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This press release is wildly overselling this research. It's not anywhere near as simple as calcium deposits causing vascular disease. CAC (coronary artery calcification, where this has been most examined) is essentially an inevitable byproduct of the process of atherosclerosis; calcification anywhere is a halmark of necrotized cells. Since atherosclerosis results from necrotic cells (primarily macrophages) which have invaded the vasculature, the extent of coronary artery calcification is a good marker of the extent of atherosclerosis that has occurred and is thus a good predictor of future coronary events.

However, that does not imply that removing coronary calcium will reduce coronary events. In fact, statin therapy by itself actually increases coronary artery calcification.

It turns out that calcified and fibrotic atherosclerotic plaques are not the plaques that rupture and cause thrombosis and myocardial infarction; in fact, the responsible plaques tend to be large, lipid-rich plaques with a thin cap (called thin cap fibroatheromas). Calcium can actually be protective in helping to form robust caps over plaques. There is a lot of work on characterizing cap-Calcium microstructure. Theoretically, removing calcium somehow using drug agents could have an adverse effect.




You seem to be knowledgeable in this matter. I have a question for you. Several years ago, I heard about a theory that these burst-prone "large, lipid-rich plaques" are essentially "band-aids" created for deficiencies in arterial walls. Does that description align with some of the literature you have read on the subject?


Not the op, but I encountered this theory through Dr. Malcolm Kendrick’s blog [1]. I’m only have a basic medical education (studied clinical psychology at a medical university), but I find the theory plausible. Kendrick’s criticism of the currently dominant cholesterol/statin paradigm is definitely worth looking into

1. https://drmalcolmkendrick.org/2016/01/21/what-causes-heart-d...


I have not heard of this particular phrase. It doesn't quite make sense to me off the top of my head; band aid implies they are beneficial, but lipid-rich plaques are not providing structural integrity or protecting against defects. They are harmful sonce they predispose to MI.

It is likely true that they tend to form where there are surface defects; this idea is decades old and a component of Virchow's triad.


>>" Since atherosclerosis results from necrotic cells (primarily macrophages) which have invaded the vasculature"

I would be interested in reading more about this. Do you have any recommendation for a layman?



I'd just look up atherosclerosis on Google to be honest. To state the basic steps in a straightforward fashion: damage of the surface endothelium, entry and oxidation of cholesterol particles and possibly other circulating junk, entrance of macrophages due to immune signaling, necrosis of extravasated macrophages, structural weakness, breaking of the endothelium, thrombosis, infarction, death of whatever was getting the blood flow distally.

There a lot of knobs at each step but that's basically it.




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