Do Stents Work? Part 1

Did you ever wonder if the food you eat has a direct effect on your health, well-being – and longevity?  Well, I’m here to end that mystery.  You ARE the foods you eat.  Welcome to the Nutrition Facts podcast – I’m your host, Dr. Michael Greger.

Today, we look at stents – those tiny tubes that doctors insert into a blocked artery to keep it open.

Did you know that there are demonstrably no benefits to the hundreds of thousands of stent procedures performed outside of an emergency setting? Here’s our first story.

The large national cardiology conferences may attract the majority of cardiologists in the entire country to one place. So, hey, if you’re going to have a heart attack, that would seem to be the place to do it. And indeed, that’s when the American Heart Association president had his, within hours of his presidential address. With so many of the nation’s top cardiologists at the conference, maybe that’s a bad time to go into cardiac arrest anywhere else, though. You don’t know, until you put it to the test.

To their surprise, they found substantially lower mortality among those going into cardiac failure or cardiac arrest during the big national cardiology meetings. Why is the death rate lower when most of the cardiologists are away? One potential explanation is that the intensity of care may be lower, suggesting the harms of such care may unexpectedly outweigh the benefits. Their results echo paradoxical findings documented during a labor strike by Israeli physicians, during which mortality rates evidently dramatically fell. And it wasn’t just one strike. This has been looked at multiple times, and in all reported cases, mortality either stayed the same or decreased. In four of the seven cases, mortality dropped as a result of the strike, and in three, there was no significant change.

The fact is that many current medical practices have been found to offer no benefit, and, in fact, potential harms. Even physicians themselves estimate that about one-fifth of medical care is unnecessary. A national summit was convened by the joint commission that accredits hospitals and the American Medical Association to identify areas of overuse—treatments that provide zero or negligible benefit—potentially exposing patients to the risk of harm for nothing. They called out five practices: for example, prescribing antibiotics for viral upper respiratory tract infections, spending a billion dollars prescribing drugs that don’t work (and if anything just make things worse). But another overused practice they identified was elective percutaneous coronary intervention––in other words, angioplasty and stents.

Just to get everyone on the same page before we dive in, coronary artery disease, the #1 killer of men and women, involves blockages in the blood vessels that supply the heart muscle itself. Low blood flow can lead to a type of chest pain called angina or, if severe enough, to a heart attack. Plant-based diets and lifestyle programs have been shown to reverse these blockages by treating the cause of why our arteries are clogging up in the first place. But, for those unable or unwilling to change their diets, there are drugs that can help, as well as more invasive treatments such as open-heart surgery to try to bypass the blockage, or percutaneous coronary intervention. That’s when doctors insert small balloons or metal tunnels, called stents, up through the large blood vessels typically in the groin, and thread them all the way up into the heart. That way, you can then get inside the blocked vessels, and try to open them up and prop them open. During a heart attack this can be lifesaving. But hundreds of thousands of these procedures are done every year for stable angina, meaning on a non-emergency basis, which can relieve symptoms but doesn’t actually reduce your risk of having or dying from a heart attack in the future.

However, not everyone knows that. They mistakenly think the procedure offers more than just symptom relief. That’s one of the reasons I’m doing this video series. As Harvard put it, stents are for pain, not protection. But then, unbelievably, it was discovered that stents may not even help with pain, as revealed in this double-blind, randomized controlled trial. Wait, you can blind people to the active treatment in drug trials by giving them a placebo sugar pill, but wouldn’t you kinda notice if you got surgery or not, whether or not they cut into your groin? Not if you got sham surgery—placebo surgery—where they cut into everyone, thread up the catheter, and at the last moment, randomly actually do or do not actually place the actual stent. And those who got the fake surgery did just as well as those who got the regular surgery. Wait, there are no benefits to angioplasty and stents outside of an emergency setting? Doesn’t prevent heart attacks, doesn’t enable you to live longer, and doesn’t even help with symptoms? And since the procedure carries risks—including death—maybe stents should be used only for people who are actively having heart attacks. But wait, so hundreds of thousands of people are getting these operations for nothing? How do the doctors justify it? Is it just greed? How do they get patients to sign up? Do they just not tell them the truth? And wait, why doesn’t it work? After all, you are opening up a blocked artery. There are just so many questions, which we’ll start addressing next.

In our next story we look at how most heart attacks are caused by nonobstructive plaques that infiltrate the entire coronary artery tree.

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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