Did you have Lp(a) measured ?

Before my heart attack they were only doing the standard lipid panel, which I don’t think includes apoB.

LDL was 103, 65, 78, 65, 83, 91, 87

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I wouldn’t be surprised if you’re Lp(a) positive with those numbers. “Good” by conventional standards, but not sufficient over long time periods, especially with high Lp(a)

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Related, where was your blockage that caused the heart attack?

High Lp(a) tends to be associated with aortic valve stenosis:

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Per the attached reference:
ApoB considerably underestimates risk in individuals with high Lp(a) levels. The association between apoB and incident CHD is diminished or even lost. These phenomena can be overcome and explained by risk-weighted apoB.
Lipoprotein(a) and risk-weighted apolipoprotein B: a novel metric for atherogenic risk - PMC

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Thanks. Clearly with an average LDL of about 80 mg/dL, 99% of doctors would say your LDL is perfect. (And they would be wrong, but that’s the state of our sickcare system…)

Are your LDL and apoB discordant now? Or are they always almost identical?

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Another issue our healthcare system may miss is the negative effect of inflammation on what the LDL or the ApoB numbers mean. If inflammation is high, as measured by hsCRP (high sensitivity C Reative Protein), then it may be that levels of OxLDL (oxidized LDL) are relatively high and may be detrimental to health.
Further, the spectrum of LDL particle sizes is also an issue. If particles are larger, they may not have an effect on the vascular wall, but if particles are small and dense they may be more easily absorbed to create soft plaque.
hsCRP is a separate test.
OxLDL is a separate test
particle size can be obtained by nmr by Lipofit

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So… what effect does a relatively high LP(a) have on the discordance measurement ?
Looking for “one metric to rule them all” may not be the wisest choice in trying to understand CVDz which is clearly multifactorial.

ApoB and Lp(a) is rate limiting, so if you lower them enough and early enough you can’t get atherosclerosis (stroke, heart attack, vascular dementia…). That’s the point, and why they are the one metric to rule them all… But do the other things as well for other reasons and to target residual risk from already developed soft and calcified plaques. That should be obvious.

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Only 20% of people have the genetics to have LP(a)
For this unfortunate 20%, nothing they do (diet, exercise, meditation, drugs) will lower their genetically induced LP(a) levels.
Statins which effectively lower ApoB… have no effect on LP(a)
Perhaps that’s why ApoB and Lp(a) are independent risk factors for CVDz
Fortunately, newer medications such as PCSK9i medications do lower LP(a).

For those who are interested, there is a phase 3 trial enrolling to evaluate whether a siRNA medication (Lepodisiran) can reduce MACE in those with elevated LP(a) > 175nmol.
Run by Eli Lilly, with whom I have no financial interest
A Study to Investigate the Effect of Lepodisiran on the Reduction of Major Adverse Cardiovascular Events in Adults With Elevated Lipoprotein(a) (ACCLAIM-Lp(a))

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Pharmaceuticals to reduce LP(a) are very close to being released onto the market. Soon there will be a treatment to help. It’s just going to take a few years until a cheap generic will be available.

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I assume I would be rejected based on using rapa and already having it lowered sub 175 from using repatha.

Soon there will be a treatment to reduce LP(a) …
…yes, for several thousand $ / year.

A few years until a cheap generic.?
… I’d be surprised if we would have this in 5 years, as Big Pharma will do all it can to maximize profit.

The current laws in India mean that India Pharma will probably develop a generic in less than 3 years. Let’s wait and see.

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You should qualify IF you are 55 or older (that’s the only reason I didn’t, and my Lp(a) sits around 175 these days).

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You don’t even need Indian laws: drugs cost 10x less in Europe. So if obicetrapib is approved then you’ll get an affordable Lp(a)-lowering in 18 months.

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A rapa news meetup in Paris to save money buying rx’s to protect our hearts… Really, what could be better?

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The benefits of statins have been discussed a lot before, as well as some of the side effects. I have used statins with Ezetimibe and then tried Bempedoic Acid instead of statins, but after a couple of months, I developed quite severe stomach pain and had to stop, which could perhaps be a topic for its own thread. Now I’m considering restarting statins or possibly starting PCSK9i if I can get a prescription. I’m well aware of the widely proven benefits of statins in treating heart disease, but I’m a bit concerned about statin-induced coronary artery calcification (CAC), although it’s said that it has a plaque-stabilizing effect. Apparently, it can increase CAC even if there isn’t much plaque present.

Apparently, at least partially, statins interfere with the function of vitamin K, which leads to calcification.

In the case of Pravastatin, other mechanisms have also been suggested. The mechanism involves activation of intestinal Bacteroides fragilis.

I’m wondering if statins can induce CAC in completely plaque-free arteries?

Is it even reasonable to use statins if Lp(a) is high, as they tend to increase Lp(a) levels in many people? Currently, I’m only using Ezetimibe. Also taking Dapagliflozin and Berberine HCL 1000 mg per day.

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Obviously, I can’t recommend you take any drug, I can only give my one rat n-1 report. I have had lifelong high cholesterol (TC 240-270, LDL 140-180, HDL 70-100) that is completely resistant to any and all lifestyle diet, exercise, supplements interventions. After turning 60, I went on atorvastatin 10mg/day. Initially the statin worked miraculously, got my LDL to 75, TC 155. I was jumping for joy. That was the first year. Every subsequent year it seemed to get less and less effective and I’m back to trash lipids - this past October, TC 239 LDL 146. Oh, and my Lp(a) is a lovely 111. My ApoB is 120. Absolute garbage.

I decided to get s CAC scan at the end of 2023 at age 65 after 5 years of 10mg/day atorvastatin.

The result was a score of ZERO. I could hardly believe it. After a lifetime of toxic levels of lipids with garbage Lp(a), after 5 years of a statin, I have a CAC score of zero. Unbelievable. I don’t fully trust this, so next month I’m getting a CIMT for another data point. Eventually I’d like to get an angio to see if there’s any soft plaque. FWIW, I’ve been supplementing with vitamin K2 for close to 20 years. It was usually just MK-7, but in the last few years I’ve also taken a combo with high MK-4. I have also been taking vit. D3, for some 25 years. Whether that has had any impact on my arteries I don’t have the faintest clue, though yes, I’ve been supplementing with K2 and D3 exactly with the hope that it may help my arteries (and bone health, prostate cancer prevention etc.).

In any case I can’t get my insurance to pay for a PCSK9i, and my PCP has no further ideas to control my lipids, so I’ve taken matters into my own hands. I’ve dropped the atorvastatin back in November of last year and gotten on 4mg/day of Pitavastatin (Indian Pharmacy). I will get a full lipid panel in April to evaluate. I don’t expect miracles from the pita, so I’ve already purchased a modest amount of bempedoic acid and separately a goodly amount of bempedoic acid 180mg + ezetemibe 10mg combo. I will first add the BA for 3 months just to see the effect on my lipids, and then the BA+EZ. I want to crush my LDL to below 60 at a minimum, preferably to 40. We’ll see.

However my point here is that there exist statins that purportedly don’t increase your risk of diabetes, or raise your blood sugar, or cause muscle problems. Pitavastatin allegedly is one like that, plus it is outstanding in MACE prevention. It also has much less interaction with other drugs. And another point is that regardless of your statin use, you are not doomed to have calcified plaque in your arteries. It’s not a certainty as I have found out. Of course, YMMV, and we are all unique individuals with a variety of physiological parameters and reactions to pharmaceuticals.

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In which unit? mg/dl or nmol/L