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Bret Scher, MD

@bschermd

Jun 12 • 10 tweets • 2 min read • Read on X

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1/ A new RCT in @JAMACardio found that vitamin K2, specifically MK7, slowed coronary artery calcification progression compared to placebo in 180 adults over two years.

Promising finding. But it raises a fascinating question about how we measure cardiovascular disease. 🧵

2/ And the finding makes sense. Vitamin K2 activates proteins that direct calcium away from arteries and toward bone where it belongs. Sounds like a good thing. But does it help heart and vascular health?

3/ The study randomized 180 adults to either 360 micrograms of MK7 daily or placebo for two years, with CAC and CTAs repeated at baseline, 12 months, and 24 months. Serial measurements, same scanner, two years. That is reasonably rigorous for a supplement trial.

4/ But here is where it gets interesting. A baseline CAC score is genuinely valuable for cardiovascular risk stratification. It helps identify who is at higher or lower risk. That clinical utility is well established.

Serial CAC scoring is a different story.

5/ When CAC increases it could mean two very different things. New plaque forming, which is concerning. Or existing non-calcified plaque turning into calcified plaque, which may actually reflect disease stabilization rather than progression.

CAC alone cannot tell you which one it is. That is a fundamental limitation of serial CAC as a monitoring tool.

6/ And this study's own CTA data sheds light on this. Increases in CAC correlated with the partial calcification of non-calcified plaques, but apparently not with new plaque formation. So one possible conclusion is that rising calcium in this study reflected stabilization of existing soft plaque, not necessarily new disease.

7/ But the CTA data also showed something fascinating. There was no significant difference between K2 & placebo in total plaque progression or stenosis severity on CTA. All 3 plaque categories increased in both groups.

K2 slowed calcification but did not appear to reduce overall plaque burden on CTA.

8/ This is precisely why CTA with quantitative plaque analysis is more informative than serial CAC alone. It tracks total disease burden, not just the calcified fraction. As radiation doses continue to fall and AI-guided plaque quantification becomes more standardized, CTA-based analysis should become the new gold standard for tracking CAD progression.

9/ Of course there are plenty of caveats. What about a higher dose of K2? Or longer duration? All good questions. But from what the trial shows, CAC decreased, but we are left wondering if that is a good thing or not.

So be careful reacting to a headline about decreased coronary calcium over time. It may not mean what you think.

Here's a link to the study jamanetwork.com/journals/jamac…

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More from @bschermd

Bret Scher, MD

@bschermd

Jun 8

A new study called NATURE-CT gives us something genuinely valuable: a look at how coronary plaque progresses naturally in relatively “low-risk” adults on no lipid-lowering therapy.

But the way some people are using it online concerns me. Let's talk about what the data actually shows and how it relates, or does not, to ketogenic therapy. 🧵

205 adults, mean age 55, no prior cardiac events, no lipid-lowering therapy, all with a baseline CAC under 100, had plaque analysis by CTA five years apart.

Total plaque volume roughly doubled.

Non-calcified plaque grew fastest. Even low attenuation plaque, the most dangerous kind, increased.

Genuinely useful reference data.

And worth noting: mean baseline LDL was only 111 mg/dL. Plaque still progressed. That should prompt us to look beyond LDL as the sole driver.

Here is something critically missing from the discussion.

Maybe the subjects weren’t as healthy as we think.
25% had hypertension. They had a suboptimal average TG:HDL ratio of 2.3.

We know nothing else about insulin resistance, fasting insulin, visceral adiposity, etc. Metabolic dysfunction may be one of the most powerful drivers of plaque progression.

A population that looks low risk on paper is not always as metabolically healthy as we would like to assume. This is a meaningful limitation for interpreting these findings and assuming they were “low risk.”

Read 10 tweets

Bret Scher, MD

@bschermd

Jun 5

Cardiology calls statins miracle drugs. Social media calls them poison.

Both sides cite published scientific papers. How can they be looking at the same evidence and reaching opposite conclusions?

As a cardiologist, I think both sides are are on to something. Let me explain. 🧵

The mainstream cardiology position: LDL and plaque cause heart disease/attacks, statins lower LDL and stabalize plaque, therefore statins prevent heart attacks and save lives. For preventing heart attacks, the trials are numerous and the guidelines are clear. (for saving lives, the data is weaker, but the guidelines remain clear.)

The social media position: statins are overprescribed, LDL is protective, and the side effect burden is being systematically underreported.

Here is the uncomfortable truth. Neither position is entirely wrong.

And as a caveat, yes, we have many other ways to lower LDL, but statins are often the “poster child” for this, so I will use them as the focus in this discussion.

Yes, statins reduce cardiovascular events. That evidence is real across multiple large randomized trials. For patients with established heart disease, the benefit can be meaningful, and in this situation, I prescribe them regularly.

But the question that might not get asked with sufficient rigor is: by how much, and for whom?

Read 12 tweets

Bret Scher, MD

@bschermd

May 18

I'm at the @APApsychiatric conference, and there is a conversation happening here that deserves a much wider audience.

Psychiatric medication deprescription. When to taper, how to taper, and who should be making that call. It is one of the most underserved questions in mental health care. 🧵

The administration has called for greater discussion about deprescribing psych meds. That has created real controversy here.

APA leaders openly acknowledge overprescription is a problem, especially with antidepressants. But these medications are also genuinely necessary and life-changing for many people. Both things are true.

So how do we talk about deprescription responsibly without encouraging people who need their medications to stop taking them?

Here is the framing I keep coming back to. This conversation should be directed at prescribing clinicians more than individual patients.

Read 9 tweets

Bret Scher, MD

@bschermd

Apr 14

In metabolic health, the most dangerous words a clinician can say are 'the science is settled.'

Here are six debates that are very much not settled, and that affect every patient I see. 🧵

Controversy #1: The Lipid “Paradox”

Is elevated LDL/ApoB inherently causative of heart disease for everyone?

Or is it one of many contributing factors that is less “causal” if your:
→ BP is normal
→ TGs are low
→ HDL is high
→ Inflammation is near zero?

Should we be studying this more?

Controversy #2: GLP-1s - Bridge or Destination?

Industry says these are lifelong drugs for a chronic disease.

Metabolic clinicians ask: Can we use them as a "bridge" to establish a muscle-sparing, metabolic health promoting lifestyle and then successfully taper off?

Seems reasonable!

Read 9 tweets

Bret Scher, MD

@bschermd

Apr 9

Your veins and arteries carry the same blood. Same LDL. Same ApoB. Same everything. Yet veins almost never get plaque. Arteries constantly do.

Maybe you've seen the recent discussions about this. It's an interesting question that provides clues in cardiovascular science, and could challenge how we think about LDL and ApoB. 🧵

If ApoB-containing lipoproteins were "sufficient" to cause the disease, we should see plaque everywhere.

But we don't.

We only see it in the high-pressure, high-turbulence environment of the arterial system.

The real "experiment" happens during bypass surgery (CABG).

When a surgeon takes a pristine vein and grafts it into the arterial circulation, something changes.

Subjected to arterial pressure, that vein suddenly becomes susceptible to atherosclerosis.

This demonstrates that mechanical factors, pressure and sheer stress, could be the primary triggers. High pressure leads to endothelial injury, which then initiates the atherosclerotic cascade.

The injury happens first; the "repair" (plaque) follows.

This leads us to a key question: Is ApoB actually sufficient for atherosclerosis, or is it merely a necessary participant that only becomes a problem once the "soil" (the endothelium) is damaged?

Read 7 tweets

Bret Scher, MD

@bschermd

Nov 6, 2022

Lowering TGs with pemafibrate doesnt lower CV events. Does that mean we can ignore TGs? No! A brief thread nejm.org/doi/full/10.10…

Changing a lab value with a drug has NOTHING to do with changing it with a lifestyle approach Just look at HDL and CETP inhibitors.

Does it mean TGs aren't independently causal for CVD? maybe. There is suggestive evidence that they are, but this study seems to imply they aren't. Does that matter? For drug development yes it does. For lifestyle therapy, not at all

Read 10 tweets

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