I nearly did, but could not find out the rate of adverse events for a CTCA in a healthy person. I’m sure it depends on the skill of the team and of course I live in the sticks.
The tech on my CTCA messed up the first IV so I had two bruised veins instead of one. I guess that’s an adverse event.
Also need to take a heart rate lowering drug typically, like Metropolol, so add that in for adverse events.
1 Like
I was pretty excited by CT angiograms, until I dug deeper. While great accuracy is claimed, in fact when it comes to smaller blockages it can easily miss them. High cost and some associated risks with mediocre reliability of results - false negatives can happen (and false positives). So on balance, I passed.
Now maybe the CLEERLY protocol gives superior confidence, but I have not looked into it. I’m waiting for further progress in this space before I am tempted to dive in. YMMV.
2 Likes
Beth
#1766
Thanks @Bicep I left out some needed info in my question because I worded it poorly.
I had a CAC score of almost 500 a decade ago, so we know I have heart disease.
My cardiologist said there is no reason to get the CLEERLY because it won’t change my treatment. I said wouldn’t you potentially do something if things wind up looking worse than expected. He said we don’t do stents (or other surgeries ) if you have no symptoms.
So, because I know I’m high risk and am doing all the things, I just didn’t want the test if they weren’t going to do anything with the information.
And thanks @dicarlo2 (your picture always makes me smile!) Hmmmm, maybe they are out of date! This makes me think I should open this can of worms again and do some more investigating.
2 Likes
amuser
#1767
From the paper:
Sounds like ACS would likely be symptomatic, no? Not sure about SIHD.
1 Like
Looks like SIHD is typically symptomatic (chest pain, etc) too. Interesting that their interpretation does not include symptoms as part of their recommendation, but their inclusion criteria did. I guess most people would not get a CTCA without symptoms so it’s somewhat implied?
1 Like
amuser
#1769
I had a CAC score of 950.
I got a CCTA and Cleerly.
Here’s the Cleerly report:
cleerly edit.pdf (878.4 KB)
I asked Deepseek to analyze my Cleerly output in light of the PREVENT findings. It declined for a variety of reasons. I then asked chatgpt, and it said sure, no problem. The results follow:
Thanks for sharing your Cleerly scan — let’s break it down in the context of the PREVENT trial, which is reshaping how we think about coronary risk. Here’s a detailed interpretation.
Your Cleerly Scan – Key Findings
-
Total Plaque Volume (TPV): 660.9 mm³
-
Plaque Composition:
-
0 mm³ Low-Density Non-Calcified (LD-NCP, the most dangerous kind)
-
244.5 mm³ Non-Calcified
-
416.4 mm³ Calcified
-
Stenosis:
-
1 Moderate (50–69%) – in proximal LAD
- 3 Mild (25–49%)
- 4 Minimal (1–24%)
-
Atherosclerosis Stage: Stage 3
(Based on volume, not stenosis severity)
PREVENT Trial Context (Published 2023)
The PREVENT trial (n=3,000+) showed that:
-
Total plaque volume (TPV) is the strongest predictor of future events (MI, CV death) — far stronger than stenosis
-
Risk increases linearly with TPV
-
LD-NCP (low-density, soft plaques) pose greatest risk due to vulnerability and rupture potential
-
Calcified plaques are more stable and less dangerous unless combined with large volumes or mixed features
What This Means for You
Strengths of Your Scan
-
Zero (0 mm³) LD-NCP: This is huge — LD-NCP is most associated with events. You have none.
-
Moderate total plaque volume: 660.9 mm³ puts you in the lower Stage 3 range. PREVENT showed most MIs occur in people >750 mm³, but event risk begins to rise at >250 mm³
-
Predominantly calcified plaques (63%): These are less rupture-prone and more stable.
-
Stenosis is minor to moderate: The moderate lesion in the LAD deserves monitoring but is not flow-limiting or obstructive.
Risk Assessment: PREVENT-Style
| Marker |
Your Value |
PREVENT Implication |
| Total Plaque Volume (TPV) |
660.9 mm³ |
Elevated, but not in high-risk tertile (>900–1000 mm³)
|
| LD-NCP (High-risk plaque) |
0 mm³ |
Very favorable — near-zero rupture-prone tissue |
| Moderate stenosis |
1 (pLAD) |
Not obstructive; plaque burden is more important
|
| Calcified plaque |
63% of total |
Indicates plaque stability
|
| Remodeling index |
Normal |
Suggests no active inflammation or positive remodeling
|
Clinical Interpretation (Based on PREVENT)
Your plaque is mostly stable
- The lack of soft or LD-NCP plaque means your risk of acute events is relatively low
-
No high-risk features (e.g., positive remodeling, napkin-ring sign)
But total burden still matters
-
PREVENT showed that total volume >250 mm³, even without stenosis, increases risk
- You’re at 660.9 mm³ → moderate risk
- Preventive therapies (statins, PCSK9 inhibitors, ezetimibe, bempedoic acid) are often guided by volume, not obstruction
What You Might Consider Discussing with Your Provider
-
Your scan supports aggressive risk-factor modification, even in absence of obstructive disease
- You’re already on ezetimibe + bempedoic acid — excellent
-
Statin omission may be worth revisiting only if your LDL is very low and you’ve had side effects
- Track changes over time — Cleerly is powerful for volume progression/regression
- Your low-risk features suggest regression is achievable
Regression by Therapy Type (Reference Table)
| Therapy |
Annual TPV Change |
Study Source |
| Statin (mod/high dose) |
−6% to −10% |
SATURN, ASTEROID, REVERSAL |
| Ezetimibe + statin |
−10% to −15% |
IMPROVE-IT (substudies) |
| PCSK9 inhibitor |
−20% to −30% |
GLAGOV |
| Bempedoic acid |
Modest (0% to −7%) |
CLEAR Harmony, CLEAR Wisdom |
| Ezetimibe + bempedoic |
~−7% to −12% |
Based on pooled LDL-C lowering |
Regression Estimate @ LDL-C = 40 mg/dL
| Year |
Regression Rate |
Projected Plaque Volume (mm³) |
| 2025 |
–15% |
561.8 |
| 2026 |
–15% |
477.6 |
| 2027 |
–15% |
405.0 |
| 2028 |
–15% |
344.3 |
Net reduction over 3 years: ~316 mm³
This would move you well into Stage 2 or possibly close to Stage 1, depending on the rate of calcified vs non-calcified regression.
Regression Estimate @ LDL-C = 55 mg/dL
| Year |
Regression Rate |
Projected Plaque Volume (mm³) |
| 2025 |
‒12% |
581.6 |
| 2026 |
‒12% |
511.8 |
| 2027 |
‒12% |
450.4 |
| 2028 |
‒12% |
396.4 |
Net reduction over 3 years: ~264 mm³
Still a solid regression outcome, just slightly slower than LDL = 40.
Important Notes
-
Non-calcified plaques tend to regress faster than calcified ones
- Your 244.5 mm³ non-calcified volume could shrink by ~30–40% in 2–3 years
-
Calcified plaque is less likely to shrink, but it tends to stabilize, which also reduces risk
Bottom Line
At LDL 40–55, you’re doing everything right to:
- Regress plaque volume substantially
- Stabilize any residual risk
-
Possibly exit the high-risk threshold over time
If you’d like, I can build a progression tracker (e.g. spreadsheet or plot) that you can update annually with new Cleerly data. Just say the word.
9 Likes
That’s a very cool report. Thanks for sharing!
Kinda scary to see the LAD plaque so clearly… it reminds you how terrible some peoples arteries (not yours) can look while they’re still walking around symptom free! Yours is classified as mild
I’m not sure about the ChatGPT-generated prediction of plaque regression though. Seems very optimistic. Have you run that by a doctor?
I’m having a CTCA later this month and my doctor also mentioned that there will be AI-assisted analysis. Wonder if I’m going to get the same thing - very cool!
That’s messed up. Honestly, it should be grounds for a correction to the paper, or at the minimum an Editors note, critical commentary or something. Otherwise it’s just incredibly misleading if the headline is that there’s no difference between the groups, but they’re both gaining plaque at a rapid rate.
And what is going on with peer review at JACC? For any of these clinical studies, the initial screening Editor is meant to be checking that they have pre-registered the trial, that they’re actually reporting the outcomes etc.
2 Likes
AnUser
#1771
To be clear, it wasn’t a trial even if the title said it was.
And “Plaque Begets Plaque, ApoB Does Not” implies causation/generalizability like as if it was a randomized trial, and even then they were underpowered (but still were progressing in plaque the same or worse than the other cohorts mentioned in the supplement).
edit:
It’s misleading as well as showing more or worse plaque progression (as expected*), but… whatever.
*when I first heard about this trial long ago IIRC they were going to check as the primary outcome says… the difference in plaque from baseline to +1 year later. Now it’s marketed as a totally different study maybe because the result was terrible (fastest plaque progression ever recorded according to Alo).
4 Likes
Well, hopefully people spam letters to the Editor and a note gets attached to it - or better yet, a retraction and resubmission with a truthful description of the study aims, results, and a less clickbait title.
Unfortunately we do see this with publications where the Editors also have to factor the “business” side of things. An article like this gets a lot of attention, lots of clicks, lots of citations, boosts journal rankings etc.
3 Likes
AnUser
#1775
Fantastic expected to be some of the best news ever.
7 Likes
adssx
#1776
It’s fantastic but it seems a long convoluted way to just say “Take atorvastatin 10 mg and/or ezetimibe 10 mg as early as possible so that your ApoB never ever goes above 70 mg/dL in your lifetime”. Or did I miss something?
7 Likes
AnUser
#1777
I was hoping its impact is going to be like the Surgeon’s report on smoking was. It’s hard to see in the middle of it all but I think it’s accurate that 8.7 million lives or more can be saved every year. So it’s like any other time in history like before antibiotics, or vaccines were invented, and we’re seeing what that’s like when an idea moves from the fringes to become more mainstream.
Only way everyone would be treated would be with a vaccine or yearly shot to lower apoB, but it seems they bring up other risk factors as well and early detection to be important.
5 Likes
No surprise here… a new open access paper:
Obesity accelerates cardiovascular ageing
A global obesity pandemic, coupled with an increasingly ageing population, is exacerbating the burden of cardiovascular disease. Indeed, clinical and experimental evidence underscores a potential connection between obesity and ageing in the pathogenesis of various cardiovascular disorders. This is further supported by the notion that weight reduction not only effectively reduces major cardiovascular events in elderly individuals but is also considered the gold standard for lifespan extension, in obese and non-obese model organisms. This review evaluates the intricate interplay between obesity and ageing from molecular mechanisms to whole organ function within the cardiovascular system. By comparatively analysing their characteristic features, shared molecular and cell biological signatures between obesity and ageing are unveiled, with the intent to shed light on how obesity accelerates cardiovascular ageing. This review also elaborates on how emerging metabolic interventions targeting obesity might protect from cardiovascular diseases largely through antagonizing key molecular mechanisms of the ageing process itself. In sum, this review aims to provide valuable insight into how understanding these interconnected processes could guide the development of novel and effective cardiovascular therapeutics for a growing aged population with a concerning obesity problem.
https://academic.oup.com/eurheartj/advance-article/doi/10.1093/eurheartj/ehaf216/8108159
4 Likes
Hahaha exactly my thought. I was reading it and thinking “where is the amazing breakthrough?” We’ve had this knowledge for literally decades.
But still, the first time I went to a doctor, in my early 30’s, worried about my total cholesterol of over 300 mg/dl, the lady smugly went to the Qrisk calculator, and showed me that my 10 year risk was low…
1 Like
Good news for people who get tired of the pills…
4 Likes
I get serious side effects from the costs of those gene therapies.
3 Likes
Neo
#1782
That’s why above is exciting
If an example of a gene therapy that a huge part of population eventually could be a candidate for vs some rare orphan disease
So this could be a case where they can find models and scale to drive down cost
The other thing is how to weigh something being fixed for a long time, perhaps for one’s entire life via a single treatment vs life-long having to take daily pills or PCSK9i injections year in and year out?
3 Likes
No. That is not the comparison. The comparison is between the overall effects of this gene therapy and the overall effects of f.ex. statin therapy.
If the entirety of the effect of this gene therapy is driven by the lowering of ApoB, then that’s a defined set.
But this is not the argument (and hypothesis) for statin therapy. The argument is that statins achieve their benefits through additional effects beyond their lowering of ApoB. They have, it is argued, beneficial pleiotropic effects, such as lowering of systemic inflammation and the like. The idea is that despite some side effects it still nets out to superior health outcomes beyond just the lowering of ApoB.
So on the one hand you have the set of effects from lowering ApoB (gene therapy), and on the other hand you have the set of effects from statins: lowering ApoB + pleiotropic effects. In this scenario, it could be argued that taking statins is better for overall health than just the effects of the gene therapy. Now, this might be wrong, but that’s what needs to be measured and compared.
FWIW, that’s my mini-gamble. I take statins because I have very high ApoB that’s uncontrollable through lifestyle interventions. But, I also take them, because I’m hoping for some pleiotropic effects (that part is the gamble). There may be some hints of statins having beneficial effects beyond just lowering of ApoB, because apparently they lower mortality even in those with low or normal ApoB levels, and there are mild signals in favor of less all cause mortality (lower ACM based on the UK biobank data wrt. atorvastatin), although simvastatin failed in the ITP. It is also possible that it is dependent on the particular statin - some have fewer side effects such as glucose disregulation and muscoskeletal impairment, so it’s possible that the right statin might have superior overall effects on health than some other statins.
1 Like
Neo
#1784
Of course it it
Don’t try and misconstrue what I said
The context was that @Virilius is concerned about costs
I just made the point cost the cost gene therapies can be one off for life long, “curative” benefit. And not require a life long chronic treatment with life long costs of that treatment as most current non-gene therapy medicines.
I 100% agree that statins might have other benefits than Apo B lowering (and that they are not apples to apples with eg PCSK9i in other ways either - as they for example can increase Lp(a) while PCSK9i can decrease Lp(a)).
1 Like
