Cholesterol Experts Say Everyone Needs a LP(a) Test

#121

Sadly, yes. That said, there’s some new thinking in some quarters, that the Lp(a) situation is highly complex, and while the particle may be much more atherogenic than plain LDL, there’s some indication that there is some conditionality involved too, where it may end up not being particularly involved in plaque progression under some circumstances. FWIW, I had a CAC done at age 65 1/2, and my score was zero. Now, it’s possible that my arteries are riddled with soft plaque, but it’s still a surprising score to me, as I have had life long high LDL (165-185 mg/dL), and have only been on atorvastatin 10mg/day for about 5 years (and btw. not very effective, last October my LDL was 146 mg/dL, TC 240).

Anyhow, your LDL has been crushed at 32. Lp(a) is nasty, but fortunately it’s not a big component numberwise of your blood lipids, it’s dwarfed by LDL, so if you crush LDL, the Lp(a) is small change. Of course, the danger of Lp(a) is the calcification of the valve leaflets, so yeah, good drugs against it can’t come soon enough.

And your rosuvastatin is not very high intensity, so you don’t need more at 32mg/dL.

I’m awaiting my results. Right now, as of the past 6 months I’m on 4 mg/day of pitavastatin. Depending on what my lipid panel shows, I intend to push my LDL to below 60 mg/dL at least, or lower. For that I’m looking to 180 mg/day of bempedoic acid, and ezetimibe 10 mg/day… hopefully that will be enough.

But lipids lowering is only one CV therapy. I think, depending on the rest of your physiology, metabolic biomarkers, you may want to add a SGLT2i like empagliflozin that’s cardioprotective, perhaps an ARB, like telmisartan to keep your BP firmly below 120 SYS. Maybe additional therapies - rapamycin can be cardioprotective. Point being, you can’t just look at lipids. There is a lot more we should be doing to keep the CV system working, it impacts the brain too. Work in progress.

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#122

FWIW I asked my cardiologist about LPa last visit about 5 months ago and whether I should be tested. He said the meds I’m taking (statin, aspirin and ARB) are pretty much what I’d take if they found my LPa abnormal, so not to worry too much about it.

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#123

Mostly right, with a couple of caveats. First, it’s true, as long as you bring your ApoB/LDL low enough. If you have little Lp(a), you have a little bit more leeway, depending on other risk factors (such as the presence of plaque). But if you have high Lp(a), you really must crush your ApoB/LDL. If you can do it with just a statin, great. But many people can’t - we are talking LDL well below 60 mg/dL. Here’s the second factor, PCSK9i enters the picture, both because they can help you reach your ApoB/LDL target, and because they can slightly lower Lp(a), by about 20% (whereas statins tend to raise it).

Bottom line, if you are below 60 mg/dL on just a statin, aspirin, and ARB, fine. But if not, I do think more can and should be done. I’m not a doctor and not offering medical advice, but if it were me, I’d get a second opinion in that scenario (of LDL above 60).

And sure, the ARB and aspirin can control other risk factors, like high BP, but ApoB/LDL is the biggest factor for MACE by far. It’s critical to get that under control.

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#124

Thanks for that information.
My LDL hangs around 60 on 5mg crestor. The doc seemed pretty happy about being on 5mg and lipids staying pretty low. Definitely a balancing act.

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#125

You’re probably very similar to me; heterogenous familial hypercholesterolemia (HeFH). Though fortunately I’ve caught it relatively early (at 32 years old). Mine was the same as you describe, where a statin alone had very little effect, but combined with Ezetimibe it was very effective. (I did also try Ezetimibe monotherapy which was also not very effective).

IMO, with your age and lifelong LDL of >160mg/dl, you should have a positive calcium score if you built plaque. I feel it’s very unlikely that you’d have all soft plaque and nothing calcified at 65yo.

As for whether I’ve built any plaque, I’m going to find out with a CTA next week… fingers crossed.

Yeah, this is definitely a valid viewpoint, and I shared this until recently. However, according to the PESA study, you can still build plaque with “low” LDL-C of 60mg/dl. If your Lp(a) is indeed high, it’s an argument to take ApoB even lower, and to perhaps be more aggressive with other risk factors (blood pressure targeting 100-110 rather than 120 etc).

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#126

I just added Ezetimibe 10 mg with my Crestor 10 mg. Hoping for a 20% reduction in ApoB. Lp(a) is not a problem for me. My numbers are on Crestor alone are:

LDL-C = 48 mg/dl
HDL-C = 62 mg/dl
Trigs = 53 mg/dl

Lp(a) = 10.5 mg/dl
ApoB = 68 mg/dl

Will report back in 2 months. Calcium score is 23. 78 yo. male

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#127

Those are great numbers, and I’m going to guess your ApoB goes below 50 mg/dl with addition of Ezetimibe

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#128

I put this in the GH/longevity thread as well, but I noticed a reference to this study on an older thread, which showed a doubling of Lp(a) after GH replacement therapy in GH-deficient adults. Might be worth monitoring for anyone who might be dabbling in GH or GH-releasing peptides:

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#129

thanks! Was very informative.

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#130

OK, as a result of this thread, I am headed to my local Quest tomorrow for a much needed hormone panel and tests for LP(a) and ApoB.
See what you folks made me do? :slight_smile:
I will post results when I get them, fingers crossed.

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#131

I’m like you - 71 female LDL 160, total 120ish never on statin so got calcium score recently was 0. Thinking of getting that non invasive test that checks soft plaque. I heard Peter Attia say if someone has our numbers and 0 score, must have some other protective mechanisms going on.

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#132

Meant Total 240 and ApoB 126.

#133

Yes, the key here is age. A CAC score of zero at age 40 means nothing, because the vast majority at that age have a score of zero, even if they have soft plaque. However a CAC score of zero in your mid-60’s and older means that your body is not very atherogenic for whatever reason, because by that age, the majority have some calcification, or conversion of soft plaque. Now, that does not mean you’re completely out of the woods, you may still have some soft plaque, or more likely the atherogenic process is much slower, and you might still accumulate measurable plaque down the line. But yes, it’s generally good news to have a score of zero in your late 60’s onward.

But what to do with high LDL/ApoB, especially if you have high Lp(a), is up to you. A completely individual decision. I have personally elected to go ahead and go on a statin (4 mg/day pitavastatin) six months ago, and likely crush my ApoB numbers with the addition of bempedoic acid and ezetimibe. I am doing this because I am persuaded that there are benefits to statins completely apart from MACE avoidance, and keeping LDL below 60 mg/dL has health benefits on balance. Now, I am not going to go crazy and crush below 40 mg or whatnot, but 50-60 is good enough for me. But I am very statin tolerant, and have picked pitavastatin specifically so your calculus may be quite different. I’m also monitoring the rest of my biomarkers pretty carefully, and will adjust as needed. It’s a work in progress, always subject to revision, as my situation evolves and medical science progresses. YMMV.

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#134

I did go on 5mg Crestor finally and numbers came down after 3 months but I seemed unusually tired so now I just take 2.5mg a couple times a week. I’ll get rechecked in a few months if up again will do more, but I need to ask for that Lp(a) my doc only does the usual, had to ask her for the ApoB and then she didn’t include in the recheck but LDL came down to 88, total 174 and HDL 67. ( just looked, had forgotten it improved that much.) Good enough for me but that 2.5mg twice a week may not be doing the trick, although I read with some it does. Good luck getting your numbers where you want them!

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#135

Ezetemibe does wonders (especially if you’re a hyper-responder like me) with no side effects. It should be the number one treatment before statins IMHO.

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#136

Thanks Chris I’ll ask for it if numbers have gone back up. Since I already have “chronic fatigue” it’s hard to know for sure if it is Crestor but I did seem even more tired.

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#137

Traditionally, Ezetimibe monotherapy kinda sucks though. Maybe a 20% lowering of LDL-C.

The real magic happens when it synergises with a statin.

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#138

IMG_0563
IMG_05631179×1657 203 KB

https://jamanetwork.com/journals/jama/article-abstract/2833204

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