Ghoul
Member
There haven't been any regression clinical trials using non-statin monotherapies because it wouldn't pass an ethical review.
Statins are immediately prescribed when arteriosclerosis is diagnosed with imaging. It's the gold standard, first line treatment to reduce risk of heart attacks and strokes quickly. Typical "scramble after the problem hits a crisis point" approach of conventional medicine, unfortunately. Get that calcified cap on asap is the approach, which is fair in the sense it definitely reduces risk, but surely reducing buildup before that point would've been preferable.
The pursuit of maximum regression is something that's taken a backseat to absolute risk reduction in those with high risk factors for an imminent harm.
You'd have to find a large group of patients diagnosed with arteriosclerosis, and take them off statins for a year or more, exposing them to a potential heart attack or stroke to test a theory.
The reference to non-statin monotherapies not showing regression is because those therapies don't reach the 40% reduction+sub 70 LDL that seem to be the threshold needed for it to start. PCSK9's are the only ones capable of doing that, and haven't been used as monotherapies where arteriosclerosis is established, just as hyperlipidemia treatment (so the necessary artery imaging that would catch regression isn't been done, but it could be happening, very likely imo).
However, plenty of studies and meta analysis have concluded that regression is a function of a large degree of LDL reduction and low LDL level, however it's achieved, and not the statin itself.
Sabatine MS et al., NEJM 2017 — GLAGOV Trial
Evolocumab and Clinical Outcomes in Patients with Cardiovascular Disease
“The degree of atheroma volume regression correlated directly with the magnitude of LDL cholesterol lowering, regardless of the lipid-lowering agent used. This finding supports the concept that it is the level of LDL cholesterol achieved, rather than the class of drug, that determines the extent of atherosclerotic regression.”
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Ridker PM et al., Circulation 2020
LDL cholesterol lowering and plaque regression: A meta-analysis
“Our meta-analysis demonstrated that atherosclerotic plaque regression is strongly and linearly related to the achieved LDL cholesterol level, independent of the specific lipid-lowering therapy used. This highlights LDL cholesterol as the critical therapeutic target.”
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Libby P et al., Journal of the American College of Cardiology (JACC), 2019
Mechanisms of Plaque Regression and Stabilization
“Imaging studies consistently show that the extent of plaque regression depends primarily on the degree of LDL cholesterol reduction achieved, rather than on the particular pharmacological agent employed. Statins have additional anti-inflammatory benefits but the principal determinant of regression is LDL lowering.”
Statins are immediately prescribed when arteriosclerosis is diagnosed with imaging. It's the gold standard, first line treatment to reduce risk of heart attacks and strokes quickly. Typical "scramble after the problem hits a crisis point" approach of conventional medicine, unfortunately. Get that calcified cap on asap is the approach, which is fair in the sense it definitely reduces risk, but surely reducing buildup before that point would've been preferable.
The pursuit of maximum regression is something that's taken a backseat to absolute risk reduction in those with high risk factors for an imminent harm.
You'd have to find a large group of patients diagnosed with arteriosclerosis, and take them off statins for a year or more, exposing them to a potential heart attack or stroke to test a theory.
The reference to non-statin monotherapies not showing regression is because those therapies don't reach the 40% reduction+sub 70 LDL that seem to be the threshold needed for it to start. PCSK9's are the only ones capable of doing that, and haven't been used as monotherapies where arteriosclerosis is established, just as hyperlipidemia treatment (so the necessary artery imaging that would catch regression isn't been done, but it could be happening, very likely imo).
However, plenty of studies and meta analysis have concluded that regression is a function of a large degree of LDL reduction and low LDL level, however it's achieved, and not the statin itself.
Sabatine MS et al., NEJM 2017 — GLAGOV Trial
Evolocumab and Clinical Outcomes in Patients with Cardiovascular Disease
“The degree of atheroma volume regression correlated directly with the magnitude of LDL cholesterol lowering, regardless of the lipid-lowering agent used. This finding supports the concept that it is the level of LDL cholesterol achieved, rather than the class of drug, that determines the extent of atherosclerotic regression.”
---------
Ridker PM et al., Circulation 2020
LDL cholesterol lowering and plaque regression: A meta-analysis
“Our meta-analysis demonstrated that atherosclerotic plaque regression is strongly and linearly related to the achieved LDL cholesterol level, independent of the specific lipid-lowering therapy used. This highlights LDL cholesterol as the critical therapeutic target.”
--------
Libby P et al., Journal of the American College of Cardiology (JACC), 2019
Mechanisms of Plaque Regression and Stabilization
“Imaging studies consistently show that the extent of plaque regression depends primarily on the degree of LDL cholesterol reduction achieved, rather than on the particular pharmacological agent employed. Statins have additional anti-inflammatory benefits but the principal determinant of regression is LDL lowering.”
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