won't prescribe it, insurance won't cover it, yet life threatening levels of plaque can be present (again, especially under 45). How often do we see "I have a zero CAC I'm gtg"?

If plaque blocks an artery, chest pain would be a warning signal. Because of plaque outward remodeling, it's often a silent, undetected threat.

 

[Wizbang]

And just to be clear I am on vascepa (icosapent ethyl) without elevated Triglycerides (My last lipid panel this year had them at 49) I believe and the data shows it has beneficial effects that extend well beyond TG reduction.

 

[RockyP]

And just to be clear I am on vascepa (icosapent ethyl) without elevated Triglycerides (My last lipid panel this year had them at 49) I believe and the data shows it has beneficial effects that extend well beyond TG reduction.

Same. That’s how I read the conclusions also. The benefits were had with ldl and trig not changing much

 

[explodingHeart]

I could've phrased that better.

I don't mean it's undetectable in the sense of technology, rather that dangerous levels of plaque accumulation go undetected. With a zero CAC score, and no symptoms, a clinician won't prescribe it, insurance won't cover it, yet life threatening levels of plaque can be present (again, especially under 45). How often do we see "I have a zero CAC I'm gtg"?

If plaque blocks an artery, chest pain would be a warning signal. Because of plaque outward remodeling, it's often a silent, undetected threat.

If OP takes a pcsk9 inhibitor and gets his LDL down to <= 30 or so, and his BP down to 120/80 morning bp (so 105 or so at night), can he get rid of most of his risk?

Obviously plaque can't regress much, but can he stop adding more? He still wants to compete and he knows the risks. I'm just curious what would happen from here on out.

 

[Type-IIx]

how is spine density different from bone density? ain't it just the density of the bones that make up your spine or am I misunderstanding something?

Think you're reading too deeply into a quick post I fired off in a couple sentences, stream of consciousness… there are differences in femoral neck/lumbar spine bone and shit though, but this thread's for a guy's health/almost had a heart attack

 

[Avies48]

I am trying to get my doc to get me one.

Usually
Paid out of pocket and i also one one wnd the prenuvo scan whole body… but i gotta sell a testicle first…

 

[newguy2]

No not pointless! If you have a positive CAC score you can definately use that as a guide (and insurance approval) for more aggressive treatment (pcsk9) and advanced imaging.

It's just that if it's zero, you can't assume you're in the clear and don't need to do anything else, especially as an AAS user.

AAS use by default puts us all in, at least, the lower end of "high risk", but unfortunately the risk scores and guidelines don't explicitly address it, though a (good) cardiologist would use this info to follow "high risk" guidelines for treatment decisions despite other factors putting you in a low risk category.

Not all the things that make AAS use a cardiovascular risk factor are understood yet. Some are obvious like lipids, BP, inflammation, but from the limited research there's even more going on, because risk appears higher than those other traditional factors can account for.

I've seen theories, for example, that micro vessels within heart muscle tissue may be harmed by AAS use in unique ways, hinted at in autopsies of young bodybuilders, but the mechanism isn't understood yet.

Thanks for this, I got the calcium score and it all came back at 0. I have not told my doc about AAS or even TRT as I don't want it to cause an insurance denial or some such trouble.

 

[RockyP]

Thanks for this, I got the calcium score and it all came back at 0. I have not told my doc about AAS or even TRT as I don't want it to cause an insurance denial or some such trouble.

Are you under 45? I had one around age 40, also score zero, and I'm already up by doc's ass for another one in a few years.

 

[newguy2]

Are you under 45? I had one around age 40, also score zero, and I'm already up by doc's ass for another one in a few years.

I turn 45 in a month. So right there.

 

[RockyP]

I turn 45 in a month. So right there.

Well, a score of zero is a great place to start - but we (you, me, and many others) need to be sure to repeat that shit in 5 years. We're in a cohort of possible false negatives. Not trying to worry you, but we need to remain vigilant.

 

[Ghoul]

Well, a score of zero is a great place to start - but we (you, me, and many others) need to be sure to repeat that shit in 5 years. We're in a cohort of possible false negatives. Not trying to worry you, but we need to remain vigilant.

A genuine negative for calcification, but plaque, unless you've had sub 60 LDL your entire life, you have some degree of accumulation. During the Korean War the US started checking soldiers during autopsies, and for example, 85% of 22 year olds had established plaque, some even had arteriosclerosis!

Within a generation or two this disease will be extinct. You'll get a lifetime PCSK9 inhibitor, essentially a heart disease "vaccination" during childhood that'll neutralize PCSK9 for good and there won't be any accumulation of plaque.

 

[RockyP]

A genuine negative for calcification, but plaque, unless you've had sub 60 LDL your entire life, you have some degree of accumulation. During the Korean War the US started checking soldiers during autopsies, and for example, 85% of 22 year olds had established plaque, some even had arteriosclerosis!

Within a generation or two this disease will be extinct. You'll get a lifetime PCSK9 inhibitor, essentially a heart disease "vaccination" during childhood that'll neutralize PCSK9 for good and there won't be any accumulation of plaque.

This makes me wonder if there are PED users walking the earth with genetic polymorphisms for PSCK9 that enable them to blast the shit out of gear with obscenely bad lipid profiles and live to tell about it. However, as I write this i realize that it's highly unlikely that they can also control (on say 3+ grams per week) for other things that kill bodybuilders like HTN-related effects, the downstream effects on kidneys, LVH, other organ damage, etc.

 

[ChemBB]

Dropped the Tren + Mast, now just on 300 Test.

Decided it wasn't worth the risk.

Seems like in terms of cardiac remodeling + LDL risk, Test/Nandrolone/Primo are the ways to go.

But I'm not made out of money, so Test + Nand it'll be for the foreseeable future.

 

[Sera]

And just to be clear I am on vascepa (icosapent ethyl) without elevated Triglycerides (My last lipid panel this year had them at 49) I believe and the data shows it has beneficial effects that extend well beyond TG reduction.

High dose (1-2g a day) EPA gave me a really scary heart arrhythmia, just be careful if you are prone to things like that. Thankfully it never came back after stopping.

 

[IndividualMan]

Dropped the Tren + Mast, now just on 300 Test.

Decided it wasn't worth the risk.

Seems like in terms of cardiac remodeling + LDL risk, Test/Nandrolone/Primo are the ways to go.

But I'm not made out of money, so Test + Nand it'll be for the foreseeable future.

you had a MI and kept running tren until now??
good call on dropping most things that severely negatively affect lipids tho

 

[DugPrime]

Same. I haven’t seen one over 40 from “one of us” in a while. But that’s why I’m so aggressive with LdL lowering. My HDL is dogshit so I want my ldl so low that the HDL issue becomes unimportant / less important.

And as far as I recall there’s no real data to show that chasing HDL to try to raise it has any positive impact on cardiac events, especially if you’re ldl is under 60-70.

I agree with you, isolated low HDL isn't a cardiac risk, it's more about the LDL/HDL ratio, and especially total cholesterol.

 

[RockyP]

I agree with you, isolated low HDL isn't a cardiac risk, it's more about the LDL/HDL ratio, and especially total cholesterol.

LDL is where the action is.

That said, i prob wouldn't go run Tren and anavar for 16 weeks straight to see how low my HDL could get, but aggressive LDL management is what's most important. And being very honest and accurate about our risk stratification, which does not show up so easily on paper. I appear to be low risk on paper but when you factor in my family history and gear usage, along with a good 15 years of shit lipid management under my belt, I'm in the LDL under 55 category, full stop. I run Pitavastatin 4 mg and just added Vascepa (not for lipids but for ancillary CV benefits). If my LDL is over 60 in 6 weeks, I'll add Zetia 10 mg daily.

 

[Banana Joe]

Dropped the Tren + Mast, now just on 300 Test.
Decided it wasn't worth the risk.

Please just consider scaling that back to 200mg. At least for the next 3 months or so.
I know why you want to keep taking at least those 300mg, and everyone else in this thread does, but please try to take a step back.
Nobody here wants you to stop posting for good, or come back after a four week hiatus, with a new thread being called "Had another heart attack a few weeks ago".


If you don't mind, and for others that will find this thread later, could you post a summary of everything you have posted so far? In regards, to your medical and gear history, how your lipids were etc.
Because at least on paper you didn't seem like a prime candidate to have a heart attack at age 30.