The Amazing Human Heart

“Do-it-yourself cardiac bypass surgery: All you need is walking shoes.” —Harvard Medical School

Doctors have believed forever that the human heart is so fragile and helpless that it can’t heal itself. The heart can only be improved after a heart attack, they believe, by putting the hapless patient through a car crash—excuse me, coronary artery bypass surgery. They are wrong.

Medical science is wrong for a whole bunch of reasons, one of which I discussed last week—angiogenesis. Angiogenesis is the formation of new blood vessels, provoked by protracted and at least periodically vigorous exercise. Another reason the docs are wrong is arteriogenesis, the improvement of existing blood vessels.

When coronary arteries begin to occlude—that is, close up—other arteries can expand to help increase blood supply to the heart. A heart attack (assuming the patient survives) has a similar effect. This process of expansion is called arteriogenesis.

Arteriogenesis begins with mechanical stress on the walls of the blood vessel. In other words, as one artery occludes, more blood attempts to pass through other arteries. This stresses the blood vessels, which in turn stimulates the production of a protein called monocyte chemoattractant protein 1, or MCP-1.

There follows a cascade of events that culminate in the increased diameter of the vessels until the pressure on the vessel walls is normalized. And as we will all recall, Poiseuille’s Law of Flow posits that as the diameter of a tube (a blood vessel, for example) increases, the total flow capacity of the tube increases by a power of four. Thus, even small increases in vessel diameter result in very large increases in blood supply.

Interestingly, arteriogenesis happens only when the vessel is stressed in a repetitive manner. This typically happens during transient coronary artery occlusion, when an artery becomes nearly blocked, then unblocks itself, then becomes partially blocked again and so on over and over. Constant stress on the vessel wall, on the other hand, doesn’t stimulate arteriogenesis. (Think high blood pressure.)

But we don’t have to wait for blocked arteries or a heart attack to launch the process of arteriogenesis and improve the capacity of our blood vessels. We can stress the vessels just as well, or even better, by undertaking an exercise program that repetitively and intermittently pressures the vessels.

The most effective form of exercise (for producing arteriogenesis) appears to be interval training. Competitive athletes typically have advanced arteriogenesis, but ordinary people can accomplish much the same thing through an exercise regime that mimics sprint training.

For example, we could design a moderate exercise regime in which we walk (on a track, sidewalk, or treadmill) on level terrain for a few minutes, then climb steeply for a few minutes, then walk downhill for a few minutes, flat for a few minutes, and so on.

The important aspects of this regime are that a) the heart needs to be stressed intermittently, b) the degree of difficulty of the exercise needs to reach aerobic levels, and c) the exercise should be continued for about thirty minutes and be repeated several times per week.

Competitive sprinters will, of course, work much harder than this, but that’s because they are trying to win races. To stimulate the production of MCP-1 and launch the process of arteriogenesis, we only need to stress the blood vessels intermittently and regularly at a minimum aerobic level.  Anything beyond that will be useful for winning races, but not for initiating arteriogenesis.

Angiogenesis and arteriogenesis are remarkable phenomena, and they give the lie to the long-held medical opinion that the heart cannot heal itself. But there’s more. A closely allied phenomenon is blood vessel collateralization.

All mammals have very small collateral vessels in their hearts, running between and connecting the coronary arteries. Under normal conditions these collaterals are “closed,” that is, no blood is running through them, and they are almost invisible. But under certain conditions the collaterals “open” and blood begins to flow through them to the main arteries.

What are these conditions? They are the same conditions that launch angiogenesis and arteriogenesis—stress on the heart resulting from coronary occlusion, heart attack, or exercise. When a coronary artery becomes occluded, collateral vessels spring into action, bypassing the blocked portion of the artery.

As noted in the quote that heads this post, collateralization is essentially identical to what a heart surgeon does in a CABG procedure—bypassing clogged points in the arteries so that blood flow can resume. Except that your chest isn’t being sawed open, your heart ripped out of your chest cavity, etc., etc.

So effective is vessel collateralization that researchers at UCL, Yale and other institutions found that heart patients with significant vessel collateralization had a 36 percent reduced chance of dying from a heart attack. To put that in perspective, it is nine times as effective as the best statin.

Combining the therapeutic effects of angiogenesis, arteriogenesis, and collateralization, we find that the human heart is actually extraordinarily robust. As far as I know, no one has studied the combined effect of these three phenomena on heart patients. But I wouldn’t be surprised to find that individuals who have managed to engage all three of these natural therapies would have at least twice the chance of surviving a heart attack.

But even that is not the end of the heart’s ability to heal itself, as we’ll see next week.

Next up: Opening the Medical Mind, Part IV