Passed a Stress Test With Flying Colors and Had a Heart Attack on the Way Home, How Could That Happen?

Tomorrow I’ll have another “Medical Monday” talk taped for our local TV station.

It’s set up more like an interview but I still have to prepare it like a talk. It’s a little speech I give to patients several times per week, but it still causes some raised eyebrows, so I think it’ll be useful for a bigger, more general, audience.

I think I’ll say something like this:

The reason you can have a heart attack even after a normal stress test is that it isn’t necessarily the biggest blockages that cause heart attacks.

Big blockages, or plaques, don’t develop overnight. They take a while, and are more likely to either be silent (if other blood vessels take over the blood flow, like when commuters start to choose the side streets because the highway gets too congested) or to cause what we call stable angina.

Stable angina is chest pain after a certain work load, say two flights of stairs but not one.

Big blockages don’t always cause people to have chest pain if they push themselves too hard; diabetics, for example, often don’t feel pain when the heart is suffering lack of oxygen from its diminishing blood supply, because diabetics can have all kinds of nerve damage, not just in their feet.

Medium sized blockages, say 30-50 percent ones, are the scariest ones, because they may not limit blood flow enough to cause EKG changes or any visible decrease in the radioactive glow we measure in a nuclear stress test.

But 85% of all heart attacks happen as a result of plaque rupture. The wall of the plaque breaks and the “gooey stuff”, cholesterol and other lipid particles, oozes out into the blood stream and a clot forms around it. That’s why we give “clot busters”, fast acting blood thinners, to people who are teeter-tottering on a heart attack. This is what we call Acute Coronary Syndrome.

A couple of decades ago, doctors first gave Lipitor to people with Acute Coronary Syndrome and their pain went away. Lowering cholesterol doesn’t happen that quickly, so what was that all about? More on that in a bit.

Of course, big blockages can rupture, but they are more likely to cause warning symptoms before that happens, while the smaller ones are undetectable unless you do a heart catheterization on everybody.

(CT scans can be used to look for calcified plaque, but the non-calcified, softer plaque might actually be more dangerous.)

So, let me come back to he smaller blockages.

The first thing to make clear is that our arteries are not metal pipes, or even plastic tubes. they are living tissue. And just like our skin renews itself every thirty days or so, our arteries are undergoing all kinds of repair and renewal.

One important aspect of how healthy our arteries are is whether there is inflammation, and we are talking coronary arteries here, but the same thing holds true for the blood vessels to our feet and our brains, too.

When there is inflammation in, say a knee or on the skin, there is redness and swelling and all kinds of chemical reactions that work great if you need to heal broken bones or open wounds. But that kind of reaction can also lead to unwanted bone spurs, thick and peeling skin or, in our arteries, plaque formation.

And sure enough, people with inflammation, be it rheumatoid arthritis or chronic gum infections, on average have more plaque and more heart attacks than you would expect from looking at just the classic list of risk factors, like blood pressure and cholesterol.

Another alarming tidbit here is that some foods cause inflammation, like sugars and refined carbohydrates, while other foods like fish and olive oil reduce it.

In addition to lipid blood testing for determining heart attack risk, we sometimes use blood tests we call “inflammatory markers” (one of them is CRP, or C-Reactive Protein) to decide who should take drugs to lower their heart attack risk.

And this is where Lipitor, now generic atorvastatin, comes in.

It was one of many “statin” drugs developed for lowering harmful LDL cholesterol. It also lowers inflammatory markers in the blood, and as we found out after years of study, it decreases, and in high doses it can even reverse, plaque buildup in the neck arteries as measured by ultrasound, and it can reduce heart attack and stroke risk by 30-50%.

There are other, non-statin drugs (like Zetia), that lower cholesterol and inflammatory markers, but have nowhere near the impact on heart attack risk that the statins have.

So what’s going on?

We now know that Lipitor and the other statins actually do five things:

1) THEY LOWER CHOLESTEROL AND LDL, and that means something but is probably not their main action.

2) THEY MAKE THE PLAQUE WALL LESS BRITTLE, LESS LIKELY TO RUPTURE.

3) THEY PREVENT PLAQUE BUILDUP AND CAN SHRINK EXISTING PLAQUE.

4) THEY HAVE ANTI-CLOTTING PROPERTIES THAT ARE DIFFERENT FROM THE WAY ASPIRIN WORKS.

5) THEY RELAX THE LITTLE MUSCLES IN THE WALLS OF OUR ARTERIES THAT CAN CAUSE “CORONARY SPASM”.

The second through fifth of these mechanisms are well known by now, but we can’t measure them, so people still spend a lot of attention on the numbers that we can measure.

And speaking of measures: In 2013 the American Heart Association and the American College of Cardiology issued a new lipid guideline, with an update added this past year.

Instead of dividing people into just high, medium or low risk for heart disease, the new guideline has a calculator that lets you figure out somebody’s ten year risk. You can then compare this to the best case scenario, and also see what the impact would be of treating blood pressure, quitting smoking or taking Lipitor.

Now, I don’t mean to be overly enthusiastic about Lipitor. It can have unwanted side effects, from brain fog to rising blood sugars to muscle aches. But I am enthusiastic about how much better we understand how heart disease develops.

And I am also excited about what other research has shown: Our diet and lifestyle can address the same five mechanisms of action that Lipitor does. There is more and more proof that avoiding junk food and soda, following a plant based OR a Paleo OR Mediterranean diet, being physically active, sleeping well, managing stress and so on, can have the same impact and reduce a person’s heart attack risk by half.

I’m sure there will be reasons to ad-lib, answer questions, go in depth or off on tangents, but this is the framework I’ll start out with.

3 Responses to “Passed a Stress Test With Flying Colors and Had a Heart Attack on the Way Home, How Could That Happen?”


  1. 1 Brenda Wells August 17, 2019 at 11:32 pm

    The more things change, the more they stay the same.
    Thanks for pulling information together in a concise practical method. Enjoyed your blog.

  2. 2 John R. Dykers, Jr. MD, Davidson Class of 56, UNC Class of 60 August 18, 2019 at 3:37 pm

    So well said/written. Wish we could have practiced together. Just had angioplasty and stent of 96% lesion in LAD! Just found “skinny fat” diabetes at 84. Lipitor I had taken for 35 years incinerated when home burned down 22 Feb and my knee with the 15 year old triple tear in the medial meniscus stopped hurting! Switched to simvastatin and much better liped lowering and knee does not hurt. (took one 20 mg atorvastatin before my angio and the knee hurt like hell!)

  3. 3 James Adrian MD UCLA class of 65 August 19, 2019 at 11:27 am

    Excellent. Probably you have that in a handout to go with your talk or they could take it home, study it and then come back for the talk.


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Osler said “Listen to your patient, he is telling you the diagnosis”. Duvefelt says “Listen to your patient, he is telling you what kind of doctor he needs you to be”.

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