No Time to Die From an MI

Steven Kornweiss, MD cardiovascular, preventive medicine Leave a Comment

“I would rather be ashes than dust! I would rather that my spark should burn out in a brilliant blaze than it should be stifled by dry-rot. I would rather be a superb meteor, every atom of me in magnificent glow, than a sleepy and permanent planet. The function of man is to live, not to exist. I shall not waste my days trying to prolong them. I shall use my time.” — Jack London

Each year, for roughly one in eight Americans, their time ends with a fatal obstruction of the coronary arteries, the vessels that supply blood to our hearts.

When a major coronary artery is suddenly obstructed, oxygen-rich blood ceases to flow to the corresponding area of heart muscle (myocardium). If blood flow is not quickly restored, the myocardium dies. This is commonly known as a heart attack; in medical terms: a myocardial infarction (abbreviated MI).

If the obstructed artery is a large one, a vast area of heart muscle will lose blood flow. This can result in sudden death. If the victim survives, their heart may be severely weakened. Trivial activities like taking out the trash or climbing the stairs now leave them breathless.

While I’ve been thinking more and more about the balance between living a full life and a long one, I’d prefer not to die from an MI while pondering such existential questions.

I think often about cardiovascular disease.

Cardiovascular risk assessment and prevention is complex. Many risk factors can be considered. Among these, there are familiar factors like smoking, high blood pressure, obesity, diabetes, and "high cholesterol."

The first four are relatively non-controversial, but the last one, "high cholesterol," has been the center of controversy for decades.

Currently, guidelines suggest measuring LDL-cholesterol in all patients starting at a young age. Depending on age and other risk factors, as well as LDL-cholesterol level, guidelines often recommend that doctors prescribe statins to reduce LDL-cholesterol levels. This is one of the primary strategies used by nearly every primary physician and cardiologist to reduce the risk of heart attacks.

Here’s an example of one guideline:

In patients 20 to 75 years of age with an LDL-C level of 190 mg/dL or higher (≥4.9 mmol/L) maximally tolerated statin therapy is recommended.

In other words, if you’re between the ages of 20 and 75, and your LDL-C is greater than or equal to 190, your doctor is directed by the guidelines to prescribe the most potent statin drug that you can tolerate. Typically, this means you would take 80 milligrams of Lipitor once daily, unless you have side-effects. The most common side effect is statin myopathy, which manifests as muscle pain.

While the strategy of lowering LDL-cholesterol is effective when applied across a large population, it’s not clear that it works with equal efficacy in each individual member.

That is, if you have a group of 100 people, and a treatment helps 80 of them, but fails to help 20, the net benefit will be seen as positive. Guidelines will recommend this treatment for all patients. But, we know that some percent will not be helped. In most cases, we even accept that some will be outright harmed.

For this reason, though it’s very hard to do, I believe we should try to avoid applying guidelines without attention to the particular features of each individual patient.

With that in mind, we should find out if LDL-cholesterol is really a helpful diagnostic and therapeutic metric for all patients.

Consider this:

LDL-cholesterol is a poor predictor of heart attacks. Here is an excerpt from an article published in the American Heart Journal in 2009.

In the present study, almost half of patients hospitalized with CAD have admission LDL <100 mg/dL, and 17.6% of patients had LDL <70 mg/dL. Even when only patients without prior history of CHD, other atherosclerotic vascular disease, or diabetes were studied, 72.1% have admission LDL <130 mg/dL and 41.5% had LDL <100 mg/dL. Thus, a substantial proportion of patients present with their first or recurrent CHD events well within the current guideline-recommended targets for LDL.

In other words, three-quarters of patients in this study who were hospitalized for coronary artery disease had LDL-cholesterol levels that were considered acceptable, and in many cases, optimal.*

To my interpretation, this is one strike against relying solely on LDL-cholesterol for individual risk assessment and treatment.

Next, consider this case of a woman with familial hypercholesterolemia whose LDL-cholesterol was five times the normal level.

She developed severe coronary artery disease and suffered a heart attack at the age of eighteen.

This woman had markedly elevated LDL-cholesterol levels, and there is little controversy that this was the cause of her condition.

In this case, high LDL-cholesterol definitely correlates with severe coronary heart disease and MI.

Last, let’s look at this case of a man with lifelong LDL-cholesterol five times the normal level – roughly the same as the woman in the case above.

His coronary arteries?


He’s never had a heart attack. He’s had multiple CT scans of his coronary arteries which have failed to show signs of any coronary disease.

How can it be that two patients, each with the same markedly elevated LDL-cholesterol numbers, have such different disease states? One has a near fatal heart attack at the age of eighteen, but the other is in perfect health at age seventy-two.

Both the population statistics and cases such as these are clear: high blood levels of LDL-cholesterol are not sufficient on their own to cause atherosclerosis and heart attacks. And, on the other side, levels of LDL-cholesterol that are considered acceptable are not a guarantee that an individual will not develop atherosclerosis or heart attacks.

There must be other factors that matter above and beyond the mere quantity of LDL-cholesterol in the blood.

Experts in lipidology and longevity will tell you that this is, in fact, the case.

Knowing this fact, if we’re to understand how we should think about the mitigation of atherosclerosis and heart attacks, which are a leading killer of both men and women in the United States, we need to start by understanding its cause a little bit better.

Did you know, for instance, that LDL-cholesterol, perhaps counterintuitively, is not even a type of cholesterol? LDL stands for low-density-lipoprotein. LDL is a type of lipoprotein particle. These particles vary in size, content, and function. One component of LDL-particles is cholesterol.

What does this cholesterol have to do with the development of coronary artery disease and heart attacks?

If you’re interested in understanding this topic in more detail, I suggest you read this next article, which I’ve written to help answer the following questions:

  • What is cholesterol?
  • What is the function of cholesterol?
  • Where does it come from?
  • How does it get into and out of your body?
  • How does cholesterol move around in the blood?
  • Why do people say that LDL-cholesterol is bad?
  • Is it true that higher LDL-cholesterol is bad and lower is good?

— Steve

Read the next article in this series: What is LDL-Cholesterol?

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