Which impact has Bempedoic Acid on atherosclrosis plaque stability ?
Mechanism of action
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2 Answers
Haitham Jowah
This is a great question, and I'm really excited about it. One way to think about how bempedoic acid affects plaque is as a strong one-two punch.
First of all, it does the obvious job very well. It was smartly made so that it only works in the liver, where it strongly lowers LDL cholesterol, which is the "bad" cholesterol. For decades, we've known that lowering LDL levels aggressively is important. It takes away the fuel that the plaque needs to grow, which makes it smaller and more stable over time. That's the main benefit.
But here's the most interesting part: it also seems to put out the fire.
The big clinical trials show that it lowers inflammation markers like hs-CRP a lot, and this isn't just because it lowers cholesterol. The idea is that by hitting its target enzyme (ACL), it also cuts off the resources that inflammatory cells in the plaque need to stay "angry" and do damage. It helps calm everything down, which makes it less likely that the plaque will break.
So, even though we are still waiting for direct human imaging to show us this happening in real time, the evidence is strong. The lower number of heart attacks isn't just because of better numbers; it looks like the drug is changing the plaque itself.
In short, it takes away the fuel (LDL) and puts out the fire that causes inflammation. That's a strong mix for keeping plaque stable and what makes it such an intriguing drug.
First of all, it does the obvious job very well. It was smartly made so that it only works in the liver, where it strongly lowers LDL cholesterol, which is the "bad" cholesterol. For decades, we've known that lowering LDL levels aggressively is important. It takes away the fuel that the plaque needs to grow, which makes it smaller and more stable over time. That's the main benefit.
But here's the most interesting part: it also seems to put out the fire.
The big clinical trials show that it lowers inflammation markers like hs-CRP a lot, and this isn't just because it lowers cholesterol. The idea is that by hitting its target enzyme (ACL), it also cuts off the resources that inflammatory cells in the plaque need to stay "angry" and do damage. It helps calm everything down, which makes it less likely that the plaque will break.
So, even though we are still waiting for direct human imaging to show us this happening in real time, the evidence is strong. The lower number of heart attacks isn't just because of better numbers; it looks like the drug is changing the plaque itself.
In short, it takes away the fuel (LDL) and puts out the fire that causes inflammation. That's a strong mix for keeping plaque stable and what makes it such an intriguing drug.
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Muhammed YUSUF
Preclinical data summarized in recent reviews demonstrate that liver-specific ACLY inhibition attenuates atherosclerotic lesion development and reduces macrophage-driven inflammation, mechanisms consistent with improved plaque stability. Clinically, sustained reductions in hsCRP (~20–30%) further support an anti-inflammatory, plaque-protective profile.
However, direct human imaging evidence confirming changes in plaque composition or fibrous cap thickness (IVUS/OCT/CCTA) remains limited. Thus, current evidence supports biological plausibility and indirect stabilization, with definitive confirmation awaiting dedicated plaque-imaging studies.