#1624

The difficulty here, of course, is that mice tend not to be euthanised because the researchers think they are about to have a heart attack.

#1625

Umm, that would mean that miraculously mice never got heart attacks before they got cancer, and were it not for that pesky cancer they’d all succumb to rashes of heart attacks. A rather exotic hypothesis, if I may say so.

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#1626

The issue is really one as to the extent to which mice get CVD. I don’t know I don’t really look that much at mouse studies. I only found out about the euthanasia issue by having dinner with researchers who have lots of issues where animal welfare skews the results. I am not myself saying we should not be concerned about animal welfare, but when it has changed the results that should be reported transparently.

So if you have a lifespan experiment and the mice have actually been euthanised rather than just found dead in a cage then that should be reported separately even if it is counted in a summary as the date of death.

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#1627

Well, that I can agree with. That said, it’s not just animal welfare. Many trials are stopped before completion if a clear and dramatic benefit is shown in the treated arm vs placebo, with the justification that it would be unethical not to provide the same benefit to the control group. That is fine as far as it goes, but very frequently we hear regretful comments that while stopping the trial was the right thing to do from an ethical point of view, from a purely scientific perspective, valuable data was not gathered because of the premature stoppage. So there are tradeoffs.

#1628

Indeed you are right. There are tradeoffs, but what is important is to know what is actually happening.

With all the Robust Mouse Rejuvenation charts what is actually really the cause of the death of the mice. Is it an opinion of an animal house welfare worker? Do different welfare workers take different views and does that affect the median lifespan?

(I know the answer to the second question is yes, but the effect may not be material)

#1629

Do they euthanize in the ITP?

#1630

I don’t know. I know what happens particularly in the UK and the rules on these things tend to be similar in “western” countries. However, I don’t know and the reporting on this is inadequate.

In the end my own practical research is all in Homo Sapiens.

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#1631
7 Likes
#1632

Also

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#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.)

3 Likes
#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).

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#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.

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