UNBREAK MY HEART
David Faxon is a pioneer of angioplasty techniques, keeping the heart free and clear of blockage.
by Christopher TedeschiThrough three blood vessels, each the diameter of a shoelace, the human heart supplies itself with the vital oxygen needed to pump blood to every tissue in the body.
David Faxon, M.D., would like to make sure those tiny vessels are allowed to do their life-essential job by eliminating blockages caused by coronary artery disease.
When an accumulation of fatty deposits restricts blood flow in its two main arteries, the heart can be slowly deprived of oxygen. Atherosclerosis-the disease process that gradually deposits plaque in the arteries-can lead to heart attack and stroke. One way to make sure that blood keeps serving the heart muscle is with a bypass operation, in which a blood vessel from elsewhere in the body is used as a surgical detour around the arterial roadblock.
But another way to re-open a clogged artery is with angioplasty-snaking a long wire and catheter directly into the targeted blood vessel from a point near the groin, and physically pushing the blockage out of the way by stretching open the artery. Physicians have been using angioplasty to open clogged heart vessels for nearly two decades, and now, upwards of 450,000 angioplasties are performed each year in the U.S.
Faxon has been pioneering angioplasty techniques since he studied interventional cardiology with angioplasty innovator Andreas Grüntzig in the late 1970s. After 19 years at Boston University, Faxon left his native New England in 1993 to assume the role of USC professor of medicine and chief of cardiology.
It did not take long for Faxon to settle in as one of the top heart specialists in Southern California. In 1996, he was named one of the best doctors in Los Angeles by Los Angeles magazine and one of the best cardiologists in the United States by Good Housekeeping magazine. He currently serves as president of both the Los Angeles Affiliate of the American Heart Association and the Society of Cardiac Angiography and Intervention. In the clinic, he continues to improve on the growing collection of tools and techniques available to interventional cardiologists.
Since Faxon's arrival, cardiologists at USC University Hospital have expanded their repertoire to include several variations on the traditional balloon angioplasty technique, in which a catheter containing a deflated inch-long balloon is guided directly to the spot of narrowed artery, then inflated to push fatty deposits out of the way. Now, tiny catheters carry miniature diamond-tipped drills or tiny slicing mechanisms, each device having its own specialized niche to benefit different groups of patients.
One technique, laser angioplasty, which has been commonly used since 1992, has a catheter that carries a miniature laser to the site of the blocked blood vessel, and literally blasts the plaque out of the artery.
"In some cases, the laser is a better choice because we can remove the plaque from the artery instead of just stretching it," explains Faxon.
Another relatively new device, called a rotoblator, works like a dental drill. The rotoblator's diamond-tipped drill bit works best in hard, mineralized plaque lesions that a balloon might not crack, or in a tight spot that might be anatomically unfriendly to an inflating balloon.
But even with refined techniques, angioplasty is not for everyone. Important factors in the decision include age, sex, and the number and type of lesions-or narrowed areas-in the coronary arteries. Since plaque deposits usually form where arteries branch and blood flow is most turbulent, anatomy plays an important role as well.
Recent evidence also points to an increased risk for people with diabetes. Last year, in an article in the American Heart Association's journal Circulation, Faxon and his colleagues showed that the post-angioplasty mortality rate for diabetics was roughly twice that of people without the disease and that diabetics showed higher rates of heart attacks and were more likely to have bypass surgeries.
Yet, Faxon says, the increased risk should not deter people from considering the procedure. Rather, careful testing and follow-up could help physicians spot problems earlier in high-risk patients, and angioplasty could postpone traumatic bypass surgery for years.
For all patients, the biggest concern after angioplasty is that the blocked vessel will narrow once again, shutting off blood flow. Understanding this constriction, called restenosis, has been Faxon's strongest research interest since he entered the field. USC scientists have tested several new ways to prevent restenosis, and the outlook seems to steadily improve. But restenosis severe enough to block arterial blood flow still occurs in roughly 30 percent of angioplasty patients within six months after the procedure.
One way to prevent restenosis is with a tubular wire support called a stent. Like miniature scaffolding, the stent is permanently set in place during angioplasty using the same catheter that carries the balloon. The stent bolsters the section of artery that might otherwise sag in on itself. Stents help minimize the risk of eventual restenosis, as well as prevent the abrupt artery closure that sometimes occurs immediately after an angioplasty.
Along with new stent designs, USC trials have examined drugs that can be used along with devices to minimize the likelihood of restenosis. In 1995, Faxon and a colleague were awarded a U.S. patent for a catheter designed to deliver restenosis-reducing medications directly to the arterial tissue, while also carrying a balloon for expanding blocked coronary arteries.
Adding to Faxon's knowledge was a recent report from scientists at La Jolla's Scripps Clinic demonstrating that when small catheters holding radioactive beads were momentarily placed in the blocked artery directly after an angioplasty, the rate of restenosis decreased to 17 percent, less than half the rate seen in patients who had not received the radiation treatment.
Faxon and his research team recently began a similar trial on patients undergoing angioplasty for a single lesion in a coronary artery. A radioactive wire, fourteen-hundredths of an inch in diameter-about equal to three human hairs-slips inside the catheter that guides the balloon to the blocked artery, then delivers a high dose of gamma radiation over a two- to five-minute time period.
The radiation, he explains, makes the smooth muscle in the vessel incapable of responding to the injury caused by angioplasty.
"We see atherosclerosis as an inflammatory illness," Faxon explains, drawing an analogy between the wound caused by angioplasty apparatus and a cut on the skin. The area swells, the immune system kicks in, a blood clot forms and new tissue begins to grow.
Instead of scar tissue, the cells that grow inside the coronary artery are smooth muscle cells, which normally compose the middle layer of the arterial wall. Sometimes, as an artery heals, the cell growth overdoes itself and forms such a "scar" that the restored blood flow becomes hampered once again.
"The idea has traditionally been to stop the proliferation of cells, leaving less mass to narrow the artery," Faxon explains. Studies like the radiation research focus on preventing the harmful growth of muscle cells inside the artery, yet scientists are not sure if the treatment actually prevents restenosis, or just delays it.
But two years ago, new research on the process of restenosis turned much of the previous thinking on its head.
Since the mid 1980s, dozens of drug trials have attempted to prevent restenosis, either by stopping the growth of smooth muscle cells after an angioplasty or controlling the inflammation that comes along with an arterial wound.
Researchers have now suggested that the way that the artery rebuilds-or "remodels"-its supporting structure could be more important than limiting the growth of new muscle cells after angioplasty. Blood vessels remodel in response to a wound such as would be caused by an inflating balloon or a laser beam. Yet if the muscle cells can grow without blocking blood flow, there's no restenosis. It is how they grow that is really important. Remodeling may consist of a constriction of the artery, or an enlargement of the vessel without restricted blood flow.
In a February 1995 editorial in the Journal of the American College of Cardiology, Faxon and former USC colleague Jesse Currier, M.D., suggested that remodeling might be the most important player in the restenosis process.
That realization, says Faxon, could point the way to therapies that influence arterial remodeling instead of merely trying to control the new growth that occurs after an angioplasty.
Scientists, realizing that arterial constriction can occur even with a minimal amount of new growth or plaque formation, suspect collagen, the main structural protein in most of the body's tissues, as an integral part of the remodeling process.
This past spring, Faxon and his team of researchers showed that in animal models, arteries that showed restenosis after angioplasty had significantly greater amounts of collagen than those that did not. The research hinted that collagen could play an important role in the way the artery remodeled, and could suggest possible treatments aimed at minimizing the chances of restenosis.
More research on collagen and artery remodeling is on the way. The continuing collection of clinical and basic research projects, from the biochemistry of structural proteins to the effectiveness of radiation therapy, steadily grows under Faxon's supervision, along with an expanding interventional cardiology program at USC University Hospital.
And while the small armory of drills, lasers, balloons and stents now offers better angioplasty choices for greater numbers of patients than ever, ongoing research in Faxon's division of cardiology will make sure that those unclogged arteries stay that way for years to come.n
For more information about David Faxon, M.D., and the division of cardiology or any of The Doctors of USC and their specialties, please call 1-800-USC-CARE (1-800-872-2273).
