Why Healthy People Suffer Heart Attacks

Recently, I was at a dinner party when another guest, upon hearing that I was a cardiologist, turned to me and said, “My friend just passed his annual physical with flying colors. Two days later, he had a heart attack. How could this happen?” I’m sorry to say that I hear stories like this almost as often today as I did 25 years ago.

The fact is, back then, we had an excuse. We didn’t know any better. Today, we do. We know that someone can look great on paper—pass a standard exercise stress test with flying colors, have good cholesterol scores, and never have had a sick day in his or her life—but still have arteries that are a diseased and potentially lethal mess. Today we have access to cutting-edge diagnostic tests that can identify these high-risk people early enough to prevent them from having heart attacks in the first place.

The problem is that many patients destined for heart problems don’t get the benefit of our most accurate tests (see our MSN Health & Fitness interview with Dr. Agatston). Many seemingly perfectly healthy people “suddenly” are getting heart attacks because their arteries are not perfectly healthy and they don’t know it. With the proper noninvasive tests, these diseased arteries would have been identified, and the heart attacks wouldn’t have happened.

In order for you to understand how our thinking about what causes a heart attack has changed, I will give you a short course in cardiology from my new book, The South Beach Heart Program: The 4-Step Plan That Can Save Your Life. Don’t worry, it won’t hurt a bit, and you’ll be an expert in no time.

The Persistence of the Plumbing Model

More than a century ago, when pathologists first examined the arteries of heart attack victims, they reported that they were hard and inflexible. They named this condition arteriosclerosis, from the Latin word for hardening of the arteries(today we refer to it as atherosclerosis). A closer look revealed that the artery walls were not just stiffer, they were also clogged with a yellowish, waxy substance that early medical investigators called plaque, a term that we still use today. Cardiac researchers also correctly noted that most heart attack patients had something else in common: One or more of their coronary arteries was blocked, preventing blood flow to the heart muscle.

But these early investigators went on to make two understandable mistakes. First, they surmised, the higher up a blood clot forms when it blocks a coronary artery, the greater the area of heart muscle affected. If the clot occurs in the left main coronary artery, then all of the heart muscle supplied by the left circumflex and left anterior descending arteries will die, causing a deadly heart attack. Like gook in a drainpipe, plaque builds up inside an artery steadily over time, gradually narrowing the opening until it closes, blocking blood flow. Second, after observing a blood clot at the site of most blockages, they theorized that the clot had formed after the plaque had sealed off the artery, causing blood flow to become stagnant.

In fact they were mistaken. What was actually causing the blockage was not completely understood until fairly recently. Here’s what they missed: There are two kinds of plaque—soft plaque and hard (or healed) plaque. It is the soft plaque (the so-called vulnerable plaque), which is prone to rupture, that is most dangerous and that most often causes a heart attack. The best way to picture a soft plaque is to think of it as a small bump protruding from underneath the delicate inner lining of the artery (this lining is called the endothelium). The soft plaque is filled primarily with cholesterol. Suddenly, with no warning, the small plaque-filled pimple can burst open, puncturing a hole in the endothelium and exposing the contents of the soft plaque to the bloodstream. A blood clot then develops at the site of the “injury” as part of the healing process. This clot (along with spasm of the affected artery) is what most commonly causes obstruction of blood flow; the clot is not the result of obstructed blood flow, as was previously thought, but is its cause!

Why is this point so important? Knowing when and how the blood clot is formed is key to understanding the mechanism of a heart attack, which is fundamental to developing a strategy for preventing and treating heart disease. When the plaque ruptures, causing the formation of a blood clot that compromises blood flow enough to cause pain, it is called an acute coronary syndrome (ACS). If it compromises blood flow long enough to cause the death of heart muscle, it is classified as a heart attack. As I tell my patients, if you feel any pain that lasts for several minutes, call your doctor, even if the pain subsides.You’re still at risk. That’s because until it heals, the blood clot at the site of vessel injury can still grow and cause a heart attack. This healing process can take several weeks.

The good news is that most plaque ruptures do not result in a heart attack or even in chest pain. In as many as 99 out of 100 ruptures, the clot is largely broken up or dissolved by natural clot-busting enzymes produced by your body. When the ruptured plaque in a vessel wall heals, it scars over (like any cut or wound) and often calcifies. These healed plaques are rarely the source of further problems. They form the hard plaques described earlier. So why did it take so long for medical scientists to figure out that it’s soft plaque, not hard plaque, that is the problem? It’s because soft plaque hides inside the artery walls and, on an angiogram, it often is invisible or appears small and not obstructive.