1: “Scientists have been exploring the medical mysteries of the human heart for almost as long as poets have been probing its metaphorical depths,” Dr. Peter Attia writes in his brilliant book Outlive.
“It is a wondrous organ, a tireless muscle that pumps blood around the body every moment of our lives. . .
“And when it stops, we stop.”
Heart disease remains our deadliest killer.
We can think of it “like the scene of a crime,” Peter writes, “breaking and entering, more or less.
“Let’s say we have a street, which represents the blood vessel, and the street is lined with houses, representing the arterial wall.”
There is a fence in front of each house that is like “a delicate but critical layer of tissue that lines all our arteries and veins,” Peter notes.
This single layer of cells is a “pretty important little structure,” Peter writes. It is called the endothelium, and in addition to providing the barrier between the blood vessels (the street where the blood flows) and the wall of the artery, it also controls “the passage of materials and nutrients and white blood cells into and out of the bloodstream,” Peter writes.
In addition, it dilates and contracts to increase or decrease blood flow and regulates blood-clotting mechanisms.
“The street is very busy, with a constant flow of blood cells and lipoproteins and plasma and everything else that our circulation carries,” he writes.
2: Peter points out that the two most significant risk factors for heart disease, smoking, and high blood pressure, damage the “fence” in our analogy, which provides the barrier between the blood vessels and the artery wall.
In addition, sometimes particles will penetrate the cell barrier. In our analogy, we can think of them entering the front porch.
“Normally, this is fine,” Peter observes, “like guests stopping by for a visit. They enter, and then they leave.”
LDL particles (the “bad” cholesterol) and other particles with apoB protein, however, sometimes get stuck inside.
“The trouble starts when LDL particles stick in the arterial wall and subsequently become oxidized. . . rendering it somewhat toxic,” Peter notes. At this point, “the LDL/apoB particle stops behaving like a polite guest, refusing to leave—and inviting its friends, other LDLs, to join the party. Many of these also are retained and oxidized. . .
“I’ve been saying LDL, but the key factor here is actually exposure to apoB-tagged particles, over time,” Peter suggests. “The more of these particles that we have in our circulation, not only LDL but VLDL and some others, the greater the risk that some of them will . . . get stuck.”
Which is why we must know how many of these apoB particles are circulating in our bloodstreams. “That number is much more relevant then the total quantity of cholesterol that these particles are carrying,” he writes.
“In response to this incursion, the endothelium dials up the biochemical equivalent of 911,” Peter notes. Specialized immune cells confront and “swallow up” the intruders to remove them from the artery wall.
If they consume too much, however, these cells blow up into “a foam cell,” Peter writes, “so named because under a microscope it looks foamy or soapy. When enough foam cells gather together, they form a ‘fatty streak’—literally a streak of fat that you can see with your naked eye during an autopsy of a splayed-open coronary artery.”
These “fatty streaks” become the core of plaque.
“And this is the point where breaking and entering tilts over into full-scale looting,” Peter writes, “In an attempt to control the damage, the . . . cells in the artery wall then migrate to this toxic waste site and secrete a kind of matrix in an attempt to build a kind of barrier around it, like a scar.”
There is more bad news: “None of what’s gone on so far,” Peter notes, “is easily detectable in the various tests we typically use to assess cardiovascular risk in patients.”
As the process continues to unfold, the plaque may begin to become calcified. “This is what (finally) shows up on a regular calcium scan. Calcification is merely another way in which the body is trying to repair the damage by stabilizing the plaque to protect the all-important arteries.
“But it’s like pouring concrete on the Chernobyl reactor: you’re glad it’s there, but you know there’s been an awful lot of damage in the area to warrant such an intervention.”
When we receive a positive calcium score, it means there are plaques present that may be stabilized (calcified). Or not.
“If the plaque does become unstable, eroding or even rupturing, we’ve really got problems,” Peter writes. “The damaged plaque may ultimately cause the formation of a clot, which can narrow and ultimately block the lumen of the blood vessel—or worse, break free and cause a heart attack or stroke.”
3: Despite all these dangers, there is some good news.
“We are fortunate that many of these conditions can be modulated or nearly eliminated—including apoB—via lifestyle changes and medications,” Peter writes.
“I have all my patients tested for apoB regularly . . . I take a very hard line of lowering apoB, the particle that causes all this trouble. (In short: get it as low as possible, as early as possible.)”
His recommendation: Ask for the apoB test the next time we see our doctors. “Don’t be waved off by nonsensical arguments about ‘cost’: It’s about twenty to thirty dollars.”
More tomorrow.
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Reflection: How aware am I of the risks of heart disease?
Action: Talk to my Primary Care Physician about Peter’s work.
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