Below is an approximation of this video’s audio content. To see any graphs, charts, graphics, images, and quotes to which Dr. Greger may be referring, watch the above video.
Angioplasty, which is when a tiny balloon is inserted into a narrowed coronary artery feeding your heart to force it to open wider to improve blood flow, wasn’t put to the test in a randomized controlled trial until 1992. And it failed to prevent heart attacks, and it failed to show any survival benefit. But they only followed them out six months, and included people with relatively minor disease who maybe were just not sick enough to benefit. Enter the MASS trial, enrolling those with severe blockage high up in their widow-maker artery (or widower-maker, since coronary artery disease is also the #1 killer of women), and followed them out for years. And there was no difference in subsequent mortality or heart attacks. Okay, but there were only about 200 patients. Maybe the benefit was so subtle that you just needed a greater number of patients to tease out the effect. Enter the RITA-2 study, randomizing more than a thousand patients, and they did indeed get a clear difference in the risk of future death and heart attack––but it was in the wrong direction. The angioplasty group suffered twice the risk, compared to those randomized to forego surgery.
Okay, but that was all before stents came into vogue. Instead of just ballooning up the artery, how about permanently inserting a stent––a metal mesh tube to prop the artery open. Surely, that’s got to help, which brings us to MASS-II and … still no benefit. Okay, but that was after just one year, but still no benefit after five years, or even ten years later. The courage Trial was the biggie, randomizing thousands of patients, and it fell flat on its face.
Yes, but those were mostly bare metal stents, not the fancy new drug-eluting stents that slowly release drugs. And what about high-risk groups: those with diabetes, those with more serious disease, those with 100 percent blocked arteries days after a heart attack? And meta-analysis after meta-analysis—five trials with 5,000 patients—and no reduction in death, heart attack, or even angina pain. Ten trials with more than 6,000 patients, and no benefit for survival, heart attacks, or pain relief. Now, we’re up to more than a dozen major trials, and nothing: no benefit from angioplasty and stents. “Furthermore, multiple analyses have failed to identify a single high-risk subset with stable disease that benefits …” How is that possible? You’re physically opening up blood flow.
The reason it doesn’t work is because the majority of heart attacks in real life are caused by narrowings under 70 percent. So, the plaques in your arteries that kill you tend not to be the ones that are restricting blood flow. Here are two atherosclerotic plaques. This one is squeezing off the blood flow so much you can see it on angiogram, and go after it with a stent. Problem solved, life saved, right? No, because it was the invisible one that wasn’t even impeding blood flow that was going to kill you all along. Most heart attacks are caused by nonobstructive plaques that don’t even cut blood flow 50 percent.
There’s this clogged pipe misconception that has been difficult to dislodge, imagining where cholesterol plaques slowly, inexorably encroach on blood flow, eventually cutting it off completely, triggering a heart attack. In reality, coronary artery disease is an inflammatory disease in which the cholesterol from the blood being deposited in the artery walls causes an inflammatory reaction, like a pimple. When those pimples pop, they cause the blood in the arteries to clot at the site. Before rupture, these plaques often do not limit flow, and may be invisible to angiography and stress tests. They are, therefore, not amenable to angioplasty and stents.
Old plaques are like old scarred pimples. The tightest blockages are made up of mostly just calcified and dense fibrous scar tissue. They can still rupture and kill you, but there are so many more of the smaller lesions brewing, which are hidden from view. The way we visualize coronary arteries is with an angiogram, where X-rays are taken where we inject this black-looking dye into the arteries; so, we can only see plaques that encroach on the blood flow. That’s why you get these kinds of tip-of-the-iceberg illustrations, the point of which is to emphasize that most of the atherosclerotic plaque in the coronary arteries is not seen well by angiography. To really understand what’s going on in people’s arteries, we must turn to autopsy. William Clifford Roberts is probably the most preeminent cardiovascular pathologist in the world. What did he learn after studying coronary arteries for 50 years? After digging around in nearly 2,000 bodies, he learned that atherosclerosis is a systemic disease.
“In patients with fatal coronary artery disease, . . . the quantity of plaque is enormous. There is not just 1 plaque here, another plaque there, with normal [clean arteries] in between plaques. Plaques are continuous! Not a single 5-mm segment in the entire coronary artery tree is devoid of plaque …” So, isolated coronary disease is a myth. There are no such things as “1-vessel disease,” “2-vessel disease,” or “left main disease. Plaque is in all of [them] if it’s in one of them.”
Adding up the lengths of the four main coronary arteries that feed the heart (the right coronary artery, the left main, the circumflex, and the left anterior descending), they add up to about 11 inches of coronary arteries, which for examination can be cut into about 50 quarter-inch slices. And this is what you see. Not plaque gunking up one or two slivers, but all throughout the coronary arteries. If you look at over a thousand of these slices from dozens of patients who died of heart attacks, not a single segment was devoid of plaque. So, no wonder why just stenting open one area has no impact on heart attacks or death.
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