Is My Stent Open?
Here’s a scenario that we cardiologists occasionally see.
A patient comes into the hospital with chest pain. He goes to the cath lab where he’s seen to have 90% narrowing of one of his critical vessels, which his cardiologist opens with a small metal coil called a stent (see previous post for more information on how this is done).
Several months later, the man begins having discomfort that is similar to his previous episode. He immediately wonders about his stent and heads straight to the ER. Another angiogram follows and the diagnosis is made: “In-stent restenosis.” The stent has closed down (“stenosis” is Latin for “narrowing”). Technically, the configuration of the stent remains the same; it’s just that the cells of the interior of the blood vessel have grown into the center of the stent and reduced the effective space through which blood can flow. The patient needs another angioplasty to open the clogged artery.
I narrate this vignette to illustrate what goes through the mind of many patients who receive stents. I believe it is nearly inevitable for a person with a coronary stent to wonder “Is mine still open?” Many of my patients ask me about this (and those who don’t are probably wondering this in the backs of their minds): “When are you going to do a test to see if my stent is still open?”
The answer? We don’t.
Such a reply doesn’t sit well with many people.
Imagine the following exchange. You’ve recently been diagnosed with a life-threatening cancer and survived a surgical excision. Your oncologist sums up the therapy going forward: “We’ve cut out the cancer and we’ll see you periodically to check up on you. The one thing we won’t do, however, is repeat the CT scan or do any blood testing to see if the cancer comes back. We know that the tumor will recur in a percentage of patients, but our policy is to simply keep you on medication and hope for the best.”
How long would it take for you to find another cancer doctor? How well could you sleep at nights knowing that your physician is planning no monitoring whatsoever to see if your cancer recurs? I’m no oncologist, but I have to believe that it is an engrained part of their specialty to periodically perform some test to see if the tumor has returned. Even cancers where the cure rate is quite high need to be followed, for peace of mind if nothing else.
So why don’t we do the same with coronary stents? Shouldn’t we be doing some type of periodic testing to make sure the vessel is still open? The answer is complicated and requires a history lesson in coronary intervention.
Years ago, when balloon angioplasty was first pioneered, the chance that the vessel would close down (a process called restenosis) within months of the procedure was quite high. With angioplasty you simply expand a balloon in the narrowed artery and cram aside all the cholesterol plaque. The balloon is deflated after a minute or so and then you just hope for the best. At the six-month mark you stand about a 40% chance of having the narrowing return (higher with more complicated blockage or smaller vessels).
Back in those days it was common for us to do testing to evaluate the artery, a strategy that made sense since nearly half of all patients needed a repeat procedure. It wasn’t unusual to do an elective angiogram at 6 months as a matter of course.
Stents came into common use in the early 1990s and with them the rate of restenosis dropped from 40% to about 20%. Still, the rate remained high enough that doctors insisted on routine evaluation for stent patency—generally with stress testing. Despite having a metal coil inside the vessel to prop it open, the interior lining of the artery still managed to grow closed in up to a third of patients.
About 10 years ago we started using stents coated in chemicals—borrowed from the world of cancer therapy—that inhibit the excessive growth of the arterial cells. The so-called drug-eluting stents (DES) have proven to be remarkably helpful at decreasing the rate of restenosis, now to well below 10%. We still use the old-fashioned plain stents, but we reserve these for larger vessels where the rate of restenosis will be low regardless of the type of stent used. The other breakthrough that has decreased the rate of restenosis is the more widespread use of medications—such as aspirin, Plavix, and statins—that improve the likelihood that the stent will remain open.
With all these changes we’ve reached the point where the chance of a stent closing down has become increasingly uncommon. The story at the beginning of this blog post is one that we cardiologists are familiar with, but such a clinical scenario is becoming more the exception than the rule.
In the mind of the patient, however, the fact that stent restenosis is an infrequent occurrence among the general population may not be all that reassuring. They still wonder, “Why not just do a stress test every year to be sure?”
The problem lies in the numbers. Even the most rigorous stress tests have a modest rate of what we call false positives—where the test suggests an abnormality in a person, but no problem actually exists—that is high enough to make stress testing unhelpful. If you, as the owner of a stent, undergo a stress test in the absence of symptoms, your chance of a false positive could be as high as 75%. In other words, your likelihood of restenosis has dropped so low that even an abnormal stress test will not compel your cardiologist to believe that your stent has closed down.
I spoke with one of our interventionalists to gain perspective on this. Dr. Jeffrey Carstens faces this question regularly and explained to me how he handles it.
“When my patients ask about this I remind them of a couple things. First, the rate of restenosis has now dropped so far that stress testing is no longer useful. In fact, the most current edition of our guidelines (from the American College of Cardiology) actually classifies routine stress testing in the symptom-free patient as ‘class 3,’ meaning not helpful and even possibly harmful.
“Second, in the patient who feels fine, a repeat angioplasty will provide the person no benefit at all. Stenting has been shown to improve symptoms only and not to impact survival. So, in the absence of suspicious chest pain or difficulty breathing, I adopt a type of ‘if it ain’t broke, don’t fix it’ approach.”
What Dr. Carstens emphasizes is important: if you’re having chest pain after receiving a stent you need testing, but if you’re healthy and free of chest pain, then coronary studies aren’t beneficial.
This doesn’t mean that routine testing among asymptomatic people doesn’t happen. Many cardiologists and primary doctors are so accustomed to such testing that they continue to ask for it despite good evidence to the contrary. Similarly, patients who have had annual examinations for many years express concern when we abruptly change our game plan. Like most doctors I have been guilty of giving in to patient anxieties and ordering a stress test even though I know that it may produce results I can’t rely on.
It took us a couple decades to get to the point where the typical coronary intervention represents a stable and durable procedure. It may just take a little longer for the public—and many doctors, for that matter—to catch up with this.