Lp(a) of 390 nmol/L!

[Nocturne]

Just got the results of two tests that had not come back before my meeting with my cardio doc. One was good except my Large HDL count was much too low (despite HDL reaching 45, which I had seen as a bit of unexpected good news).

The other was my lipoprotein A level. A score of 75 nmol/L or below is below the 75th percentile and considered optimal.

My score was 390. I do not know the percentile there but I could hazard a guess.

From what I have read, high Lp(a) is basically a genetic thing that is pretty much unaffected by diet and exercise. It puts a person at high risk for CAD, stroke, and aortic stenosis.

So I think it's a mystery solved as far as why I developed CAD and AS at such a young age. Just the other week I found a risk calculator online and plugged all of my OLD numbers into it -- from before the diet, weight loss, exercise, and statins -- and got a result of under 3% chance of developing heart disease OVER THE NEXT DECADE. High Lp(a) is synergistic with high LDL, so it basically punishes you a lot more than the average Joe for stepping out of line WRT your lipids.

And it looks like there is nothing you can do to treat it. Niacin, maybe, but even with optimal response mine would still be through the ceiling.

I am so worn out, so depressed, so ANGRY. This isn't just cheating ME, it is going to cheat my KIDS -- 50% chance for each, and I have 4. I am sick and tired of bad news about my heart and body.

 

[Nocturne]

OK - a ray of hope:

http://www.lipoproteinafoundation.org/page/AkceaPhaseII

If all goes well there could be a new Lp(a) lowering drug on the market in a few years -- and this one seems really effective too. Note that elevated levels of Lp(a) are significantly associated with calcific aortic stenosis.

In many ways it is too late for me -- but it's not too late for my kids.

 

[Warrick]

I don't know much on any of this but I know have high cholesterol, think it's genetic as my brothers worse than mine, my kids were all checked for BAVD and all negative, understand you there, but then their kids and so on? Genetics is about as fixed as the earth going around the sun

sounds like it's time to step back and see the trees

 

[Agian]

I'm getting 109mg/dL from 390nmol/L (please check)
Evolocumab should get that down into the 70s
Crystalline Niacin and DHEA (you're low in testosterone right?) might get it below 50mg/dL
This would still make it a little high, but not dangerously so. You can compensate by getting your LDL even lower
The Repatha will reduce your LDL and increase your HDL

My feeling is that we inherit a predisposition for high Lp(a). Chances are both your parents had high Lp(a), for yours to be that high
If your children's mother has a normal Lp(a) it is unlikely theirs will be as high as yours
It peaks in childhood anyway, before reaching a lower baseline in adulthood
I'm not convinced of this on/off 50% thing you quote (doesn't make sense), as the recommended 'normal' is just a guesstimate (think it through)

Anyway, now you know what's driving your plaques, you can address it
You can reverse soft plaques, but not calcium. So, your CAC score will not go down. It might even blip up a bit as the calcium percentage of your plaques increases, as the polystyrene regresses

Persevere and you'll improve things

 

[Nocturne]

Agian, as far as I know, Evolocumab has no effect on Lp(a), bad Lp(a) is highly heritable, and CAC scores go up steadily over time and do not "freeze". If you can find me any actual data to the contrary I would like to see it.

I do have low T and am being treated for it. As it turns out, TRT is one of the few things that actually does lower Lp(a). I wonder how bad it was BEFORE...

Found a foundation for Lp(a) and watched this patient testimonial:

https://vimeo.com/205088669

This woman's story is very similar to my own.

I am am still sad, and angry, and scared -- but at the same time I feel a sort of peace, knowing WHY. My case makes SENSE, now. I needed to know WHY.

 

[Nocturne]

Agian, as far as I know, Evolocumab has no effect on Lp(a), bad Lp(a) is highly heritable, and CAC scores go up steadily over time and do not "freeze". If you can find me any actual data to the contrary I would like to see it.

I do have low T and am being treated for it. As it turns out, TRT is one of the few things that actually does lower Lp(a). I wonder how bad it was BEFORE...

Found a foundation for Lp(a) and watched this patient testimonial:

https://vimeo.com/205088669

This woman's story is very similar to my own.

I am am still sad, and angry, and scared -- but at the same time I feel a sort of peace, knowing WHY. My case makes SENSE, now. I needed to know WHY.

 

[Nocturne]

Sorry, I've just... I've been carrying that for a while now.

More info on Lp(a) as a cause of aortic stenosis here:

http://www.jlr.org/content/57/6/917

It seems that most people dealing with AS at a younger age have bicuspid valve. When I first came here, I felt very alone and confused because no one else seemed to be dealing with calcific degenerative AS; no one anywhere near my age, at any rate. The community here should be aware that extremely elevated Lp(a) is a thing that is strongly associated with calcific degenerative AS.

 

[Agian]

https://www.ebs.tga.gov.au/ebs/picmi...42316114622483

I'm on the **** myself.

Sigh, I've already posted heaps about the reversibility of CAD.
Calcium doesn't JUST materialise and doesn't in itself cause heart attacks. It makes up about 20% of plaques and they use it (because you can see it on Xrays) to estimate plaque burden.

 

[Nocturne]

"In clinical trials, in patients with primary hypercholesterolaemia [Heterozygous familial hypercholesterolaemia (HeFH) and atherosclerotic cardiovascular disease (CVD)], Repatha reduced LDL-C, TC, ApoB, non-HDL-C, TC/HDL-C, ApoB/apolipoprotein A1 (ApoA1), VLDL-C, TG and Lp(a), and increased HDL-C and ApoA1."

Well that is good news and I thank you for it. How much did did it lower your Lp(a)?

I'm aware of what CAC is and how it is a measure of plaque burden. I am also aware that it marches steadily upward regardless of statin use or anything else, unless you are talking about the extreme dietary restrictions advocated by Dead Ornish, Esselstyn, et. al. that have never been tested on a large scale (presumably because they cannot find a large number of people who are capable of subsisting on leaves).

(Edit -- I have seen evidence that aged garlic extract slows the progression of CAC significantly. Which is why I take it. Hoping this bears fruit.)

 

[Nocturne]

OK I'm seeing a 30% reduction in Lp(a) from Repatha? I know this is a relatively new drug, but it still feels odd that even the Lp(a) foundation doesn't seem to mention it on their website.

I cannot find a conversion from nmol/L to mg/dl for Lp(a) anywhere online. Which is frustrating. But if 390 is cut in half, it is almost 200, which is still well past the 125 "extremely high risk" cutoff.

 

[Agian]

I'm talking to someone who got their Lp(a) down to 80 from 130 plus (Higher than yours). He was put on Fenofibrate by his cardiologist. He is taking DHEA and Niacin, as well. No Evolocumab.

My Lp(a) is now normal. Started at about 60. Evolocumab got it down to 45 (30% reduction as promised). Down to 24ish with Niacin, DHEA, fishoil, almonds, flaxseed. So more than total 50% reduction. If you replicated my results, yours should get lower than 50.

Ornish and Esselstyn's claim to fame is reversal without statins. Keep in mind that their diet will actually reduce HDL and increase Lp(a). Ornish started his journey in the 80s and was influenced by some guru, yoga, mediation etc.

Fish eaters have lower Lp(a) than vegetarians.

I learnt the DHEA trick from William Davis.

If I were you I would trial Evolocumab, Niacin, DHEA.

 

[Agian]

But if 390 is cut in half, it is almost 200, which is still well past the 125 "extremely high risk" cutoff.

I got 109 for your result (see above).

 

[Nocturne]

Thank you,Agian, but this report would seem to question the validity of your calculations:

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5067066/

As for Niacin: "At present, no effective drug therapy is available for Lp(a) – nicotinic acid was withdrawn from the market in Europe after two studies showed no positive effect on cardiovascular events and a rather high rate of adverse events (AEs)."

As for Evolucumab: "PCSK9 inhibitors reduce Lp(a) levels up to 30%; however, in patients with very high Lp(a) concentrations, this effect is much less or even absent. An elevation of Lp(a) represents no indication for the administration of PCSK9 inhibitors, but these drugs could be used in patients with a parallel elevation of LDL-C."

Apheresis, however, DOES lower Lp(a) and DOES have a positive effect on cardio outcomes for people with high Lp(a). Interestingly, my father has been donating platelets through apheresis every two weeks for years -- I doubt it is the same apheresis procedure that lowers Lp(a), but it would be a measure of poetic justice if he has accidentally been protecting himself from heart attack by selflessly taking the time to donate platelets!

Other than that, my best hope -- and the best hope for my kids -- most likely lies in the new generation of drugs being trialed right now:

http://www.lipoproteinafoundation.or...e=AkceaPhaseII

These drugs are relevant to the AS community because high Lp(a) has been shown to be strongly linked to AS.

And I have to wonder -- if this is so, could it be that one reason people with AS tend to have lower relative survival as compared to the norm after AVR is that they tend to also have high Lp(a)? If that is true, then these new drugs may be even more important for the AS community.

 

[Nocturne]

I'm talking to someone who got their Lp(a) down to 80 from 130 plus (Higher than yours). He was put on Fenofibrate by his cardiologist. He is taking DHEA and Niacin, as well. No Evolocumab.

My Lp(a) is now normal. Started at about 60. Evolocumab got it down to 45 (30% reduction as promised). Down to 24ish with Niacin, DHEA, fishoil, almonds, flaxseed. So more than total 50% reduction. If you replicated my results, yours should get lower than 50.

Ornish and Esselstyn's claim to fame is reversal without statins. Keep in mind that their diet will actually reduce HDL and increase Lp(a). Ornish started his journey in the 80s and was influenced by some guru, yoga, mediation etc.

Fish eaters have lower Lp(a) than vegetarians.

I learnt the DHEA trick from William Davis.

If I were you I would trial Evolocumab, Niacin, DHEA.

Did not see this entire post for some reason.

I am glad the Evolucumab worked for you, but see above.

Will look into DHEA; have already read some about it on the testosterone forum I frequent.

Doc told me that the Ornish/Esselstyn data was scant, that Esselstyn had been using the same small study for too many years to prove his theories. In any event it is a diet that would leave a person genuinely jealous of the dietary freedoms of people who have both diabetes AND Celiac. That is a major hit to quality of life, any way you slice it, and to take it on based on scant data... Eh. Sounds nice in theory.

 

[Nocturne]

I'm talking to someone who got their Lp(a) down to 80 from 130 plus (Higher than yours). He was put on Fenofibrate by his cardiologist. He is taking DHEA and Niacin, as well. No Evolocumab.

I have been reading that it is not possible to convert the measurement in nmol/L to mg/dl for some reason. In any event I have yet to find a converter or conversion formula anywhere online. So I am not really sure if your friend is higher than me -- although it is entirely possible. 80 is still bad, and again the end game benefits from Niacin (ie fewer heart attacks) have not materialized.

We'll see what my cardiologist says, but thanks for the suggestions. Going to look up Fenofibrate.

 

[Nocturne]

Wait -- Fenofibrate INCREASES Lp(a)? Why would I want to take that?

http://journals.lww.com/cardiovascu...ct_of_Fenofibrate_on_Lipoprotein_a__in.2.aspx

I mean sure, my triglycerides are great, actually, so maybe this doesn't apply to me, but... Something seems odd here.

 

[Agian]

No, the studies suggest there is little additional benefit in taking Niacin on top of Statins. If your ldl is already low then the benefit of adding Niacin is outweighed by the potential side-effects. But, this does not factor in high Lp(a).

Lp(a) is not a widely recognised risk factor and therefore evolocumab is not marketed for Lp(a) reduction.

Adverse effects of Niacin and temporary. Look up the Niacin flush. However, the slow release variety can accumulate and cause liver problems. The crystalline form can be taken twice a day and it's short half-life protects you from liver problems. You will feel uncomfortable when you first take it, but if you build up slowly you won't have any problems.

If you have a low lp(a) then 30% may not be much numerically. Therefore in contradiction to your comment the reductions tend to be MORE dramatic (Not less) with higher initial levels.

The conversion I found was for micromoles. Just move the decimal point. 109 sounds about right.

Going vegan is not that hard. Your taste for meat goes away after 60 days. I still eat fish/fishoil.
Esselstyn says no fats, no nuts. This is likely to decrease HDL and increase lp(a), which is not what you want.
if you had high ldl and normal lp(a), then yeah... but you don't.

 

[Paleowoman]

I have been reading that it is not possible to convert the measurement in nmol/L to mg/dl for some reason.

To convert nmol/L to mg/dL you divide by 2.5. To convert mg/dL to nmol/L you multiply by 2.5.

From wikipedia:

Lipoprotein(a) - Lp(a)

Desirable: < 14 mg/dL (< 35 nmol/L)
Borderline risk: 14 - 30 mg/dL (35 - 75 nmol/L)
High risk: 31 - 50 mg/dL (75 - 125 nmol/L)
Very high risk: > 50 mg/dL (> 125 nmol/L)

 

[Agian]

Wait -- Fenofibrate INCREASES Lp(a)? Why would I want to take that?.

Does it? I won't insist. That's not what this dude's cardiologist reckons. His did go down, but it might have been the other stuff that did it.

 

[Agian]

To convert nmol/L to mg/dL you divide by 2.5. To convert mg/dL to nmol/L you multiply by 2.5.

From wikipedia:

Lipoprotein(a) - Lp(a)

Desirable: < 14 mg/dL (< 35 nmol/L)
Borderline risk: 14 - 30 mg/dL (35 - 75 nmol/L)
High risk: 31 - 50 mg/dL (75 - 125 nmol/L)
Very high risk: > 50 mg/dL (> 125 nmol/L)

The conversion depends on the stuff you're measuring. You mean for lp(a)? Possible. What did you get for 390?