Just last week I saw a patient who suffered a sizable heart attack. He came to the hospital quickly and my partners were able to whisk him into the cath lab and open his blocked artery before much muscle damage occurred. By the time I saw him the next morning he was feeling great and was eager to find out when he could go home.
While he was satisfied with his expeditious treatment he was confused and a little upset about one particular detail of his medical care. It seems his primary doctor had ordered a stress test just a month earlier as part of an overall check-up and the man passed with flying colors. So how was it, he asked, that he could ace a stress test and only a month later suffer a heart attack?
It’s an excellent question.
Many of you have probably heard the same story from friends or relatives. “Uncle Cletus passed his stress test and dropped over from a heart attack the next day. What gives?” Is stress testing unreliable and inaccurate? Is it a waste of time, money and effort? If it can’t screen for a heart attack then what good is it?
To answer this I have to once again resort to a discussion of anatomy, physiology and disease progression. I know, it’s dry and boring, but my blogging contract with Alegent Health Care stipulates that I produce a truly mind-numbing article at least once each month—so far I’m ahead of schedule for 2011.
The normal coronary artery is a smooth elastic pipe that delivers blood from the aorta to the cardiac muscle, thereby allowing your heart to provide you with 2.3 billion contractions during your lifetime without a single day off. During the course of your life—as you consume your way through thousands of greasy meals and spend hours lounging on the couch—cholesterol builds up in the wall of the vessel and crowds the inner diameter.
Most people mistakenly believe that this is a gradual and steady process (actually, most people never think about this—that’s what keeps me in business), but in fact it progresses in leaps and bounds. Let’s say a heart catheterization at age 50 finds you to have a 20% blockage and ten years later a repeat procedure shows that your blockage has progressed to 70%. In those intervening 10 years your blockage has not narrowed steadily at a rate of 5% per year; rather, it was probably stable at 20% until one day it jumped to 70%.
How this happens is best described by giving you a microscopic look at the exact anatomical make-up of your coronary blockage. (And no, I’m not talking about shrinking a team of scientists and injecting them into your vessels. While that seems like a good idea, you would have a hard time convincing Raquel Welch to sign on to such a crazy idea for a second time. And without her, what’s the point?)
The cholesterol (and other gunk) in the plaque is a fairly noxious mix and, if allowed to come in contact with blood, would immediately trigger formation of a clot as the body tries to seal off the offending muck. Thankfully, blood flow through the center of the artery is partitioned from the cholesterol core by a layer of sturdy cells that makes up the “fibrous cap.” A thick cap keeps the vessel stable and protects against sudden clot formation. A thin one, on the other hand, can easily crack and allow blood to seep into the cholesterol cavity and launch the clotting cascade. A vessel that was previously only 30% blocked almost immediately progresses to 100% and a heart attack ensues. If, by chance, the clot doesn’t totally plug the vessel, it often leaves the artery far more narrowed (thus can a 30% progress to a 90% almost instantly).
About 20 years ago some clever researchers took a look at patients who underwent cardiac catheterization and who had the bad luck of suffering a heart attack within the next few months. They reviewed the patients’ previous angiogram films to determine what the coronary vessels looked like just before the heart attack. To their surprise, the arteries that went on to cause the heart attack were not those with 80% or 90% blockage. Instead, the so-called “infarct-related vessels” were the benign-appearing mild blockages with narrowing most frequently at 50% or less.
These findings had a profound effect on how we understood the progression of coronary disease. The person who will have a heart attack next week may today have a blockage that is so mild that it produces no meaningful obstruction to flow. This point is critical since our stress tests have the ability to detect coronary blockage only if it occludes 70% or 80% of the inner diameter.
A typical story, then, is the patient who has a 40% narrowing in the critical left anterior descending artery who sails through the stress test. On a microscopic level, his artery is a ticking time bomb with a fibrous cap that is thin and unstable with a dense cholesterol plaque lurking beneath. The day after the stress test the man rests in his La-Z-Boy and triumphantly smokes a cigarette under the false reassurance that his heart is impervious to his life of indiscretion. The nicotine surge triggers the release of enough adrenalin to destabilize the delicate cap and his cholesterol cache is exposed to the blood stream. Doing what it thinks is right, the blood tries to seal off the crack with a sturdy clot. The blood flow through the artery occludes, the man grasps his chest in bewildered surprise, and his wife calls 911 (over his objections, of course). The rest is history.
Now that you understand the cascade of events involved in a heart attack you can readily see how unhelpful stress testing is in screening people for heart disease who exhibit no symptoms. As you can surmise, a normal stress test in no way guarantees the patient won’t have a heart attack while walking out of the clinic.
So then, you may ask, what use is stress testing? Since it is good at detecting tight but stable blockages (the 90% narrowing that pinches off normal blood flow) the test is helpful in assessing patients who experience chest pain, especially on exertion. In such a patient the abnormal stress test would lead to a cardiac catheterization where the blockage could be treated with angioplasty and stenting, thereby ameliorating the unpleasant chest pain the patient suffers.
At present we have no test that can look inside a patient’s heart and accurately predict who is destined to have a heart attack. Not even cardiac catheterization—which, like stress testing, gives us only the degree of diameter narrowing and not the composition of the plaque—can predict the future behavior of the blockage. For now, the answer to this dilemma is the same as I’ve given on countless other occasions: limit your risk factors, take your medications, get your exercise, and call 911 at the first sign of trouble.
Who knows? Maybe the eventual answer will entail shrinking someone down to the size of a red corpuscle. When that happens I’ll be the first one to call Raquel Welch.