So what is a layperson with "high" LP(a) (mine is 109, which was flagged as high) to do? I had a calcium score done (zero), and a cardiologist recommended my LDL be under 100 (currently 102, brought down by red yeast rice and berberine, apparently, since I won't take statins). Now I hear stations can raise LDL. Since red yeast rice has the same active ingredient as statins (monacolin k), do I need to get my Lp(a) retested only to find out it's gone higher? Good grief, this is rather maddening.
I went down this path because my mom had heart disease and a couple of strokes and died at 78, and my dad had heart disease and died at 92 of a failed valve replacement.
My sister says her Lp(a) is normal, I guess I got the bad genes.
I love this so much! In my large cardiology group I have felt like I’m the outlier as I make exactly this arguments against routine testing. Had a completely healthy 44 year old woman crying in my office because she was convinced she wouldn’t see her kids grow up after PCP found elevated Lp(a). The harm is real!
Love this by Dr Marine: “Labeling patients with a new disease (? Lp(a)-itis) has psychological consequences, especially if there is no specific treatment for it.”
Lp(a)-itis is the new disease that warrants expensive R and D of new fancy, expensive and lucrative (for pharmaceutical companies) drugs!
I’m so grateful for Sensible Medicine Substack to provide solid direction.
Thank you for your insightful essay. I am rather tired of population screenings because they very rarely lead to a reduction in overall mortality. Sadly, as in the case of your colleague, they appear to be designed to cause fear. Ultimately, I think they are used to medicalize being alive. Obviously, we want to prevent untimely deaths, if possible, but all people die at some point of something. Are we so arrogant that we think we can prevent death?
A family member had this test recently and his LP(a) value came back very high (279). This caused significant distress. He immediately started a statin, which cut his LDL in half but also raised his LP(a) even more, into the 300s. He refused the CAC scan, since its only utility seemed to be potentially motivating him to start a statin, which he'd already decided to do. His PCP agreed with this reasoning. The statin did cause unpleasant side effects for the first few weeks, which seem to have abated, thankfully. Now we're waiting for the results of the several ongoing trials of the clinical benefit of lowering LP(a). In the meantime, we're taking comfort in the fact that all of his other modifiable risk factors for CVD are quite low, thanks to diet and lifestyle (and a blood pressure medication). At this point, I don't know if we'd say we're glad he had it tested. I suppose it depends on whether being on a statin meaningfully changes his risk of a cardiac event, which seems like more of a hope than a certainty. The pyschological stress has definitely been a notch in the "con" column.
In the case report, the patient's Lp(a) is NOT high! Look at the labs reference ranges: 125 should have been reported as 'moderate'. So, all the fear is completely misplaced. The ordering physician should have had clinical common sense and reassured the patient. However, that the doctor ordered it in the first place tells me that he/she lacks clinical reasoning 101.
This fits the overall picture discussed by Dr Marine. Even if the Lp(a) value were 126, it should make no difference in how the doctor counsels his/her patient.
I don't see the steelman case for this addressed in article. My understanding as a non-expert is that negative cardiovascular outcomes from Lp(a) basically follow the same pathways as those of high ApoB, so given high Lp(a) we should more aggressively treat ApoB, which should mitigate negative outcomes from both.
I'd be curious to hear from those of you more knowledgable why that would not work.
This is a fantastic overview. One of the lowlights of a typical clinic day for me is a patient bringing in an elevated Lp(a) someone else ordered. Whatever happened to the maximum "Don't order a test unless you know what you're going to do with it"?
The suspicion that universal testing ( including first degree relatives!) is a ploy for future pharmaceutical sales is well founded. Seems Lp(a) testing should be confined to research settings until an effective treatment exists and it shows absolute clinical benefit that outweighs the risk and cost. A marginal improvement at enormous expense is worse than no treatment at all.
I would say I am a relatively healthy patient (hypothyroidism, h/o breast cancer 20 years) and in my 50's no cardiac history or family cardiac history or any lab abnormalities with lipids. (My LDL and HDL are almost identical fyi 1:1 ratio) Exercise, eat well etc etc. and my new doctor (very academic) wanted to get this test. I said why ? even if its abnormal I'm not doing anything differently. She said good to have at least once to know. I gave in even though I thought it was a bit silly. Of course it was normal. I know in general i am getting "good care" but even at the "best" institutions these types of un needed things happen and the doctors believe so much pharma and association propaganda.
What about for p-tau217 ? And when the dog catches up with the car, what’s he going to do? As mentioned in prior topics, medicalization of everything has potential to harm. “ Primum non nocere “ No need to be like the ostrich but …. I’m sure Dr A. I. Geepiti will have an answer
Thank you for this . I have an older friend who was tested for this came back high and was told to contact a cardiologist about result. It caused anxiety and not sure of benefit for 80 year old who is proactive with her health
So what is a layperson with "high" LP(a) (mine is 109, which was flagged as high) to do? I had a calcium score done (zero), and a cardiologist recommended my LDL be under 100 (currently 102, brought down by red yeast rice and berberine, apparently, since I won't take statins). Now I hear stations can raise LDL. Since red yeast rice has the same active ingredient as statins (monacolin k), do I need to get my Lp(a) retested only to find out it's gone higher? Good grief, this is rather maddening.
I went down this path because my mom had heart disease and a couple of strokes and died at 78, and my dad had heart disease and died at 92 of a failed valve replacement.
My sister says her Lp(a) is normal, I guess I got the bad genes.
I love this so much! In my large cardiology group I have felt like I’m the outlier as I make exactly this arguments against routine testing. Had a completely healthy 44 year old woman crying in my office because she was convinced she wouldn’t see her kids grow up after PCP found elevated Lp(a). The harm is real!
Love this by Dr Marine: “Labeling patients with a new disease (? Lp(a)-itis) has psychological consequences, especially if there is no specific treatment for it.”
Lp(a)-itis is the new disease that warrants expensive R and D of new fancy, expensive and lucrative (for pharmaceutical companies) drugs!
I’m so grateful for Sensible Medicine Substack to provide solid direction.
Thank you for your insightful essay. I am rather tired of population screenings because they very rarely lead to a reduction in overall mortality. Sadly, as in the case of your colleague, they appear to be designed to cause fear. Ultimately, I think they are used to medicalize being alive. Obviously, we want to prevent untimely deaths, if possible, but all people die at some point of something. Are we so arrogant that we think we can prevent death?
A family member had this test recently and his LP(a) value came back very high (279). This caused significant distress. He immediately started a statin, which cut his LDL in half but also raised his LP(a) even more, into the 300s. He refused the CAC scan, since its only utility seemed to be potentially motivating him to start a statin, which he'd already decided to do. His PCP agreed with this reasoning. The statin did cause unpleasant side effects for the first few weeks, which seem to have abated, thankfully. Now we're waiting for the results of the several ongoing trials of the clinical benefit of lowering LP(a). In the meantime, we're taking comfort in the fact that all of his other modifiable risk factors for CVD are quite low, thanks to diet and lifestyle (and a blood pressure medication). At this point, I don't know if we'd say we're glad he had it tested. I suppose it depends on whether being on a statin meaningfully changes his risk of a cardiac event, which seems like more of a hope than a certainty. The pyschological stress has definitely been a notch in the "con" column.
In the case report, the patient's Lp(a) is NOT high! Look at the labs reference ranges: 125 should have been reported as 'moderate'. So, all the fear is completely misplaced. The ordering physician should have had clinical common sense and reassured the patient. However, that the doctor ordered it in the first place tells me that he/she lacks clinical reasoning 101.
This fits the overall picture discussed by Dr Marine. Even if the Lp(a) value were 126, it should make no difference in how the doctor counsels his/her patient.
Bottom line: Treat patients, not lab results.
I don't see the steelman case for this addressed in article. My understanding as a non-expert is that negative cardiovascular outcomes from Lp(a) basically follow the same pathways as those of high ApoB, so given high Lp(a) we should more aggressively treat ApoB, which should mitigate negative outcomes from both.
I'd be curious to hear from those of you more knowledgable why that would not work.
Statins can actually raise Lpa measurement quite significantly.
This is a fantastic overview. One of the lowlights of a typical clinic day for me is a patient bringing in an elevated Lp(a) someone else ordered. Whatever happened to the maximum "Don't order a test unless you know what you're going to do with it"?
This is a maxim I try to follow. As I mature in clinical practice, I try to order as few tests as possible.
Thanks for the well reasoned commentary.
The suspicion that universal testing ( including first degree relatives!) is a ploy for future pharmaceutical sales is well founded. Seems Lp(a) testing should be confined to research settings until an effective treatment exists and it shows absolute clinical benefit that outweighs the risk and cost. A marginal improvement at enormous expense is worse than no treatment at all.
I would say I am a relatively healthy patient (hypothyroidism, h/o breast cancer 20 years) and in my 50's no cardiac history or family cardiac history or any lab abnormalities with lipids. (My LDL and HDL are almost identical fyi 1:1 ratio) Exercise, eat well etc etc. and my new doctor (very academic) wanted to get this test. I said why ? even if its abnormal I'm not doing anything differently. She said good to have at least once to know. I gave in even though I thought it was a bit silly. Of course it was normal. I know in general i am getting "good care" but even at the "best" institutions these types of un needed things happen and the doctors believe so much pharma and association propaganda.
What about for p-tau217 ? And when the dog catches up with the car, what’s he going to do? As mentioned in prior topics, medicalization of everything has potential to harm. “ Primum non nocere “ No need to be like the ostrich but …. I’m sure Dr A. I. Geepiti will have an answer
Testing for risk of AD seems even less useful than for Lp(a).
Oh yes, let's all test for p-tau217!! Then we'll know if we need to start saving money for 24/7 care...
Last one out turn the lights off …
Thank you for this . I have an older friend who was tested for this came back high and was told to contact a cardiologist about result. It caused anxiety and not sure of benefit for 80 year old who is proactive with her health
“Pre-test probability matters; ARR matters “: a statement that should drive every discussion and shared decision making in clinical medicine.