Plaques are continually being removed from arteries by natural mechanisms within the body. Statin use, when combined with aggressive dietary changes, can slow down the rate of plaque deposition to the point that the rate of plaque removal is actually higher than the rate of plaque deposition, and, as a consequence, plaque thinning can be observed.
Reducing plaques faster (plaque liquefication) has some potential, life threatening drawbacks.
- We've all seen how ice cubes, when frozen together into a clump and then placed in a water bath, dissolve. Some ice cubes break off from the main structure and float away to dissolve separately. The same thing can happen with a large plaque deposit. If a piece of the plaque breaks off during the liquefication process and continues to travel through the blood stream it can lead to downstream blockages, particularly in the brain (stroke). Rapid dissolution of plaques would increase the risk for such adverse events.
- While plaques form more or less everywhere as relatively uniform deposits, the real concern is areas where plaques have grown to large size and begin to block arteries. It has been found that these larger deposits are initiated by events related to damage of the arterial wall at that specific location. The damage leads to infection (that's why highly sensitive C-reactive protein [hs-crp] measurements are routinely made in conjunction with cholesterol measurements). The body mobilizes the immune system to fight the infection; microphages and white blood cells are directed to these infection sites. Once this happens deposition of other materials (lipids, calcium, etc.) start at the infection site and abnormal plaque growth results. Because of the 1) initial damage, 2) the infection and 3) infection fighting, the arterial wall becomes abnormally thinned at the site. To some degree, the plaque actually serves to stabilize the thin wall preventing wall rupture and leaks. Rapid removal of the plaque would increase the chances for the wall to rupture, producing adverse events and increasing mortality.
So while it is likely that drugs could be designed to remove the plaque extremely fast (e.g. liquefication), the risks might far outweigh the benefits.
would the liquefied plaque be eliminated as regular fluid is through
the kidneys?
A major component of plaque is lipoprotein. Lipoprotein is transported by blood as insoluble particles of varying density and size. Lipoprotein itself is an assembled complex of proteins and fats. The fats are various esters of glycerol including esterified cholesterol. The lipoprotein transports cholesterol and fats, via the bloodstream to cells where these compounds are needed for biosynthesis. After the lipoprotein has released the transported molecules it returns to the liver where it is "reloaded" and sent out again. Lipoproteins are not eliminated (unless damaged) from the body, but are rather recycled.
If a large amount of lipoprotein were suddenly released into the body, I'm sure some would be eliminated through the kidneys. Certainly the lipoprotein receptors would sense this event and stop synthesis of new lipoprotein until systemic balance was restored. it seems likely that adverse events like kidney damage, gallstones, bile duct clogging, etc. would occur.
Since statins were first released onto the market, drug companies have been considering where to go next. I have to believe that plaque liquefication was among the options considered. While the reduction of plaque build up (statins) have their share of problems, I would guess that these problems are minor compared to the possible problems that can result from liquefication (discussed above). Indeed, with the recent announcements (see here for example) of monoclonal antibodies achieving plaque reductions superior to statins, it seems that drug companies are continuing to focus on avoiding the problem in the first place, rather than fixing things (liquefication) down the road.
