Most heart attacks are caused by nonobstructive plaques that infiltrate the entire coronary artery tree. There is no such thing as “1-vessel disease,” “2-vessel disease,” or “left main disease.” Atherosclerotic plaque is continuous throughout the coronary arteries of heart attack victims.
Why Angioplasty Heart Stents Don’t Work Better
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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.
Please consider volunteering to help out on the site.
- Blausen Medical Communications. Wikimedia Commons.
- Parisi AF, Folland ED, Hartigan P. A comparison of angioplasty with medical therapy in the treatment of single-vessel coronary artery disease. Veterans Affairs ACME Investigators. N Engl J Med. 1992;326(1):10-16.
- Hueb WA, Bellotti G, de Oliveira SA, et al. The Medicine, Angioplasty or Surgery Study (MASS): a prospective, randomized trial of medical therapy, balloon angioplasty or bypass surgery for single proximal left anterior descending artery stenoses. J Am Coll Cardiol. 1995;26(7):1600-5.
- Coronary angioplasty versus medical therapy for angina: the second Randomised Intervention Treatment of Angina (RITA-2) trial. RITA-2 trial participants. Lancet. 1997;350(9076):461-8.
- Blausen.com. Medical gallery of Blausen Medical 2014. WikiJournal of Medicine. 2014;1(2).
- Hueb W, Soares PR, Gersh BJ, et al. The medicine, angioplasty, or surgery study (MASS-II): a randomized, controlled clinical trial of three therapeutic strategies for multivessel coronary artery disease: one-year results. J Am Coll Cardiol. 2004;43(10):1743-51.
- Hueb W, Lopes NH, Gersh BJ, et al. Five-year follow-up of the Medicine, Angioplasty, or Surgery Study (MASS II): a randomized controlled clinical trial of 3 therapeutic strategies for multivessel coronary artery disease. Circulation. 2007;115(9):1082-9.
- Boden WE, O'Rourke RA, Teo KK, et al. Optimal medical therapy with or without PCI for stable coronary disease. N Engl J Med. 2007;356(15):1503-16.
- BARI 2D Study Group, Frye RL, August P, et al. A randomized trial of therapies for type 2 diabetes and coronary artery disease. N Engl J Med. 2009;360(24):2503-15.
- Mancini GB, Hartigan PM, Bates ER, et al. Prognostic importance of coronary anatomy and left ventricular ejection fraction despite optimal therapy: assessment of residual risk in the Clinical Outcomes Utilizing Revascularization and Aggressive Drug Evaluation Trial. Am Heart J. 2013;166(3):481-7.
- Hochman JS, Lamas GA, Buller CE, et al. Coronary intervention for persistent occlusion after myocardial infarction. N Engl J Med. 2006;355(23):2395-407./
- Stergiopoulos K, Boden WE, Hartigan P, et al. Percutaneous coronary intervention outcomes in patients with stable obstructive coronary artery disease and myocardial ischemia: a collaborative meta-analysis of contemporary randomized clinical trials. JAMA Intern Med. 2014;174(2):232-40.
- Thomas S, Gokhale R, Boden WE, Devereaux PJ. A meta-analysis of randomized controlled trials comparing percutaneous coronary intervention with medical therapy in stable angina pectoris. Can J Cardiol. 2013;29(4):472-82.
- Mitchell JD, Brown DL. Harmonizing the Paradigm With the Data in Stable Coronary Artery Disease: A Review and Viewpoint. J Am Heart Assoc. 2017;6(11):e007006.
- Doenst T, Haverich A, Serruys P, et al. PCI and CABG for Treating Stable Coronary Artery Disease: JACC Review Topic of the Week. J Am Coll Cardiol. 2019;73(8):964-76.
- Rothberg MB. Coronary artery disease as clogged pipes: a misconceptual model. Circ Cardiovasc Qual Outcomes. 2013;6(1):129-32.
- Roberts WC. Quantitative Extent of Atherosclerotic Plaque in the Major Epicardial Coronary Arteries in Patients with Fatal Coronary Heart Disease, in Coronary Endarterectomy Specimens, in Aorta-Coronary Saphenous Venous Conduits, and Means to Prevent the Plaques: A Review after Studying the Coronary Arteries for 50 Years. Am J Cardiol. 2018;121(11):1413-35.
- Pantaleo MA, Mandrioli A, Saponara M, et al. Development of coronary artery stenosis in a patient with metastatic renal cell carcinoma treated with sorafenib. BMC Cancer. 2012;12:231.
- Friedewald VE, Ambrose JA, Stone GW, Roberts WC, Willerson JT. The editor's roundtable: the vulnerable plaque. Am J Cardiol. 2008;102(12):1644-53.
- BruceBlaus. Wikimedia Commons. 2013.
- Al-Lamee RK, Nowbar AN, Francis DP. Percutaneous coronary intervention for stable coronary artery disease. Heart. 2019;105(1):11-19.
Video production by Glass Entertainment
Motion graphics by Avocado Video
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.
Please consider volunteering to help out on the site.
- Blausen Medical Communications. Wikimedia Commons.
- Parisi AF, Folland ED, Hartigan P. A comparison of angioplasty with medical therapy in the treatment of single-vessel coronary artery disease. Veterans Affairs ACME Investigators. N Engl J Med. 1992;326(1):10-16.
- Hueb WA, Bellotti G, de Oliveira SA, et al. The Medicine, Angioplasty or Surgery Study (MASS): a prospective, randomized trial of medical therapy, balloon angioplasty or bypass surgery for single proximal left anterior descending artery stenoses. J Am Coll Cardiol. 1995;26(7):1600-5.
- Coronary angioplasty versus medical therapy for angina: the second Randomised Intervention Treatment of Angina (RITA-2) trial. RITA-2 trial participants. Lancet. 1997;350(9076):461-8.
- Blausen.com. Medical gallery of Blausen Medical 2014. WikiJournal of Medicine. 2014;1(2).
- Hueb W, Soares PR, Gersh BJ, et al. The medicine, angioplasty, or surgery study (MASS-II): a randomized, controlled clinical trial of three therapeutic strategies for multivessel coronary artery disease: one-year results. J Am Coll Cardiol. 2004;43(10):1743-51.
- Hueb W, Lopes NH, Gersh BJ, et al. Five-year follow-up of the Medicine, Angioplasty, or Surgery Study (MASS II): a randomized controlled clinical trial of 3 therapeutic strategies for multivessel coronary artery disease. Circulation. 2007;115(9):1082-9.
- Boden WE, O'Rourke RA, Teo KK, et al. Optimal medical therapy with or without PCI for stable coronary disease. N Engl J Med. 2007;356(15):1503-16.
- BARI 2D Study Group, Frye RL, August P, et al. A randomized trial of therapies for type 2 diabetes and coronary artery disease. N Engl J Med. 2009;360(24):2503-15.
- Mancini GB, Hartigan PM, Bates ER, et al. Prognostic importance of coronary anatomy and left ventricular ejection fraction despite optimal therapy: assessment of residual risk in the Clinical Outcomes Utilizing Revascularization and Aggressive Drug Evaluation Trial. Am Heart J. 2013;166(3):481-7.
- Hochman JS, Lamas GA, Buller CE, et al. Coronary intervention for persistent occlusion after myocardial infarction. N Engl J Med. 2006;355(23):2395-407./
- Stergiopoulos K, Boden WE, Hartigan P, et al. Percutaneous coronary intervention outcomes in patients with stable obstructive coronary artery disease and myocardial ischemia: a collaborative meta-analysis of contemporary randomized clinical trials. JAMA Intern Med. 2014;174(2):232-40.
- Thomas S, Gokhale R, Boden WE, Devereaux PJ. A meta-analysis of randomized controlled trials comparing percutaneous coronary intervention with medical therapy in stable angina pectoris. Can J Cardiol. 2013;29(4):472-82.
- Mitchell JD, Brown DL. Harmonizing the Paradigm With the Data in Stable Coronary Artery Disease: A Review and Viewpoint. J Am Heart Assoc. 2017;6(11):e007006.
- Doenst T, Haverich A, Serruys P, et al. PCI and CABG for Treating Stable Coronary Artery Disease: JACC Review Topic of the Week. J Am Coll Cardiol. 2019;73(8):964-76.
- Rothberg MB. Coronary artery disease as clogged pipes: a misconceptual model. Circ Cardiovasc Qual Outcomes. 2013;6(1):129-32.
- Roberts WC. Quantitative Extent of Atherosclerotic Plaque in the Major Epicardial Coronary Arteries in Patients with Fatal Coronary Heart Disease, in Coronary Endarterectomy Specimens, in Aorta-Coronary Saphenous Venous Conduits, and Means to Prevent the Plaques: A Review after Studying the Coronary Arteries for 50 Years. Am J Cardiol. 2018;121(11):1413-35.
- Pantaleo MA, Mandrioli A, Saponara M, et al. Development of coronary artery stenosis in a patient with metastatic renal cell carcinoma treated with sorafenib. BMC Cancer. 2012;12:231.
- Friedewald VE, Ambrose JA, Stone GW, Roberts WC, Willerson JT. The editor's roundtable: the vulnerable plaque. Am J Cardiol. 2008;102(12):1644-53.
- BruceBlaus. Wikimedia Commons. 2013.
- Al-Lamee RK, Nowbar AN, Francis DP. Percutaneous coronary intervention for stable coronary artery disease. Heart. 2019;105(1):11-19.
Video production by Glass Entertainment
Motion graphics by Avocado Video
Republishing "Why Angioplasty Heart Stents Don’t Work Better"
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Title
Why Angioplasty Heart Stents Don’t Work Better
LicenseCreative Commons Attribution-NonCommercial 4.0 International (CC BY-NC 4.0)
Content URLDoctor's Note
Most heart attacks are caused by nonobstructive plaques that infiltrate the entire coronary artery tree. Atherosclerotic plaque is continuous throughout the coronary arteries of heart attack victims. That’s why we have to treat the cause and prevent the buildup of plaque in the first place, which means keeping your LDL cholesterol low. I talk more about how to do that later in this video series. Next, l talk about the risks of stents.
This is the second in a seven-video series on stents. If you missed the first one, check out Do Angioplasty Heart Stent Procedures Work?.
Stay tuned for:
- The Risks of Heart Stents
- Angioplasty Heart Stent Risks vs. Benefits
- Do Heart Stent Procedures Work for Angina Chest Pain?
- Why Are Stents Still Used If They Don’t Work?
- Heart Stents and Upcoding: How Cardiologists Game the System
As I say over and over in this video series, during a heart attack, in an acute setting, angioplasty can be life-saving. As I reiterate, when I’m talking about stable CAD, I’m talking nonemergency situations. In an upcoming series I talk about pros and cons of statin drug therapy. Spoiler: If you have a history of heart disease or stroke, taking a statin is recommended. All of these videos, including the upcoming statin series, are available on a digital download of a webinar I did last year. You can find it here.
UPDATE: A new meta-analysis was just published last month and alas, there is still zero survival benefit to stent placement for stable coronary artery disease, but at least there were fewer heart attacks. Since this still didn’t translate into actually living any longer, the foundation of treatment remains medical and lifestyle management. Hat tip to Dr. Bitterman!
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