Hidden Epidemic: Heart Disease in America
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Watching: The Hidden Epidemic - Heart Disease In America

Chapter 8: Within the Walls [12:43]

Repeated high-tech cardiovascular surgery cannot arrest the progression of heart disease. A new technology reveals why.

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Transcript: Chapter 8 - Within the Walls

Repeated high-tech cardiovascular surgery cannot arrest the progression of heart disease. A new technology reveals why.

NARRATOR: In hospitals across the country, there's a relentless stream of heart disease patients.

DR. PETER LIBBY: We've gotten so good at keeping people from dying during the acute phase of a heart attack that we have many more survivors accumulating.

DR. PETER LIBBY: Because we have made such tremendous inroads in cardiovascular diagnosis and therapy, many in the public perceive cardiovascular disease as a done deal, as a problem solved. Nothing could be further from the truth.

NARRATOR: Over six million operations or other interventions for heart disease are preformed in American hospitals each year.

NARRATOR: Many of them are done on patients who are having a second, third, or fourth prcedure. 500,000 people each year have a repeat heart attack, and in some hospitals, 40% of bypass surgery is done on patients who've had the operation at least once before.

DR. STEVE NISSEN: It's sort of a patchwork solution, you know? You can bypass the arteries, but if you don't stop the disease you're fighting a delaying action.

DR. STEVE NISSEN: And so I think that we are, in fact, patching people up and sending them back into an environment where the disease is going to recur.

NARRATOR: Figuring out why so many people have repeated incidents of heart disease, and what to do about it, are the primary goals of current research.

DR. PETER LIBBY: We used to view atherosclerosis or hardening of the arteries as a simple plumbing problem. We viewed the arteries like pipes, and when there was an excess of bad cholesterol, it would clog up the pipes and when that blockage got very severe it could lead to a heart attack. Our simple plumber's concept has undergone tremendous revision as we've learned more and more about how this disease really works.

DR. STEVE NISSEN: And many of us believe that the future is to get to the fundamental source of the disease. And that means its bio—the biochemical and genetic aspects of the disease. What's driving that disease?

NARRATOR: Figuring out what's driving heart disease has been a process full of unexpected twists and turns. Patient like Ken Christianson have provided surprising clues during their own fights with the illness. His problems started 19 years ago.

KEN CHRISTIANSEN: February first, '88 I had a massive heart attack. I was clinically dead three minutes and came back. About three or four or five years later, that's when I started getting a little worse, you know weaker, tireder, all the time.

NORA RITTER: His heart functioning was decreasing all the time. By the time we got to Cleveland clinic, it was like five to seven percent.

NARRATOR: Ken endured years of treatments, but in the end his heart was so badly damaged the only option left was a transplant. It's a successful procedure today, but it had a rocky start when it was first performed almost 40 year ago. In those early days many patients died within days after their surgery. Most of the time their bodies rejected the donated hearts. Even when better anti-rejection drugs came along, a significant percentage of treatment patients still died in five years or less. Doctors began to suspect there was something more fundamental going on inside transplanted hearts that was making them fail so fast.

DR. STEVE NISSEN: What limits life expectancy after a heart transplant, is the development of accelerated coronary disease, and it can actually happen so quickly, that within five years, the transplanted heart is no longer working.

NARRATOR: More than 60,000 American each year need a hear transplant, but only about 2,000 get one. With such a limited resource at stake, it was critically important to figure out why some transplanted hearts stayed healthy, an some developed that fast-moving form of heart disease.

DR. MURAT TUZCU: And it was a very frustrating problem for transplant heart disease doctors to hear 'that man was doing just well last night, there was no problem.' And next day he died suddenly or had a massive heart attack.

NARRATOR: Doctors need a way to find early sings of trouble inside the heart. The only tool they had was an angiogram. Since the 1950's it had been the gold standard for detecting blockages in the arteries. Pictures similar to x-rays could clearly show if plaque was obstructing the flow of blood, which could lead to a heart attack. But some cardiologists thought there had to be something more going on, something they couldn't see.

DR. STEVE NISSEN: We sometimes saw people that didn't have a lot of disease on the angiogram but had a heart attack anyway, so we suspected we were missing something.

NARRATOR: In the late 1980's, Steve Nissen began working on a bold new idea. He wanted to use the same technique as an angiogram, but instead of making an x-ray image of the center of the artery, Nissen was going to use a miniaturized ultrasound probe to scan the cells that line the artery walls. There was just one problem.

Dr. Steve Nissen at computer: interview clip: At the time we were doing this development, the smallest ultrasound devices were about the size of your fist. And we thought we could make an ultrasound device so small that we could actually put it in the coronary arteries. Now, coronary arteries are very very tiny. They're about the size of a pencil lead. And so like a radar dish goes around, it rotates around, sending and receiving these sound waves, just like sonar and when it sees the reflections come back, it makes a picture from those reflections. I will tell you it was very frustrating. A lot of the work was done in animals because of course you can't test something like that in humans until it's been perfected. And we would go into the animal lab and we would not get a picture. We would say, all right, let's go back to the drawing board. But by about 1989 or 1990, we were making pictures.

DR. STEVE NISSEN: We put one of these catheters in the coronary artery, and there it was, all that plaque that we couldn't see any other way. You could see on a television screen just as if you were literally there, and it really was like a fantastic voyage. It was a trip inside the arteries.

NARRATION: The new Technology—called Intravascular Ultrasound, or IVUS—was working and the Cleveland team was shocked by what it reveled.

DR. STEVE NISSEN: So here's an example of—of how much you miss if you just look at the old fashioned way at the angiogram. And this is an angiogram, you don't have to be a cardiologist to understand it. So you see this is the dye in the coronary, and you see everything's nice and smooth, nothing is actually narrowed. So now we're going to take you inside that artery, and we're going to show you what the ultrasound looks like. Now remember that the ultrasound's going to look at the artery in cross-section, like you took a sausage and sliced it up, and there's a gigantic plaque, which I've colored in gold for you. And then this is another huge plaque on this side of the artery, right there. So those angiograms we'd relied on since 1957, what we realized in the 1990's is that they were showing us 1% of the real disease burden.

NARRATOR: This was a dramatic new insight. A huge amount of plaque was growing in the walls of the arteries, not just clogging the center. The Cleveland team decided to test this new imaging technique on transplant patients. Maybe IVUS could help uncover which patients were developing rapid heart disease that would destroy there new hearts.

DR. STEVE NISSEN: If you're going to develop accelerated coronary disease after a transplant, it shows up after the first year. So it's very important to look after that first year, and we do this in every transplant, to find out whether there's plaque building up in the coronaries.

NARRATOR: It's one year after Ken Christianson's transplant.

NARRATOR: The ultrasound probe is carefully threaded into his heart.

NARRATOR: The doctors will compare today's image to those taken a year ago, right after Ken's transplant. If they see any new plaque, Ken's chances of surviving more than five years are slim.

DR. MURAT TUZCU: There doesn't seem to be any new development as far as I can see right now. There is really no difference from last year. We have to take this to the lab now and to compare what we see here with what we have seen last year. But it looks so far I think quite good. It is very promising.

DR. STEVE NISSEN: If you want to defeat a disease, you've got to see it, and if you want to understand it you have to be able to measure it. And that was a pivotal role that intravascular ultrasound was to play.

NARRATOR: IVUS research studies had made it clear that there was much more plaque hidden in the artery wall than anyone ever imagined. This posed a new question if there was so much plaque in the arteries—but it wasn't blocking the center—how could it still cause heart attacks?

NARRATOR: In Boston, Peter Libby had spent years researching the biology of heart disease and he was looking for answers to that question.

DR. PETER LIBBY: The disease plays tricks on us. So the patient can have no symptoms or warning and the cardiologist, using traditional tools, could be misled into thinking that things are just fine, when in fact, concealed, hidden within the artery wall, there is trouble brewing.

NARRATOR: Libby was convinces that the hidden plaque in the artery walls was the key to the unpredictable was the disease attacked, and the stubborn fact that it kept coming back even after patient has the best possible treatment.

NARRATOR: The challenge was to figure out how this happened.

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