#1633

A unique way to live longer and reduce arteriosclerosis - Astaxanthin.

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#1634

The blood types most at risk for heart disease

People with type A, type B or type AB blood are more likely than people with type O to have a heart attack or experience heart failure, according to the American Heart Association.

While the increased risk is small (types A or B had a combined 8% higher risk of heart attack and 10% increased risk of heart failure, according to one large study) the difference in blood clotting rates is much higher, per the AHA. People in the same study with type A and B blood were 51% more likely to develop deep vein thrombosis and 47% more likely to develop a pulmonary embolism, which are severe blood clotting disorders that can also increase the risk of heart failure.

A reason for this increased risk, according to Guggenheim, might have to do with inflammation that happens in the bodies of people with type A, type B or type AB blood. The proteins present in type A and type B blood may cause more “blockage” or “thickening” in the veins and arteries, leading to an increased risk of clotting and heart disease.

Guggenheim also thinks this may describe the anecdotal decrease in risk of severe COVID-19 disease in people with type O blood. (Note: Since this article was first published, more research has added to the notion people with type A blood may have a higher risk of infection. This because the COVID-19 virus binds to cells slightly differently based on blood type.)

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#1635

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Trends in drug repurposing: Advancing cardiovascular disease management in geriatric populations

Open Access Paper: https://www.sciencedirect.com/science/article/abs/pii/S2452318625000054?via%3Dihub

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#1636

“Hindu Mission Hospital, Tambaram, Chennai, 600045, Tamil Nadu, India”

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#1637

It staggers me to see people still arguing against the basic science of how atherosclerosis works. It’s a relatively simple process which develops over a long time. Almost every human gets some sort of atherosclerosis, in multiple arteries. Lowering atherogenic lipoproteins is a prevention tactic which is backed by some of the strongest science we have in all of medicine.

Then you have the other aspects, like reducing endothelial dysfunction (i.e. control blood pressure, control blood glucose, don’t smoke) and reducing inflammation.

I’m a firm believer that if everybody started by doing a check for familiar hypercholesterolemia at age 6, and simply control ApoB levels, we could reduce heart attacks to negligible levels.

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#1638

Isn’t it correct that the aspects don’t matter if apoB is controlled early enough (you say this later in your post), I’ve written about this here concluding that it’s the rate limiting step in cardiovascular disease.

If true I think it’s helpful to think that way as it weighs that correctly as more important than the other factors if done early.

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#1639

I think it’s not quite correct, though between controlling blood pressure (whether pharmacologically or not) and taking medications that improve endothelial function as a side effect (Telmisartan, SGLT2-inhibitors, etc) or just maintaining good endothelial function via exercise/sleep/etc, I bet you would eliminate all non-genetic heart defect forms of heart disease. With that said, for the vast majority of the population, simply bringing ApoB below 50 would eliminate their risk for heart disease.

Note that my post below’s examples all involve compromised endothelial function (independent of plaque) or a genetic defect that needs to be repaired via surgery.

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#1640

Based on what evidence?
I don’t understand why you say it’s not correct but then later say for the majority of the population below 50 would eliminate risk for heart disease.

There are no cases of MI secondary to plaque rupture at total abetalipoproteinemia, unless if you can find any.

#1641

Here you go

  • In this systematic review and meta‐analysis of >5000 patients with suspected ischemia, nonobstructive epicardial coronary artery disease on coronary angiography, or absence of myocardial ischemia on stress testing, ≈30% of patients, equally divided between men and women, had abnormally reduced coronary flow reserve diagnostic of coronary microvascular dysfunction.
  • In these patients, we observed a nearly 4‐fold higher mortality and a 5‐fold increase in major adverse cardiac events among individuals with coronary microvascular dysfunction compared with those with normal coronary microvascular function.
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#1642

Apparently there’s a nice acronym for this case as well that you might use to find studies. MINOCA: myocardial infarction without coronary artery disease.

Here’s a review of the disease

MINOCA is considered a heterogeneous working diagnosis with an estimated prevalence of anywhere from 3 to 15% among all acute myocardial infarctions (AMI) patients (5–12). This heterogeneity is partly due to significant differences in what conditions are included in the term MINOCA and which definition is used. In a pooled analysis of 23 studies, the prevalence of MINOCA was 8.1% among 806,851 consecutive AMI patients (12). MINOCA has been reported by large national registries worldwide, including the US, Japan, Poland, and Sweden, with the incidence of MINOCA ranging from 2.9 to 10.2% (6, 9, 13, 14). Compared to MI with obstructive CAD, MINOCA patients were younger, with a median age of ∼61 years (12), and MINOCA was more common in Black (6, 8, 15) and Hispanic (16) patients. Further, MINOCA patients were less likely to present with traditional cardiovascular risk factors, including hypertension, dyslipidemia, diabetes, and current smoking history (12).

4 Likes
#1643

Interestingly this review, and I guess the term MINOCA does include plaque disruption.

Plaque disruption is an umbrella term that includes plaque rupture, erosion, and calcified nodules. As lipids accumulate in coronary arteries, the surge in inflammation, necrosis, fibrosis, and calcification leads to plaque formation, which may progress and be complicated by disruption (43). Plaque rupture results in the exposure of the plaque to the coronary lumen, which results in thrombosis and thromboembolism (44), while plaque erosion results from thrombus formation adjacent to the luminal surface following endothelial cell apoptosis and neutrophils’ recruitment without rupture (45). Female sex and smoking history are associated with an increased risk of plaque erosion compared to rupture (46). Plaque rupture can be detected utilizing intravascular imaging including intravascular angiography ultrasound (IVUS) or coronary optical coherence tomography (OCT); whereas the higher resolution of OCT is needed to assess plaque erosion (47). In a multi-center prospective study, plaque rupture (and ulceration) existed in 38% of females with MINOCA (n = 16/42) who underwent IVUS (48). The HARP study reported that plaque disruption was the most common cause of MINOCA, as was evident in 43.4% of females with MINOCA who underwent OCT including 8 with plaque rupture, 5 with plaque erosion, and the rest had an intra-plaque cavity or layered plaque (27). Notably, only 59% of participants had three-vessel OCT, which may have led to an underestimation of the prevalence of plaque disruption (27).

I guess I would take this to mean given a prevalence of 3-15% for MINOCA, conservatively 50%, or 1.5% - 7.5% are from non-plaque related causes. The ones in the review are Coronary vasospasm, Spontaneous coronary artery dissection, Coronary embolism/thrombosis, MINOCA mimickers, Coronary microvascular dysfunction.

ApoB < 50 would eliminate the vast majority of MI (92.5% - 98.5%). Maintaining endothelial function likely a large remainder.

1 Like
#1644

I haven’t verified this but do you agree then it was pretty much correct to label CVD as ASCVD (I used them interchangeably)? The apoB post is a wiki so you can edit it. With so much misinformation it helps to simplify things, of course it’s a given to optimize other things as well.

1 Like
#1645

Yes. Eg this is technically correct any way you look at it

ApoB is the Rate-Limiting Step in prevention of cardiovascular disease

To be frank, the only reason I’m even somewhat aware of these other kinds of heart disease (prior to looking into it just now) is because my wife’s family has a genetic heart defect that has to be repaired at some point in their life if they have the genes for it, and my family history includes CMD. For most people, CVD = ASCVD, and worrying about the cases that are not is probably not worth most people’s time. And if it is, they’ll either know based on their family history, or never know because there really isn’t good screening (or prevention) for any of the other causes, aside from what people should be doing anyways - controlling BP and maintaining endothelial function.

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#1646

I’m unsure if HBP can cause stroke without significant plaque though, for example, but it’s important to reduce e.g risk of dementia and CKD anyway. Heart failure, and ATTR amyloidosis (25%+ at 70-80+), isn’t covered either, nor AF causing stroke. So the correct term is atherosclerotic cardiovascular disease, but which are most cases of cardiovascular disease it seems anyway. I didn’t know about ATTR when I wrote that post, but it might be much more significant in later ages (90-100+).

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#1647

I’d add Lp(a) to ApoB when it comes to screening, since high Lp(a) causes plaques even when overall ApoB is low, since Lp(a) is so disproportionately atherogenic.

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#1648

There is a lot of back and forth on the lipid hypothesis. So I decided to input all relevant data into Grok3 and see what it said. These are all the factors it considered:
age
BP
lipids APoA, ApoB, Lp(a), LDL, TC, HDL
insulin
waist to height
BMI
activity level
altitude ( I live at 6400’ - very important)
VO2 max and other fitness parameters like grip strength
CAC
CIMT
inflammation markers
medications
supplements
It spit out a long analysis based on these multiple factors which I doubt even Dr Dayspring could do a regression on and recommended against statins.
Recommendation: Skip statins unless you want maximal LDL-C reduction. Your VO2 max 50 and low-carb lean phenotype keep you in a sweet spot—CAC 108 isn’t a ticking bomb, and risk is <3-5%. The LMHR-MiHeart match reinforces this: LDL-C 149 isn’t your enemy here.
I think that this is the future of medicine

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#1649

Just be aware that the AI may be hallucinating. I’d go with Bempedoic Acid and Ezetemibe with your CAC and LDL. However, we all have our own preferences. Either way, I wish you a long and healthy life!

5 Likes
#1650

It depends on your prompt, if you ask it to reduce your risk of MACE over 10, or 20 year period, or longer and consider and prioritize correctly causal factors, and independent risk factors, it might answer differently. Best practice is to work on creating the prompt with it that you’ll feed it back to it + your data and when it should reason and about what + search. The prompt can be really long and detailed.

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#1651

MACE can put someone in the retirement home and end healthspan. Independent + causal risk factors is important for this and to weigh factors correctly. Time period is also important (is it 10, 20, 30 year risk, or longer?).

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#1652

You might also try ChatGPT Research AI version. Please let us know if you see much variance in the recommendations.

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