Anyone else out there with extremely high lipoprotein (a)?
Hi! I just found out that I have an extremely high lipoprotein (a) of 515 nmol/L. I'm terrified; it's that high. I'm 58 years old and my total cholesterol is 212. My LDL is 141, and my HDL is just 40. My cholesterol/HDL ratio is 5.3. Of course it's a long weekend and I may not be able to reach my doctor tomorrow. I have watched a couple of informational sessions online from various doctors discussing elevated LP(a), but no one mentions anything close to how high mine is. Is there anyone else out there with severely elevated Lp(a)? Thanking you in advance. Sue M.
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I googled CIMT and found 2 places near Peoria IL that does them. I went with The Cure Center in Springfield IL and cost was $199 covered by insurance 1st year but not second year. If you are in city it should be easier to find and no prescription needed. CIMT Report showed soft medium and hard plaque in carotid artery as well as thickness so more than just hard plaque like CT scan. I plan to get one yearly to see if it gets worse and stay ahead of it. Right now since I am 65 they gave me zetia and rosuvastatin and LDL is lowest ever in my life at 84. Something in my genes has been protecting me since I am only 15% blocked 1st year up to 19% second year. This could be increase or difference in operators doing it. If it gets worse I found a doctor to get PCSK9 inhibitors from which usually are not given before stroke or heart attack. I will pay for them myself if I have to. You can always write manufacturer for discount or maybe Mark Cuban’s drug site will have them. Anyway I have plan b and c to stay ahead of it. I also really liked lipidologist David Davidson in Chicago and he is going concierge medicine Jan 1 2026 but I will go to him if I get worse…pkan c. I feel so much better getting the CIMT yearly. Other option is about $1800 to $2000 ct angiogram with die and analysis and maybe the scan part could get covered by insurance depending on situation. Clearly is one of 2 companies to get this done at with no prescription. If I get more nervous I will go get that. I obviosly don’t buy into wait for it to get 50% blocked then we will start to treat tou philosophy. I actually had a cardiologist tell me that….made no sense to me.
@elle7
@bitsygirl
@elle7 my husband had LP(a) 940. Doctors had to do open heart surgery for him and he is absolutely fine since than . Doctor suggested stenting does not help with LP(a) as the stent will be covered with plaque soon so this was the only option . Hope it helps
@elle7 , how do you get a CIMT? Can you arrange it yourself or is a physician involved?
I have lp(a) of 628 nmol/dl. Found out 2 years ago and have had to search hard for treatment. 1st cardiologist said wait until you are at least 50% blocked and then we can do a stint. Had to search hard to be listened to and get plan of action. It can increase after menopause and HRT can help. I am on statins and zetia. I pay out of pocket for CIMT each year to monitor carotid artery plaque. I will get a pcsk9 inhibitor if it gets anywhere near 50% blocked. Lipidologists say because I am old if lp(a) was going to kill me I would be gone by now so did not give me pcsk9 inhibitors. I will find someone who will give me them if I get anywhere near 50% come hell or high water and how old I am. My worry is it has increased after menopause and will cause rapid plaque formations but they were men. I also found out I have osteoporosis per DXA same week as lp(a) and that was another journey of stupid in the health care system. Get a REMS Echolite test to compare to DXA if you get this chronic condition. No wonder health care system is costly…more expensive to let me live 20 years drooling in wheelchair rather than get ahead of chronic conditions.
@alana924 You're welcome. Glad this gave you some insight.
@tommy901
Thanks for your explanation!
Thank you, but I am still in a panic.
Lipoprotein(a), or Lp(a), is almost entirely determined by your genes.
About 90% of a person’s Lp(a) level is inherited. Unlike LDL cholesterol—which is strongly influenced by diet, lifestyle, thyroid function, exercise, and medications—Lp(a) is produced in the liver according to a genetic “instruction set” you were born with.
Main Causes:
1. Genetics (dominant inheritance).
If you have one parent with high Lp(a), there’s a high chance you will also have elevated levels.
Levels stay relatively constant throughout life.
2. Family history of early heart disease.
High Lp(a) often clusters in families where people have premature coronary artery disease or strokes.
3. Certain conditions can raise Lp(a) further (but aren’t the primary cause):
Kidney disease.
Uncontrolled hypothyroidism.
Inflammation / acute illness.
Menopause (levels naturally rise).
What's known to control Lp(a)?
Very few things—Lp(a) is stubborn.
Effective options:
1. PCSK9 inhibitors (Repatha, Praluent) has reduced Lp(a) by 20–30% on average.
2. Apheresis (in severe cases)
Can drop Lp(a) by 50–70% but requires repeated treatments.
3. The upcoming Lp(a) antisense drugs:
(Pelacarsen and Olpasiran):
Currently in phase-3 trials, shown to lower Lp(a) by 80–95%. Expected to be approved in a few years, possibly sooner.
What does not lower Lp(a):
Diet
Exercise
Statins
(Studies show that statin therapy can lead to an average increase in Lp(a) levels of approximately 10–20%).
Niacin (lowers it mildly but doesn’t improve outcomes, so no longer recommended).
Vitamin C, lysine and proline (no proven effect on Lp(a) levels).
Vitamin C doesn’t lower Lp(a), but studies show it supports vessel health, which may indirectly reduce plaque formation.
Vitamin C improves endothelial function by acting as an antioxidant to protect blood vessels from oxidative stress and by boosting nitric oxide production, which leads to vasodilation. It is also a cofactor for enzymes involved in collagen synthesis, which is essential for blood vessel integrity. Research shows that vitamin C supplementation can improve endothelial function in patients with conditions like heart failure, hypertension, and hypercholesterolemia.
The above information is based solely on valid Epidemiological studies over the past few years.
Hopefully, this will clarify some of the aspects of LP(a).
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