08/31/2026
1/ 🚨 NEW PAPER 🚨
At ESC, a new CAC paper came out... and almost immediately, cardiologists on social media were saying:
“Why get a coronary artery calcium scan? It won’t change management.”
Think about what that means... 🧵
2/ A test that directly measures calcified plaque in the coronary arteries is dismissed because “it won’t change management.”
In other words... the treatment decision was already made before measuring whether the patient actually has plaque.
3/ CAC creates uncomfortable situations:
• A 45-year-old with high LDL but CAC = 0
• A 60-year-old with “normal labs” but CAC = 400
Now the conversation is harder. Guidelines are less convenient. And the doctor actually has to explain absolute risk.
4/ Among people considered borderline risk by PREVENT, observed 10-year cardiovascular event rates were:
CAC 0: 1.9%
CAC 1–99: 3.9%
CAC 100–299: 7.4%
CAC ≥300: 14.3%
The same general risk category. Very different risks.
5/ CAC doesn’t always fit neatly into a predetermined pharmaceutical pathway.
But it answers an incredibly important question:
Do you actually have coronary plaque?
That seems pretty relevant to me.
6/ To be clear... statins work.
They reduce cardiovascular events and can stabilize plaque.
In STAREE, 9,971 adults ≥70 were randomized to atorvastatin 40 mg or placebo. After ~6 years, major cardiovascular events fell by about 30% in relative terms.
7/ But in absolute terms, we’re talking about a couple fewer events per 100 people treated...
And there was no significant improvement in disability-free survival, which included death, dementia or persistent physical disability.
Benefit? Yes.
But how much... and for whom?
8/ SAGA/SITE studied 1,160 adults ≥75 already taking statins for primary prevention.
After 3 years:
Death
Stop: 7.2%
Continue: 7.9%
Major CV events
Stop: 5.0%
Continue: 4.4%
Stopping was noninferior for all-cause mortality.
9/ This does NOT mean statins don’t work.
It means the magnitude of benefit matters... and patient selection matters.
Especially when real harms exist. I have personally seen rhabdomyolysis with kidney failure requiring dialysis and severe thrombocytopenia, including near-fatal cases.
10/ This is also why our recent ezetimibe paper matters.
Among 12 statin-free patients with marked LDL elevations on carbohydrate-restricted ketogenic diets, median LDL fell 50.4%...
An absolute median reduction of 137 mg/dL.
Generic. Inexpensive. Different mechanism.
11/ Small study. Retrospective. It does not prove cardiovascular benefit in this population.
But it raises a fair question:
Why are we acting as though every patient with elevated LDL must travel down exactly the same therapeutic pathway?
12/ Measure the disease.
Understand the patient’s absolute risk.
Understand why LDL is elevated.
Discuss the magnitude of benefit.
Discuss potential harms.
Then choose the intervention that makes sense for that patient.
That seems like medicine to me.
Full article and papers:
https://toward.health/why-cac-matters-statin-conversation/
