But the question is, what is she going to do differently as a result of knowing the genetic information? She’s already doing everything she’s supposed to be doing to reduce risk of heart disease and plaque buildup.
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Yes. I was wondering if I could do something different based on the data. It doesn’t seem like it.
Thank you cl-user. Yes after these results I started Metformin 1000mg twice a day.
Thank you… It has made me look up HOMA-IR and how to calculate it…
JeffW - I am wondering what else can I do change lipoprotein fractionation numbers. I am doing strength training and was doing zone 2 for 40 minutes and zone 5 10 minutes (get to above 90% of max heart rate by running fast and then walking). Since the heart attack at the beginning of April, I am only walking 3 miles a day. I plan to start strength training in 2 weeks and then slowly only zone 2.
Did you have any mental health issues that could have been driving up the plaque - stress, anger, anxiety, depression?
I had a heart attack in 2020 and I now, in retrospect, think that stress was a major contributing cause. I didn’t have any of the other risk factors for heart disease, but I did have three years of martial stress leading to a divorce in 2019.
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Sounds/looks like you were in the placebo group, unfortunately. Did they ever tell you one way or the other? The active drug should have lowered it by 90% or more (and ideally stopped or even reversed some of the plaque growth).
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I agree with @Dr.Bart.
The issue is, once you have disease, its progression can be unpredictable. It probably takes a decade of stabilization in order to see events dramatically decrease (which is why short term trials of lipid medications in high risk individuals often aren’t hugely impressive).
If Lp(a) is elevated, and the patient has no disease, I goal for APOB in the 50’s. If Lp(a) is normal, then in the 70’s. But this is with no disease present.
In general, we’d be looking at more aggressive targets with established disease. You may or may not get to those goals without a PCSK9 inhibitor - but often a statin + ezetimibe +/- bempedoic acid will do it - if you tolerate those - which most people do.
Established disease would typically have us goal APOB of 20 less than the goals without established disease.
Other factors include diet, with WFPB +/- little bit of fish vs. supplements, stress/sleep optimization, exercise, optimal insulin sensitivity, and optimal blood pressure control.
I do not find high level evidence for anything else presently - despite some studies showing various things - in totality, the items above would be the approach, and be consistent with what lipidologists (and myself) do in this space.
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An interesting issue re: Colchicine. I have had really bad tinnitus in my left ear since I had the Covid Vaccine three years ago. It was driving me nuts to be honest. I started low dose Colchicine about two months ago for cardiovascular reasons. After two weeks of taking it my tinnitus went to very low levels. Really a game changer for me.
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Thank you for the name of the cardiologist.
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DrFraser - Thank you for a well thought and detailed response. The detailed explanation regarding lipid management particularly in relation to Lp(a) levels and the target APOB levels provides invaluable clarity. PS: I wish more mainstream physicians/cardiologists emphasize tailored treatments based on individual circumstances as it would improve the health of many.
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Davin8r - I think i may be in low dosage one as the number dropped by 37%
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Thank you for this succinct summary of goals and recommended treatment.
Would appreciate your thoughts about Repatha versus bempedoic acid. I was on Repatha and it did great things for lipids but raised H1AC. Taking a break and trying to decide whether to retry PCSK9i (but nervous about what it might be doing to the pancreas) or – try BA. I am in the class with elevated Lp(a):40 before treatment, and CAC score of 0.96.
Was this prescribed to you by a Cardiologist?
I’m just confirming you have Lp(A) of 40 … so not abnl (if using the test where >75 mg/dL is abnl) and you have a CAC score that is almost 0, whereas we start getting mildly concern at CAC>100 and a lot at >400.
Please let me know if there are some details I’ve misinterpreted - but it sounds to me that you have verifiably got no CAD and have a roughly normal Lp(a). Sounds perfect and I’d not really understand what would be the push for treating anything in a random individual with this combination.
I don’t know your history - was there some cardiac event or something else that happened? Do you have horribly Apo(B) - although even if you did - you sound to verifiably, essentially have no hard plaque.
Anyway, I suspect there are some details I’m completely missing, as if I had someone with these details in my care … not knowing anything else, from a lipid standpoint, I’d be advising them, even if horrible ApoB and if they have some years on them with no CAD, that they would have the option to treat the ApoB to modest levels or simply get some serial monitoring to see if any evidence of disease.
I bet however, I’ve missed a key detail that would have one on a PCSK9 inhibitor.
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Yes. This was prescribed to me by a cardiologist.
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If CRP is up …
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Fwiw, I learned about it potentially reducing events for some 25%-ish through Attia, and when I asked my cardiologist and doc about it, they both said great idea and then gave it to me.
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Was this part of your high Lp(a) protocol to offset inflammation specific to Lp(a) or something more general? What has your CRP been?