Senator Bernie Sanders, was hospitalized after experiencing chest pain at a campaign event on October 2. He is said to have had blockages in one of his coronary arteries. Two stents were placed to open them. Several days later we learned that Senator Sanders had suffered a heart attack (also known as a myocardial infarction) as a result of the diminished blood flow to his heart muscle.
What happened to Senator Sanders is one form of a condition known as acute coronary syndrome (ACA). It is usually caused by the rupture or erosion of a cholesterol plaque in the artery. This small wound brings the contents of the plaque into contact with the blood. This leads the blood to clot. If the artery is completely blocked by clot, that causes a heart attack. A partial blockage causes pain without evident tissue damage.
This is an appropriate use for stents. Stents that open the clot during the ACS save heart muscle and saves lives.
Although Senator Sanders is 78 years old, as far as we know he has no prior history of heart disease. It is noteworthy, however, that a doctor’s letter in 2016 mentioned that he had “mildly elevated” cholesterol. We do not know if he had other risk factors for atherosclerotic heart disease (high blood pressure, diabetes, abnormal lipid profile, smoking, etc.) Nor do we know if he received any medical recommendations to lower his cholesterol.
The significance of new chest pain
Based on what we know, this was a new and unusual chest pain for him. It was, in fact, described as a chest “discomfort” in many of the media stories. Chest pains of cardiac origin may be accompanied by other symptoms, such as fatigue, weakness, sweating, and shortness of breath.
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The most important take away when we talk about a new chest pain or a change in a formerly stable chest pain pattern is that it is often a warning of an impending heart attack. It is considered an acute coronary syndrome.
And, as I mentioned it is usually caused by a rupture or erosion in a cholesterol deposit in a coronary artery. That then leads to the formation of a clot that blocks the artery. I will review this sequence of events in more detail in the next section.
Bernie Sanders is very lucky. Many people with a new kind of chest pain and clot in their artery die suddenly. Their first symptom of heart disease kills them
The cause of heart attacks and sudden death
Decades ago, it was believed that heart attacks and sudden death were the result of a fixed obstruction by a cholesterol plaque in a coronary artery. However, as long ago as 1995, Erling Falk pointed out the following based on a review of four even older studies:
- Only 14 percent of heart attacks occur at a point in the artery where the obstruction exceeds 70%
- Seventy percent of myocardial infarctions occur where the fixed obstruction is 50% or less.
- A 50 percent blockage seldom produces symptoms
Thanks to leading cardiologists like Erling Falk, Peter Libby, and Steven Nissen we now know that heart attacks and sudden death almost are almost always the result of an unstable (vulnerable) plaque that has ruptured.
The unstable plaque contains LDL cholesterol, commonly known as “bad” cholesterol. That LDL cholesterol is oxidized—chemically changed—in the wall of the artery. That causes the immune system to recognize it as foreign. The human body deals with foreign material by attacking it with white blood cells (pus cells).
So the unstable plaque is actually a microabscess or a tiny boil in the wall of the artery. When that boil ruptures, a toxic, inflamed gruel with the consistency of toothpaste comes in contact with the blood in the artery. That triggers the clotting process.
If the clot partially blocks the artery, unstable angina or an acute coronary syndrome is the result. If it totally blocks the artery, a heart attack (myocardial infarction) is the result. The blocked artery causes the death of the heart muscle downstream.
Few heart attacks occur as the result of severe chronic obstruction of the artery because the more obstructive plaques are much more stable. They have been present longer. The body reacts to those lesions by producing a thick cap over the cholesterol plaque and the inflammation produced by the white cells (pus) causes scar tissue formation. The inflamed cholesterol is bound up and rupture is more difficult.
Tying the critical facts about atherosclerotic coronary artery disease together
This scientific understanding ties the critical facts of atherosclerotic coronary artery disease together.
- It explains the fact that the anticoagulant aspirin cuts the risk of heart attack by 28% in patients who are not known to have coronary artery disease.
- It helps us understand why the clot dissolver TPA (tissue plasmin activator) aborts the heart attack process.
- Finally, it clarifies why statins have power beyond cholesterol-lowering. They also dramatically reduce inflammation and quickly stabilize plaque to prevent rupture.
Other medications like ACE inhibitors for blood pressure and metformin for diabetes have beneficial effects on the metabolism of the arterial wall to improve arterial function and diminish plaque instability.
What we already know about coronary artery disease
We already have a very solid understanding of the pathophysiology of coronary artery disease. And, we know what to do to substantially reduce the risk of heart attacks with medical treatment. Lowering blood pressure, blood glucose, and cholesterol to aggressive goals lowers the risk of heart attack and sudden death dramatically. We also know that stopping cigarette smoking (or never starting) is important to avoid developing coronary artery disease.
Dr. Steven Nissen and others have also shown that aggressive lowering of the LDL cholesterol with statin therapy stabilizes plaques and reverses the buildup of LDL cholesterol and pus in the wall of the artery.
Appropriate and inappropriate use of stents
Placing stents or by-passing acutely obstructed arteries can reduce the amount of damage to the heart muscle, particularly if done early. That is what occurred in Senator Sanders’ case.
However, stents and by-passes are NOT the best ways to approach long term treatment of coronary artery disease in order to prevent future heart attacks. Here’s what W.C. Little and his colleagues wrote about the topic as far back as 1988:
“Because it was difficult to predict the site of the subsequent occlusion in our patients from the initial coronary angiogram, coronary bypass surgery, or angioplasty appropriately directed only at the angiographically significant lesions initially present in almost all our patients would not have been effective in preventing the majority of myocardial infarctions. This does not indicate that arteries that do not have obstructive lesions should be bypassed or dilated. Instead, effective therapy to prevent myocardial infarction may need to be directed at the entire coronary tree, not just at obstructive lesions. Such therapy to prevent myocardial infarctions might rationally include avoiding smoking, reducing serum cholesterol, administering agents that alter platelet function…“
Over 30 years ago, Dr. Little was saying that bypass surgery and angioplasty could not be expected to prevent heart attacks in stable patients. This is because the atherosclerotic process affects all of the coronary arteries. In fact, it affects all of the arteries in the body to varying degrees. What was amazing about Dr. Little’s statement was that he predicted the results of the 2007 COURAGE trial more than a decade ahead of time.
That landmark trial compared optimal medical therapy with optimal medical therapy plus appropriate stenting in patients with angina, most of whom had two- and three-vessel coronary disease. There was no difference in heart attack or sudden cardiac deaths in the two groups after 5 years of therapy. How could it since it didn’t fix all of the plaques in the coronary vessels. Although these may be too small and numerous to stent, they are nevertheless the site of future blockages. Remember what I said above: Seventy percent of myocardial infarctions occur where the fixed obstruction is 50% or less.
In other words, the stent added nothing but pain relief. Additionally, in the COURAGE trial, 70% of the patients were pain-free at 5 years on medical therapy alone.
We know what we should do, why aren’t we doing it?
The “new” science of vascular disease tells us that we are doing too many catheterizations, bypasses, and stents. And, we are not doing enough aggressive medical management of risk factors to prevent people from having heart attacks in the first place.
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We have known what to do to prevent heart attacks for a long time. My question is why aren’t we doing it? Let us call it what it is—a failure of leadership on this issue. How many good men and women have to suffer heart attacks and sudden death before we finally get this right?
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This story was originally published on September 28, 2007. The author has revised and updated it for republication on October 3, 2019. Updated to provide information about Dr. Sanders’ heart attack and to highlight appropriate vs. inappropriate use of cardiac stents.1548