Another article that’s drifted across my radar screen…..apparently behind a paywall. I’m seeing a lot more information on use of technology to detect the “soft”, vulnerable plaque before it even shows on CAC or even sometimes Coronary CT angiography.
It’s really interesting though as, just like with the articles I reproduced a few days ago on the early intervention thinking, there are a couple of cholesterol denialists on that particular forum. Blokes who don’t quite grasp the concept of not waiting until signs and symptoms present themselves…..and use their own examples of high LDL-C and low HDL and they’re perfectly healthy as shown by their low/zero CAC score. Even though pretty much every link that shows up there points out that waiting until the soft plaque has become calcified….and thetefore measurable by that technology……has missed the window of opportunity for true primary prevention.
Not one of them appears to be older than 50 tops . You have to wonder about kids today.
So, because I always wonder about stuff that happens to drift across my radar screen……as in a “How long has this been happening without my being aware….???”….I’ve done a little hunt on Google and so far…..
Relevant for me because I’m in the fortunate situation of being a mother and a grandmother with the health and well-being of those future generations on my mind.
Yes, rosuvastatin significantly reduces the odds of developing and progressing soft, vulnerable plaque by lowering cholesterol, reducing plaque inflammation, and promoting plaque stabilization and regression, even decreasing lipid content and necrotic cores, making it a powerful tool for preventing heart attacks and strokes, according to studies like ASTEROID and others.
How Rosuvastatin Works on Soft Plaque:
Lipid-Rich Core: Soft plaques are rich in lipids (fats) and often have a large, unstable “necrotic core,” making them prone to rupture, says the Cleveland Clinic.
Cholesterol Reduction: Rosuvastatin (a potent statin) lowers LDL (“bad”) cholesterol, directly reducing the building blocks of plaque.
Plaque Regression: High doses can shrink plaque volume and reduce the size of the lipid core, a process called regression, according to the NIH.
Key Findings from Research:
Decreases Lipid Content: Magnetic resonance imaging (MRI) showed rosuvastatin rapidly decreased lipid content in carotid plaques.
Reduces Vulnerable Plaques: Studies found significant decreases in “thin-cap fibroatheroma” (TCFA), a type of highly vulnerable plaque.
High-Dose Efficacy: High-dose rosuvastatin (like 40mg) is particularly effective at shrinking plaque volume and improving stability, say the JACC Journals and the National Institutes of Health.
In summary, rosuvastatin helps prevent new soft plaque formation and stabilizes existing ones, reducing cardiovascular risk.
I remember reading an article many years ago about autopsies done on 18-20 year old Vietnam solders and a fair number had early coronary artery disease.
Yes….early 1970s one of our pathology lecturers emphasized his point by showing slides of autopsies he’d done on kids in their late teens/early 20s who’d died of non cardiac cause with coronary arteries showing those early fatty streaks that ultimately develop into atheromatous plaques.
Mind you, that’s not quite the early diagnosis implied in the recent articles I’ve posted
Thinking about it, he quite possibly would’ve found those early signs if it’d been me on the slab. A sobering thought to think of needing such an early start.
This is probably worth it’s own thread but it sort of falls under the same heading, i.e. the concept of earlier, more aggressive intervention than has been the norm (at least, outside of endocrinology circles)…..
I remember back in the days when we had the old Diabetic Fools board, the occasional metabolic dysfunction denialist would opine that they were “only” pre-diabetic, and I recall the regulars (Fuskie and one or two others) pointing out that it was an artificial designation and still represented a departure from good health.
It’s a long read but the take home message seems to be that pharmacologic intervention (in addition to the usual recommendation for “lifestyle changes”) at an earlier stage rather than waiting for the official designation of T2D has measurable long term benefits in downstream disease prevention.