Lipoprotein (a) connection to early aortic valve stenosis?

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CarolM

Well-known member
Joined
Sep 15, 2012
Messages
65
Location
Glassboro, NJ
On 2/12/20, I had my 2nd AVR after just 7+ years. Yes, I know there are no answers "why" some valves fail far ahead of their lifespan estimates. My cardiologist and surgeon had no thoughts; sometimes it is just "luck", or genetics. That said, I personally found it dismaying to undergo this so soon, especially given a healthy diet and exercise regime.

Sooo, I did some digging on Google. There is some information on elevated lipoprotein (a) levels and early aortic valve stenosis and CV disease. My cardiologist ordered the blood test (NOT normally checked in standard cholesterol), and my level is 238! Anything over 75 is elevated.

Lp (a) is not responsive to statins, there is a strong genetic link, and currently there is no medication to lower levels. Frankly, I am not sure what will come of this information, but I certainly find it intriguing.
 
Hi @CarolM Here’s a link to an article by Dr Malcolm Kendrick in which he wrote about the role of Lp(a) in cardiovascular disease. It’s a very long article so I’ve copied just a few bits below, but to get a better understanding of what it means, the whole article is here: What causes heart disease part VI

"There has been much discussion of Lp(a) of late. What it is, what does it do, why does it matter? The first thing to point out about Lp(a) is that it is, essentially, LDL a.k.a. LDL-cholesterol a.k.a. ‘bad cholesterol.’ However, it differs in one way. It has a special strand of protein attached to it, known as apolipoprotein A.

"This protein is very interesting, from a blood clotting perspective, in that it is chemically identical to plasminogen. Yes, the one and only clot busting enzyme, switched on by tissue plasminogen activator.

"But, big but. Apolipoprotein A is folded into a slightly different structure than plasminogen. Let us say it has a right handed thread, instead of left handed thread. (This is not fully accurate, but it is close enough).

"If you incorporate Lp(a), and thus apolipoprotein A, into a blood clot, it cannot be broken down. This is because tissue plasminogen activator cannot activate it, because it is right handed. Effectively, therefore, apoliporotein A blocks the enzymatic destruction of fibrin, thus protecting the clot from destruction. Why, you may ask, would the body create such a stupid thing?

"Well, as with everything the body does, it is not stupid. It is very, very, clever. Lp(a) is only made in animals that cannot synthesize vitamin C. Guinea pigs, fruit bats, great apes and…humans. The reason for this is that, if you are vitamin C deficient, the body cannot manufacture certain important support materials/connective tissue, the most important of which is collagen.

"Without collagen, your blood vessels start to crack apart. When this happens, blood escapes, so you start bleeding from the gums, and suchlike. This condition is known as scurvy. In scurvy you start bleeding all over the place and, in the end, you die from blood loss. It is what killed many sailors of in the olden days.

"Along to the rescue comes Lp(a).. well, it can rescue you for a bit. Lp(a) sticks to cracks in blood vessel walls and forms, impossible to break up blood clots that ‘plug’ the gaps created by collagen deficiency. So you can see that Lp(a) is actually evolution’s way of protecting animals, that cannot synthesize vitamin C, from the early stages of scurvy."

"All of which means that if you don’t eat enough vitamin C, and you have a high level of Lp(a), you will end up with a multitude of very difficult to break up blood clots scattered all over your arterial walls, and inside your arterial walls too. Thus, you are going to develop CVD at a rapid rate.

"…...vitamin C deficiency is the answer to CVD? No, it is not THE answer, but it is an answer, or a part of an answer. There is no doubt that a low level vitamin C is a bad thing. There is equally no doubt that a low vitamin C level, associated with a high Lp(a) is a double bad thing. Furthermore, there is absolutely and completely no doubt that taking extra vitamin C would be a good thing for everyone – just in case."
 
Thank you for the link. I did read it, but frankly a lot was pretty technical for my non-medical brain. The vitamin C connection is certainly interesting though.
 
On 2/12/20, I had my 2nd AVR after just 7+ years. Yes, I know there are no answers "why" some valves fail far ahead of their lifespan estimates. My cardiologist and surgeon had no thoughts; sometimes it is just "luck", or genetics. That said, I personally found it dismaying to undergo this so soon, especially given a healthy diet and exercise regime.

Sooo, I did some digging on Google. There is some information on elevated lipoprotein (a) levels and early aortic valve stenosis and CV disease. My cardiologist ordered the blood test (NOT normally checked in standard cholesterol), and my level is 238! Anything over 75 is elevated.

Lp (a) is not responsive to statins, there is a strong genetic link, and currently there is no medication to lower levels. Frankly, I am not sure what will come of this information, but I certainly find it intriguing.
Hi Carol,
yes, elevated Lp(a) is causative for aortic stenosis. Mine was very similar to yours at 243 nmol/L. This puts us both at about the 95% and increases our risk substantially for heart disease and valve disease. I have BAV, so I have the double genetic whammy of having accelerated calcification from my BAV and elevated Lp(a), which studies have shown is likely causing my valve to calcify even faster than my BAV alone. Exercise and lifestyle can lower LDL, but this is not the case for Lp(a), which is technically a type of LDL, a very bad type of LDL. There are actually some things that can be done to lower Lp(a), including one prescription medication I mention below.

While statins are great for lowering LDL, they usually will raise Lp(a) 5% to 20% for most people. I believe that statins help a great number of people reduce their risk of CVD, but for those of us who have elevated Lp(a), it is important to be careful that the statin is not raising our risk level of CVD or valve disease, by raising our Lp(a). This is where the role of individualized medicine comes into play. One can get a baseline for LDL and Lp(a) and try to find the right statin and dose that lowers LDL to target, while only minimally impacting Lp(a). The effects on Lp(a) vary statin by statin, and by individual and also tends to be dose dependent. If a statin lowers LDL by 30 mg/dl but raises Lp(a) by 30 mg/dl, you are possibly doing more harm than good.

It is for the reasons above that I went off statins and went on PCSK9-I, which has the benefit of drastically lowering LDL, but also significantly lowering Lp(a). My Lp(a) has been lowered from 243 nmol/L down to its current level of 131 nmol/L. Here is how I lowered it:
My Lp(a) dropped about 6% going off of Lipitor.- statins raise Lp(a)
There is some evidence that high level fish oil, about 4g of EPA, can lower Lp(a) for some people. It lowered my Lp(a) about 5%, but some people have obtained better movement than that. Be sure to consult your doctor before going on that high level of fish oil. For me it means taking 4 capsules per day of a brand that has 1g per capsule of EPA.
But, my Lp(a) really dropped when I went on Repatha, which is a PCSK9-I. It dropped about another 40%. I am now at 131 nmol/L. This is still elevated above the desired level of being under 75 nmol/L, but way better than being at 243. Please note that Lp(a) is measured two ways; particles, which is expressed in nmol/L and in mass as mg/dl. If ones lab measures in mg/ dl, then you want to be under about 30mg/dl. The conversion factor is approximately 2.5x for most people. So yours would be something in the range of 95 mg/dl if converted.

In a post hoc analysis of the Fourier Trial, published in April 2020, hazard ratios were found to be significantly reduced for those with aortic stenosis who were on PCSK9-I. This is not surprising, given that PCSK9-I lowers Lp(a) and Lp(a) is causative for aortic stenosis. As they always say, more studies are needed and they need to do mendelian clinical trials on this specifically, this looks very promising with hope that PCSK9-I may actually slow calcification. Also, there is an antisense drug in its 3rd phase trial, which has been shown to lower Lp(a) 80-90%, so this is even better news for folks like us who have high levels of Lp(a)

Post hoc analysis of Fourier showing lower HR for those with aortic stenosis on PCSK9-I

https://jamanetwork.com/journals/ja...amacardiology&utm_content=olf&utm_term=042920
 
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Does anyone have any proof that statins raise Lp(a) ? There is no known way to lower Lp(a) at this point. I got my LDL to 56, my total cholesterol to 101, my triglycerides to 69, my weight to 158 etc etc with a low fat vegan diet, exercise and lipitor
 
Does anyone have any proof that statins raise Lp(a) ? There is no known way to lower Lp(a) at this point. I got my LDL to 56, my total cholesterol to 101, my triglycerides to 69, my weight to 158 etc etc with a low fat vegan diet, exercise and lipitor
newarrior,
Yes, it is settled science that statins raise Lp(a). Please review the published meta-analysis below:
https://pubmed.ncbi.nlm.nih.gov/311...veals,effects on residual cardiovascular risk.

This does not mean that someone who is on a statin with elevated Lp(a) should go off statin, but just need to make sure you are seeing a doctor who is aware of the dangers of Lp(a) and aware how increasing Lp(a) could offset any statin benefit from lowered LDL. But, PCSK9-I has the benefit of lowering LDL and lowering Lp(a), this is why I went of statin and went on PCSK9-I. It lowered my LDL level even better than statin and had a huge impact on lowering my Lp(a)

" There is no known way to lower Lp(a) at this point."
Well, 20 years ago this was true. This is not accurate today. PCSK9-I lowers Lp(a) significantly. I have brought my Lp(a) level from 243 nmol/L to 131 nmol/L, mostly due to being on PCSK9-I. For most people it lowers Lp(a) about 20-40%. It lowered mine about 40%. I'm still above target, but in a much lower hazard zone than when I was 243 and in the 95th% for Lp(a)

https://www.ahajournals.org/doi/10.1161/CIRCULATIONAHA.118.037184
There is also an antisense therapeutic in its third phase trial which lowers Lp(a) 80%, expected to be approved in a few years. This could be a game changer for folks who have high Lp(a). This is a big enough impact to bring about 98% of folks into target range

https://pubmed.ncbi.nlm.nih.gov/30859384/
 
newarrior,
Yes, it is settled science that statins raise Lp(a). Please review the published meta-analysis below:
https://pubmed.ncbi.nlm.nih.gov/311...veals,effects on residual cardiovascular risk.

This does not mean that someone who is on a statin with elevated Lp(a) should go off statin, but just need to make sure you are seeing a doctor who is aware of the dangers of Lp(a) and aware how increasing Lp(a) could offset any statin benefit from lowered LDL. But, PCSK9-I has the benefit of lowering LDL and lowering Lp(a), this is why I went of statin and went on PCSK9-I. It lowered my LDL level even better than statin and had a huge impact on lowering my Lp(a)

" There is no known way to lower Lp(a) at this point."
Well, 20 years ago this was true. This is not accurate today. PCSK9-I lowers Lp(a) significantly. I have brought my Lp(a) level from 243 nmol/L to 131 nmol/L, mostly due to being on PCSK9-I. For most people it lowers Lp(a) about 20-40%. It lowered mine about 40%. I'm still above target, but in a much lower hazard zone than when I was 243 and in the 95th% for Lp(a)

https://www.ahajournals.org/doi/10.1161/CIRCULATIONAHA.118.037184
There is also an antisense therapeutic in its third phase trial which lowers Lp(a) 80%, expected to be approved in a few years. This could be a game changer for folks who have high Lp(a). This is a big enough impact to bring about 98% of folks into target range

https://pubmed.ncbi.nlm.nih.gov/30859384/
I have a 88 lpa.Hey let's take this offline My USA # 323 210 8729..email: [email protected]......Thanks !
 
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