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The Move Toward Interventional Medicine

Interventional Medicine

Unfortunately, interventional cardiologists — my specialty — are not all created equal. Some are far more adept at handling complicated cases. The less skilled a patient’s interventional cardiologist, the better the odds the patient will end up in the hands of a surgeon.

And in my experience, many patients who have suffered a cardiac event do not need the last-ditch intervention of a surgeon. They can now be treated through balloon angioplasty and the insertion of stents.

For example, a patient may have three-vessel heart disease but only one of the blockages is the source of immediate problems. A gifted interventional cardiologist will recommend addressing the major blockage with balloon angioplasty and the insertion of a stent — procedures that will see the patient home in a couple of days, feeling much better.

A less-proficient doctor might worry that his skills are inadequate to carry out such a procedure.

The talented interventionalist is also more likely to take a “wait and see approach” as to whether (once the major blockage has been addressed) the minor blockages can be remedied through medication and lifestyle adjustment.

It’s also a matter of keeping up with the latest medical research and advancements. For instance, when balloon angioplasty was introduced in 1977, it was much less reliable and effective than it is today.

Back then, doctors inflated the balloon within the artery, breaking up the plaque blocking it, and hoped the artery would “remodel,” or assume a shape and form that was more favorable. Often, these arteries did just that, as the body seemed to recognize the chance to heal itself. But not


Sometimes, the arteries would seem fine in the catheterization lab, then close as soon as the patient reached the recovery room. We soon learned that there is a “rebound effect”: Like other elastic materials, arteries that have been opened with balloon angioplasty contract after having been expanded.

Balloon angioplasty still helped, because only a slight improvement in the artery produced increased blood flow. However, it could break up the plaque in a way that produced thrombosis — clotting of the blood — which could lead to heart attack or stroke.

Arteries treated with balloon angioplasty alone re-block (a process called restenosis) at rate of 30 to 50 percent. Nowadays, the procedure is complemented with the insertion of stents, hollow tubes made of wire mesh that keep the artery open after the balloon has been removed. With the advent of stents, doctors can remodel the artery after the angioplasty, ensuring free blood flow.

There are still problems with stents, however. They can cause irritation to the arterial wall, and the body’s immune system responds to this irritation in two ways. First, the immune system prompts the natural lining of the artery — the endothelium — to absorb the stent; within six months, the artery manages to line the stent with its own cells. Usually, the immune process stops at this point, and the stent has a lining of living cells, allowing the vessel to function perfectly.

In some cases, though, the body’s immune system keeps going, and the arterial wall grows around and eventually into the stent until it becomes blocked.

The first type of stent, the uncoated stent, becomes blocked again 15 to 30 percent of the time. The way in which restenosis occurs can be likened to the formation of scar tissue. Usually, if you cut your skin, a virtually imperceptible scar will trace out the healed wound. In some cases, however, a keloid scar will form. Here, the scar tissue proliferates, turns pink, and exaggerates the size of the old injury.

The irritation to the arterial wall caused by an uncoated stent also may cause a blood clot, which can precipitate heart attack or stroke.

For this reason, people with stents must take an antiplatelet medication such as clopidogrel (Plavix) for six months, as well as daily aspirin.

We now have a second type of stent, coated stents, designed to suppress cell growth around and inside the stent. These are also called “drug-eluting stents” because they “elute” or give off a drug that suppresses the body’s immune response, which prevents the stent from being overgrown and forming blockages in the artery.

Coated stents remain open indefinitely, but because they suppress the body’s immune response they are even more prone than non-coated stents to promote blood clots. This risk rises substantially in the event of surgery for another condition. For example, if a patient with a coated stent needs to have his gall bladder removed, the chances of gall bladder surgery producing a blood clot are substantially higher.

Personally, I prefer the use of uncoated stents. If I can monitor a patient closely, and the patient takes prescribed medications and actively pursues lifestyle modification, including proper diet and exercise, then there is a great chance for success without the need for extended drug therapy.

Restenosis usually occurs within the first three to six months for non-coated stents. Monthly appointments and the administration of a stress test six months after insertion can help gauge whether there’s been an adverse reaction to the non-coated stent.

My preference for uncoated vs. coated changes, however, in certain circumstances. Diabetics are far more prone to re-closure of a stent, and for that reason they should be treated with coated stents.

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