Update on statins

She indicated the LDL needs to be sub 100.

Yeah... That still has you with a 1 in 20 or so chance of death in the next 10 years.

In answer to your earlier question, AAS use can increase plaque burden independent of lipids, or more specifically, it can cause some endothelial dysfunction, and pro-inflammatory conditions increasing the accumulation of plaque burden for whatever ApoB is present.

The good news is, if your ApoB is sufficiently low, that's less likely to occur.

If y'all are getting rosuvastatin and ezetimibe from Indian pharma, might as well throw some bempedoic acid in as well.
 
Yeah... That still has you with a 1 in 20 or so chance of death in the next 10 years.

In answer to your earlier question, AAS use can increase plaque burden independent of lipids, or more specifically, it can cause some endothelial dysfunction, and pro-inflammatory conditions increasing the accumulation of plaque burden for whatever ApoB is present.

The good news is, if your ApoB is sufficiently low, that's less likely to occur.

If y'all are getting rosuvastatin and ezetimibe from Indian pharma, might as well throw some bempedoic acid in as well.

Is there any way to test for accumulated endothelial dysfunction?
 
Is there any way to test for accumulated endothelial dysfunction?

There are some simple blood panels one can get in addition to lipids that help detect inflammatory conditions. Primarily that would be hs-CRP. I suspect you're probably also getting CBC, HbA1c, and that your blood pressure is good. Homocysteine is another good panel.

In terms of direct measurement of endothelial health, one can get a PWV (pulse wave velocity) test, which is a direct measurement of arterial stiffness.

Here's a review of PWV use in diagnosing ASCVD.

I have no idea how difficult it is to find this test or get it ordered, but it seems worthwhile for someone with advanced ASCVD (i.e. >100 CAC).
 
Anyone tried Niacin?

Niacin has zero efficacy in the treatment of ASCVD. It improves biomarkers somewhat, but has no positive effects on outcomes and potentially negative effects.

 
There are some simple blood panels one can get in addition to lipids that help detect inflammatory conditions. Primarily that would be hs-CRP. I suspect you're probably also getting CBC, HbA1c, and that your blood pressure is good. Homocysteine is another good panel.

In terms of direct measurement of endothelial health, one can get a PWV (pulse wave velocity) test, which is a direct measurement of arterial stiffness.

Here's a review of PWV use in diagnosing ASCVD.

I have no idea how difficult it is to find this test or get it ordered, but it seems worthwhile for someone with advanced ASCVD (i.e. >100 CAC).

My last CRP test was at the dead bottom end of reference range. My father never had any diagnosed ASCVD and died at 76 of kidney issues. I just had a call with my paternal uncle who had a triple bypass at 66. Had a CAC score of 320 and was able to complete his stress test to 148bpm without exertion issues. Said he had high cholesterol but could never take a statin due to horrific side effects. Said he felt as if he was run over by a vehicle. He tried multiple ones and since his bypass is now on Repatha. My brother who is a few years older had a CAC score and was told it was "all good" but he didn't have a number to tell me.

Like I said I'm getting a second opinion this Thursday (to see if more testing is warranted). But I don't really have any exertion symptoms or anything I can consider angina. I do get anxiety at times.
 
Like I said I'm getting a second opinion this Thursday (to see if more testing is warranted). But I don't really have any exertion symptoms or anything I can consider angina. I do get anxiety at times.

While you may have detectable plaque burden that doesn't imply a certainty that you will have further issues. The likelihood of MACE increases and so it's something to be managed, but I've heard anecdotes of people with very high CAC scores with no issues. It's a game of probability.
 
No, because damage to the endothelium drives CVD, and you can do plenty of damage with AAS even if your cholesterol is bottomed out.

Endothelial damage is what allows the lipoproteins to enter the subendothelial space. Both are necessary for ASCVD to progress. The lower one's ApoB, the less plaque burden will accumulate regardless of endothelial damage.

Further, as you stated, AAS *can* cause endothelial damage. The specific AAS and the dose matter, as well as the individual response.
 
Updating this thread. After one month on 10mg Lipitor my LDL went from 160 to 108 and my ApoB from 120 to 83. I haven't had any noticeable side effects from the statin. I know my cardiologist is going to have issues as my creatine kinase is 1000 (it ALWAYS is for years and years out of range due to exercise but I have never had anything close to rhabdomyolysis) and my AST/ALT values are just over the top end of reference range (always are especially since starting TRT in 2020) although my GGT is low at 17.

I went to a dedicated cardiac testing facility and had a normal ultrasound. Stress test is 2 weeks from now. I'm going to suggest adding Zetia to the protocol when she reviews the bloods.
 
Updating this thread. After one month on 10mg Lipitor my LDL went from 160 to 108 and my ApoB from 120 to 83. I haven't had any noticeable side effects from the statin. I know my cardiologist is going to have issues as my creatine kinase is 1000 (it ALWAYS is for years and years out of range due to exercise but I have never had anything close to rhabdomyolysis) and my AST/ALT values are just over the top end of reference range (always are especially since starting TRT in 2020) although my GGT is low at 17.

I went to a dedicated cardiac testing facility and had a normal ultrasound. Stress test is 2 weeks from now. I'm going to suggest adding Zetia to the protocol when she reviews the bloods.
10mg at what frequency? Daily?
 
Updating this thread. After one month on 10mg Lipitor my LDL went from 160 to 108 and my ApoB from 120 to 83. I haven't had any noticeable side effects from the statin. I know my cardiologist is going to have issues as my creatine kinase is 1000 (it ALWAYS is for years and years out of range due to exercise but I have never had anything close to rhabdomyolysis) and my AST/ALT values are just over the top end of reference range (always are especially since starting TRT in 2020) although my GGT is low at 17.

I went to a dedicated cardiac testing facility and had a normal ultrasound. Stress test is 2 weeks from now. I'm going to suggest adding Zetia to the protocol when she reviews the bloods.
Lipitor is no joke! I just ran an experiment, 10mg a day for just 3 days before blood work. The changes were
CHOLESTEROL, TOTAL 152 ---> 88
HDL CHOLESTEROL 49 ---> 23
LDL-CHOLESTEROL 86 ---> 47
 
10mg at what frequency? Daily?
Yes. Daily before bed.


Lipitor is no joke! I just ran an experiment, 10mg a day for just 3 days before blood work. The changes were
CHOLESTEROL, TOTAL 152 ---> 88
HDL CHOLESTEROL 49 ---> 23
LDL-CHOLESTEROL 86 ---> 47
My HDL remained unaffected by the Lipitor and remained in the 60 level. My triglycerides also unaffected at 50.

On the blood work discussion today she said to wait another month to see if the 10mg dose continues to lower my cholesterol. I asked about Zetia and she said the next step is not Zetia but to increase the statin to 20mg daily. I have noticed some guys on here use a low dose statin - 10mg of Lipitor or 5mg of Crestor and then tack Zetia on. Why do those who do this, do it? Why not max out the statin first?
 
I asked about Zetia and she said the next step is not Zetia but to increase the statin to 20mg daily. I have noticed some guys on here use a low dose statin - 10mg of Lipitor or 5mg of Crestor and then tack Zetia on. Why do those who do this, do it? Why not max out the statin first?

Statin mono-therapy is the standard of care recommended by the American College of Cardiology. Statins come with adverse side effects that are less common then folks seem to think, but are still present and definitely does dependent.

The fact that Lipitor was prescribed suggests an outdated approach. Typically, Crestor is more efficacious at lower doses and doesn’t cross the blood brain barrier.

Zetia and bempedoic acid both have a better side effect profile than statins and are complementary. They’ll give you incremental improvements in ApoB without increasing the risk of adverse side effects.
 
Statin mono-therapy is the standard of care recommended by the American College of Cardiology. Statins come with adverse side effects that are less common then folks seem to think, but are still present and definitely does dependent.

The fact that Lipitor was prescribed suggests an outdated approach. Typically, Crestor is more efficacious at lower doses and doesn’t cross the blood brain barrier.

Zetia and bempedoic acid both have a better side effect profile than statins and are complementary. They’ll give you incremental improvements in ApoB without increasing the risk of adverse side effects.
This week’s labs indicated Primo lowered my HDL (44 to 33), but strangely enough lowered LDL and total cholesterol. Both were already at safe levels but are now even lower. I’m taking 10mg Rosuvastatin. Do you think it would be beneficial to increase Rosuvastatin or add Zetia to attempt to raise HDL? From what I’ve read increasing HDL via medications doesn’t do much to lower risk of adverse events.
 
10mg at what frequency? Daily?
If you have enough supply built up you can do morning/evening and it will crush the numbers.

The main issue is the followup numbers that I’m currently waiting on.

Mine were related to c-reactive protein and LDL barely in range.

Now I need to change my statin script or doctor.
 
Do you think it would be beneficial to increase Rosuvastatin or add Zetia to attempt to raise HDL? From what I’ve read increasing HDL via medications doesn’t do much to lower risk of adverse events.

That is correct. If your LDL where you wanted it, I wouldn't be overly troubled by HDL, especially if the ratio is fine.
 
Screenshot_20241204-143227.webp

How would you say my cholesterol numbers are?

I would say good but better ask you experts :)
Bottom of the screenshot
 
Statin mono-therapy is the standard of care recommended by the American College of Cardiology. Statins come with adverse side effects that are less common then folks seem to think, but are still present and definitely does dependent.

The fact that Lipitor was prescribed suggests an outdated approach. Typically, Crestor is more efficacious at lower doses and doesn’t cross the blood brain barrier.

Zetia and bempedoic acid both have a better side effect profile than statins and are complementary. They’ll give you incremental improvements in ApoB without increasing the risk of adverse side effects.

I don't know this for sure bc I never asked but my assumption was that Lipitor is viewed as "safer" on the kidneys. She most likely looked at my skewed creatinine numbers and my father passing of kidney failure due and prescribed it for this reason. I can't say for sure. This doctor is young 30s and works for a major hospital in a wealthy NYC area so it seems strange she would be outdated.
 
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