Take Heart
More than 200 years ago, a British country doctor was treating a woman suffering from “dropsy,” a sickness in which fluid builds up in the tissues of the body. The outlook, he knew, was grim. There was nothing he could do.
Imagine his surprise when he reexamined the woman a few weeks later and discovered her symptoms had disappeared. A local herbalist, he learned, had given her a potion containing foxglove leaves to drink.
The doctor published his studies on the leaves--and an ancient folk remedy entered mainstream medical practice.
Today, the woman’s diagnosis would be congestive heart failure, a condition in which the heart is too weak to efficiently pump blood through the body, causing fatigue and shortness of breath as fluid builds up in the lungs, as well as swelling in the body’s extremities. Doctors now know that those leaves the woman ate contained a medley of chemicals, including one called digoxin, which help the heart beat more powerfully.
Amazingly, through all this time digoxin has remained the state-of-the-art treatment for people with congestive heart failure, along with diuretics that help kidneys pump all that extra fluid from the body. The drugs treat the symptoms of the malady. They improve people’s quality of life. But they don’t stop the heart from progressively weakening, and they don’t help patients live longer.
Now this picture is changing. Medical researchers are learning more about why heart failure happens, and why it progresses so relentlessly. By mixing that knowledge with modern technology, they’re dreaming up new therapies and mechanical devices that could one day change what it means to hear those frightening words “congestive heart failure” in the doctor’s office.
Last month, UCLA cardiologists held a one-day symposium to discuss new insights into this malady, which contributes to 260,000 deaths in America every year. Here’s a look at some of the new and future therapies they discussed.
* ACE Inhibitors. These newer drugs protect the heart by interfering with a hormone, angiotensin, that is made in greater amounts in people with heart failure. Angiotensin narrows blood vessels, helping maintain blood pressure. This may be good in the short term--but causes great harm over time.
“It means that the heart is pumping against a brick wall, which weakens it further,” says Dr. Michele Hamilton, co-director of the UCLA clinical heart failure program. Not only that, but high levels of angiotensin can make heart cells bloat up, and weaken, even die.
Lowering blood pressure with ACE inhibitors gives the heart a chance to recover--and ACE inhibitors, unlike digoxin, do appear to prolong life in heart failure patients.
* Beta-blockers. These drugs have been used to treat hypertension for decades. But until recently, doctors would have never considered them for heart failure patients. Beta-blockers, after all, make the heart beat slower--surely the last thing a person with a weakened heart would want.
The body, in fact, tries to do just the opposite. As blood pressure drops, it cranks out hormones called adrenaline and noradrenaline to spur the heart to beat faster.
But that is tough on the heart. And just as ACE inhibitors give the heart a break, so do beta-blockers if they’re administered with care. Recent studies have shown that beta-blockers also prolong life in heart failure patients--and combining ACE inhibitors and beta-blockers helps survival even more.
* Fighting TNF. As heart failure progresses, muscle cells start to, in effect, commit suicide. This self-destruction happens, scientists suspect, when a stressed-out heart produces killer chemicals such as one called TNF.
Since TNF damages heart cells in other ways, too, it’s no wonder that scientists are working to hamstring it somehow. The rationale: Inject patients with a protein that will stick to it and stop it from doing its evil. Such a TNF-busting drug is already approved for the treatment of rheumatoid arthritis, in which TNF is known to play a role. Clinical trials on anti-TNF therapy for heart failure are underway.
* Growth Hormone. “Growth hormone is what makes your heart bigger and stronger as you grow,” Hamilton says. “The question is, if you treat a thin, weak heart with growth hormone, can you make it thicker and stronger?”
A simple enough question, but the studies so far have physicians scratching their heads. One found that hearts did get thicker over several months of therapy, but these beefier hearts didn’t work better. Another found that hearts pumped better and the patients’ symptoms improved. Bottom line: No one yet knows what the potential of growth hormone will be.
* Laser Therapy. With this method, little lasers are used to zap the heart with little holes in an effort to stop heart failure from developing.
Here’s the historical rationale: Certain reptiles don’t use coronary arteries to supply their hearts with blood--they use little channels, instead. So couldn’t laser-induced channels help a human heart, if the coronary artery is blocked and can’t be unblocked with surgery?
In fact, this method does help heart disease patients, studies show, reducing chest pains and enabling better performance on treadmills. But it’s probably not because of forming channels, researchers say. More likely, the drastic treatment does its good by triggering growth of brand-new blood vessels.
* Gene Therapy. Why not grow new blood vessels without burning holes through the heart? That’s the reasoning of some scientists who injected a blood vessel-inducing gene called VEG-F into legs of some people with poor circulation, and into hearts with blocked coronaries. The result: new blood vessels and an easing of symptoms in the patients.
* Growing New Heart Cells. It would be great if we could grow new heart cells every time we lost a few. “But the heart muscle’s much like brain tissue: You’re born with a certain number of cells, and they don’t have the capacity to divide,” says Dr. Robb MacLellan, assistant professor in the cardiovascular research labs at UCLA. Scientists are trying to get past that barrier, using a medley of approaches, including gene therapy and fetal heart cell grafts, in animals, for now.
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The list of procedures and devices goes on and on. There is a kind of “tummy tuck” surgery to reduce the size of grotesquely inflated hearts, which don’t beat as well. There are “assist devices” that are implanted in the abdomen as stopgaps to help hearts pump while people wait for transplants. Such devices may one day be implanted permanently in people who aren’t transplant candidates.
“But I think the most exciting thing is the potential for an artificial heart; there really is a big need,” says Dr. Hillel Laks, director of the heart transplant program at UCLA’s School of Medicine. At any particular time, there are an estimated 60,000 people who could benefit from a transplant, he says. Yet there are only enough available hearts for 2,400 transplants a year.
Tests on one artificial heart--electric, quiet, totally encased in the chest cavity--are soon to begin at three locations, including UCLA, which plans its first transplant (into a calf) later this month. Implants into people could begin as soon as the year 2000.
All in all, says Dr. Gregg Fonarow, director of the Ahmanson-UCLA Cardiomyopathy Center, “we’ve had major advances in our understanding, and we’ve got a number of new avenues of research that look very promising. Add that to the new treatments that we already know help patients live longer and better, and it’s a very exciting time.”
