The history of treating blocked heart arteries is a tale of two steps forward and one step back. People who suffer severe blockage in a coronary artery often experience chest pain or angina.
The original solution was coronary artery bypass graft, or CABG. The trouble with bypass surgery, though, is that it involves opening the chest. This exposes the patient to all sorts of risks from the surgery itself as well as infection. Recovery can be arduous.
Enter balloon angioplasty in the late 1970s. Doctors threaded a long, thin tube into the blocked artery and inflated a little balloon attached to its tip. This opened the artery, at least temporarily.
The problem with angioplasty was that frequently the benefit didn't last. Occasionally, the artery collapsed after the balloon was removed. Almost a third of the time the opened artery would clog up again.
A decade later, cardiologists came up with an apparently elegant solution. Along with the balloon, they inserted a tiny metal mesh tube (stent) that acted as a scaffold to hold the artery open.
Stents seemed like a great idea until studies revealed that they, too, had a serious drawback. About a quarter of the patients getting stents still had trouble with the arteries closing up again. This restenosis was due to an immune reaction from the body trying to heal the injury caused by the bare metal. Smooth muscle tissue grew over the stent just as a scar grows over a wound.
Drug-coated stents were introduced in the U.S. in 2003. The metal mesh was coated with an immune-suppressing drug formulated to release the medicine gradually and prevent growth of tissue. It did the job beautifully, and many cardiologists heralded medicated stents as a breakthrough.
There was another unpredicted step backward, however. Since the immune-suppressing medicine was so effective at preventing tissue from growing over the stent, the metal mesh became a trigger for blood-clot formation. Platelets (the sticky part of blood) clumped together to form a clot that could block the artery and cause a fatal heart attack.
The solution appeared to be long-term treatment with the anti-clotting drug Plavix, often with low-dose aspirin. Plavix has become the second-most-prescribed brand-name drug in the country. Roughly 3 million people swallow a pink Plavix pill every day.
How well does Plavix work? In another step backward, new research suggests that some people have a genetic quirk that makes them less likely to benefit from this anti-clotting medicine. An estimated 2 percent to 4 percent of Americans have two less-active copies of this gene. An additional 25 percent to 30 percent have a single copy, along with a copy that is more active.
That means that as many as a third of those taking Plavix might not be getting the full benefit of their pricey pink pill. In one study, these patients were at 50 percent greater risk of a heart attack or stroke (New England Journal of Medicine, Jan. 22, 2009).
Genetic tests are expensive, and insurance companies are reluctant to pay for them. Consequently, doctors and patients often don't know if Plavix is working as intended.
Stents seemed like an ideal solution to severe heart disease. Now it looks like the story is far more complicated.
Joe Graedon is a pharmacologist. Teresa Graedon holds a doctorate in medical anthropology and is a nutrition expert. E-mail them via their Web site: www.PeoplesPharmacy.com.