A topic that is near and dear to my heart.
Pun intended.
I realize that other arteries (notably the carotid and femoral) can also get plaque, but the coronary arteries seem to be particularly susceptible. Is this true (or is it just that it’s not as much of a big deal in other arteries), and if so, why? It doesn’t seem like a very good design to me…
The heart muscle pumps 60-100 times per minute (and occassionally more) for your entire lifetime. It requires significant food and oxygent on a constant basis.
In contrast, your skeletal muscles don’t work nearly as continually, and often not nearly as hard. Their metabolics requirements are less.
Severe obstruction of leg arteries can lead to intermittent claudication, where the impaired circulation may be sufficient for the limb(s) at rest but not for sustained effort.
Unlike your leg muscles, though, you can’t just stop your heart for a rest!
Really severe arterial obstruction can lead to death of the tissue “downstream”, or limb loss but usually it’s the messed up heart circulation that kills you first.
I have done a lot of autopsies, and I can say that all arteries, minus the pulmonary, are susceptible to significant ( as in, can cause problems) plaques. The arteries of the heart may be on balance somewhat more susceptible because they come off the aorta right where it connects to the heart and thus where blood pressure is highest, although the aorta and coronaries have intrinsic ways of modulating that to an extent. As you say also, the problems caused by narrowed/blocked coronaries can be very noticeable. Keeps me in business anyway. The one that has always puzzled me is the splenic artery. In just about everyone who is older than younger, the splenic artery turns to concrete.
I’m not trained in this field, but I am interested, mainly because of my wife’s coronary condition. It seems that the problem is related to the fact that the heart is both the source of power for the circulatory system, and one of its beneficiaries. The blood brings oxygen, necessary for life, to all the tissues; and is powered by an organ whose muscle is among those tissues.
The blood vessel entering the heart is necessarily large, because it carries blood from the entire body. Branching off from this vessel are the (much) smaller vessels that feed the heart muscle. This branching occurs throughout the body, but the change in diameter, and mass flow, is most dramatic in the heart muscle. The large drop in vessel diameter (and probably direction) of blood flowing to the heart muscle causes a pressure drop, as it would in any piping or duct system. The pressure drop allows sediments to accumulate , due to turbulence, eddy currents, etc. As said, I am not trained in the field; but the explanation makes sense to me. There are also biochemical aspects to the problem, since plaque deposits are not very similar to, for example, the soil deposits that are seen when small streams branch off from large ones. But the pressure drop caused by the large drop in vessel diameter was shown to me, by a cardiologist, and was convincing as an explanation.
In other words, both hydraulics and biochemistry are involved. I think the hydraulics part is what we civilians have to accept, if we need an explanation. It is also the approach used by heart surgeons, I think.
Something to keep in mind is that the LDL that makes up most plaque, IIRC has to somehow infiltrate the endothelium of the blood vessel which is smooth tissue. It doesn’t just drop out of circulation like sediment in a stream.
There has to be a mechanism for that and IIRC at least one mechanism is macrophage cells stuffed with oxidized lipids. Oddly, this never seems to be discussed so I don’t know if there is no solid understanding of what the mechanism of infiltration is or if it is something that just never gets mentioned.
The previous two answers can be combined in that the turbulence from the flow dynamics can cause small injuries to the coronary artery endothelium, which then causes a small amount of inflammation and brings in the macrophages. While there, the macrophages engulf the oxidized LDL, which they would do anywhere as part of their basic cleaner function.
However, there has to be more to it than that. For starters, despite that everyone has the same coronary artery flow situation, not everyone gets significant (or sometimes even any) plaque buildup. Add to that that people who would seem to have one or more of the standard risk factors in more or less equal proportion can also be very differentially effected. Also, another autopsy observation is that plaque buildup can be and often is very patchy between arterial beds, within individuals. Say, one person may have highly clogged coronary arteries but clean cerebrals; the next person vice versa; the next person bad plaques in the legs but OK everywhere else.
I think the flow turbulence makes sense.
I had an emergency double-bypass at age 50. My LAD was 95% blocked at a “Y” junction. There was no other significant plaque in any of my other arteries, and I had no particular risk factors. The doctor mentioned that it might have been caused by a deformity in the artery itself.
Everyone has the same coronary artery flow, but values of LDL, VLDL, and HDL - cholesterols vary depending, in large part, on diets. HDL acts as a scavenger, picking up the LDL deposits before they becime oxidized. The trans fats both increase LDL and decrease HDL. (Trans fats are saturated fats; if 100% hydrogenated, they are no longer trans.) Cis fats can be saturated or unsaturated. Unsaturated can be mono- and poly- unsaturated. Each has different effects on the liver’s synthesis of the different factions of cholesterol and total cholesterol.
Granted. But you missed the point. The point was that people who seem to posses a similar set and degree of the standard risk factors, such as the levels of HDL, LDL, etc, are nonetheless differently affected by atherosclerosis. An additional point was that various arterial systems within the same person - and so also presumably exposed to the same set of standard risk factors - are also differently affected. This suggests to me - and it is by no means an original thought of mine - that there is more going on in the development of atherosclerosis than just the standard risk factors.
Actually, trans fats are unsaturated and saturated fats are what you get with full hydrogenation; only unsaturated fats can have a trans or cis configuration because saturated fats don’t have any double bonds (where a hydrogen atom is missing):
(it is also possible to have a fat that is both trans and cis, like CLA)
As far as coronary arteries go, one possibility is that they are constantly being squeezed by the heart, such that blood actually only flows when the heart is resting between beats; all of this squeezing could cause minor damage to the vessels, making them more likely to get plaque deposits.
I can add a little bit of “the more to it” although I am far from an expert on these matters …
Stenosis, and in particular an acute cardiac events, are not exclusively the result of plaque size but more so of plaque rupture. There are more vulnerable plaques that rupture more easily than others, with thin fibrous caps and softer cores. Mechanical forces (such as the shear forces of the beating heart) appear to play a major role in promoting both vulnerable plaque formation and rupture:
That article also goes on to discuss how mechanical stress may contribute to the fibrous cap being built of weaker material.
Thus plaques may form all over but some locations may be more prone to form vulnerable plaques that are prone to rupture causing a consequent clotting (thrombotic) event that blocks flow. It does not help it those same locations are critical spots with limited alternate routes of blood supply. The nature of the beating heart (mechanical stresses and high pressure differentials) may promote the formation of those vulnerable plaques.
The good news is that the same plaques that are the most vulnerable are the ones most susceptible to regression.
Like eightysix: said, plaques can form anywhere. During a company physical, a doctor said she wanted to listen to my femoral valves. I asked why, and she said she would listen for drag on the valves, to see if I’m building up plaques, as a test for other plaques elsewhere, presumably my heart, where the plaques were critical. I said, “Great, and thanks.” I’d forgotten the femoral artery is located at my inner thigh, and I jumped a bit when she went for that area with a stethoscope. Didn’t help she looked just like Britney Spears.