Tim Russert’s Death: Questions, Answers
from WebMD — a health information Web site for patients
June 17, 2008 — Newsman Tim Russert’s death last Friday from a heart attack caught many people by surprise.
NBC News reports that Russert, 58, collapsed at work and that resuscitation attempts were made at a nearby hospital, to no avail.
Russert’s doctor, Michael Newman, MD, says an autopsy showed that the heart attack was caused by cholesterol plaque rupturing in a coronary artery and that Russert had an enlarged heart.
Russert was known to have coronary artery disease that was well controlled with medication and exercise; he had performed well on a stress test in late April, according to NBC.
WebMD spoke with three cardiologists — none of whom was treating Russert — about Russert’s death:
* Cam Patterson, MD, chief of the division of cardiology at University of North Carolina at Chapel Hill.
* Robert Ostfeld, MD, cardiologist Montefiore Medical Center in New York.
* Douglas Zipes, MD, past president of the American College of Cardiology and distinguished professor of medicine at Indiana University.
Russert’s heart attack was caused by a sudden coronary thrombosis that happened when cholesterol plaque ruptured in an artery. Please explain how that happens.
Zipes: What happens is a cholesterol plaque builds up on the inside wall of the artery, and when the cap of the cholesterol plaque is weak, it can then rupture, spewing cholesterol and other chemicals … into the bloodstream. When the [chemicals] come in contact with platelets, the platelets clump and occlude the coronary arteries [causing a heart attack].
Patterson: Based on the physician’s report that we heard and also what we know about the natural history of this process, he’d had coronary artery disease for many, many years, if not decades, and he probably had plaque that built up over many years due to factors — some of which may be under his control, some of which may be outside of his control — that led to cholesterol buildup in the arteries around his heart. And at some point on Friday — for reasons that none of us are able to understand or predict, even with the best tests — his plaque ruptured.
Ostfeld: Atherosclerosis, the disease that may ultimately lead to a heart attack, is a disease process that develops within us over decades. This is a disease process that starts very early in life.
Is there any way to predict plaque rupture?
Patterson: Not right now. There’s no test we can do in humans to predict that. We’re working on developing tests, but they’re really in the animal model stage right now for identifying vulnerable plaque.
There are some therapies that we know reduce the frequency of plaque rupture. In particular, high-dose statin therapy. The other thing that I think is important from a therapeutic standpoint is the power of aspirin. Aspirin can certainly help to prevent or reduce the complications related to plaque rupture.
Russert’s coronary artery disease was said to be well controlled with medication and exercise. Why did his heart attack happen anyway?
Patterson: When we talk about having coronary disease being well controlled, what we usually refer to are the symptoms of chronic blockages. And it’s important to remember that chronic blockages are very different from plaque rupture, which is what killed him. He may very well have been treated very effectively to reduce symptoms from the chronic blockages, but we don’t have any therapies that specifically prevent plaques from rupturing.
Would he have been a candidate for more aggressive treatment?
Zipes: I’d need to know more about him. For example, if he had significantly reduced heart function — an ejection fraction of 35% or less — he would have been a candidate for an implantable defibrillator.
Is it possible that the care he did get actually did prolong his life?
Ostfeld: That’s a great point. That’s very possible. It’s possible that without having his medical problems treated and without having a healthy lifestyle, his heart attack may have been 10 years earlier.
The autopsy showed that he had an enlarged heart. How does that happen, and how might that have played a role?
Zipes: It could be that he had previous heart attacks, and that can then produce scarring and dilation of the heart. A heart attack, in about 10% of individuals, may be asymptomatic, so you have no chest pain associated with that. It’s even higher in diabetics, and I read some place that he was diabetic, so he could have had an asymptomatic heart attack in the past. Or he could have had other causes. … Most commonly, given the autopsy and what happened to him, it was due to the coronary disease.
Does having diabetes make it harder for people to be aware of heart attack symptoms?
Ostfeld: Yes, that’s quite possible. Sometimes people can have a “silent” heart attack where they actually had death to part of the heart muscle — the heart attack — but did not feel it, and that is reportedly more common in people with diabetes because they may have some nerve damage that may reduce their ability to feel that.
His coronary artery disease was asymptomatic — that’s silent heart disease?
Patterson: That’s silent heart disease. It’s important to remember that half of people who have heart attacks don’t have symptoms before they have a heart attack.
How would someone find out that they have that?
Ostfeld: There are a handful of ways that we can predict future risk and/or specifically screen for atherosclerosis that may not be clinically apparent. Routine screenings are things like cholesterol and high blood pressure and diabetes — things that, if elevated or present, may significantly increase your future risk of heart disease. Those should be part of routine evaluation.
Other tests include a blood test looking for inflammation in the body; one blood test is a high-sensitivity CRP test. But it is not clear that checking this blood test will always modify how we treat the patient.
There are more expensive tests that can be performed that look directly at blood vessels, looking specifically for atherosclerosis. Two such tests are a carotid ultrasound test that looks at the thickness of the blood vessel, something we call an IMT … if it’s thick, that suggests that there is atheorscloerosis present.
Another imaging study is a heart CT can or heart CAT scan, which can look for calcium in the blood vessels and or look at the blood vessels themselves to see if signs of atherosclerosis are there.
Zipes: Heart scans can be useful. In general, they’re expensive and generally not paid for by insurance, but if someone can afford it, yes, that’s a very reasonable thing to do.
Osfteld: It’s important to know that [some] CAT scans do have risk. The one that looks specifically at the blood vessels [sometimes called a “noninvasive coronary angiogram’] … has more than trivial radiation and may increase cancer risk down the line. So these are not tests that I believe should be done on everyone. Others would argue otherwise, but I believe that should be individualized as well, and, I believe, done under the care of a physician.
Russert did well on a stress test in late April. What does a stress test tell you, and if you do well on one, does that mean you’re in the clear?
Patterson: The critical question is what does it not tell you. Stress tests don’t tell you about the presence of vulnerable plaque. Plaque doesn’t have to obstruct blood flow to be vulnerable. The only thing that a stress test will tell you is if you have enough plaque to obstruct blood flow.
The fact he had a normal stress test is good prognostically; it put him in a lower-risk bundle. But it doesn’t take his risk down to zero and it does nothing to identify whether he had plaques that were vulnerable and at risk for rupture.
Ostfeld: Every test is different and needs to be interpreted differently. But if someone has an excellent stress test, that would predict a very low risk of a short-term event and is largely reassuring. However that does not obviate the need, of course, to continue to have a healthy lifestyle and to be sure problems are well controlled.
If someone already has atherosclerosis, is the goal to prevent it from worsening or is the goal to undo it?
Ostfeld: The goal is to make the person as healthy as possible and to improve the health of the blood vessels as much as possible. We’ve learned that many of our therapies, although they may not change the absolute amount of atherosclerosis in a blood vessel, they improve the health of that blood vessel very much. So it may be that the health of the blood vessel itself is the key aspect. We know that a healthy lifestyle and appropriate medical therapy can improve the health of the blood vessels, so those things are obviously very important.
A lot of people may still have the idea of plaque being something that clogs the arteries like hair in a drain. Can you explain to them how they should picture it inside the walls and how a blockage and rupture happens?
Patterson: Plaque can be the kind of buildup you’re talking about — that’s where the water doesn’t flow through the drains right. But that’s not really what a vulnerable plaque is. If you want to think about what a vulnerable plaque is, it’s like having a pimple in the side of a blood vessel wall, a pimple that’s prone to open up and rupture. It’s when that rupture occurs that the blood will clot and the heart attack will happen. So it’s really a very different process, fundamentally, than the obstruction of the flow of blood.
Would you expect that Mr. Russert’s death is a wake-up call?
Ostfeld: I think that’s a great way to look at it. Out of this tragedy, maybe positive things can arise. Atherosclerosis, and diseases related to it, is the No. 1 killer of adult men and adult women. Also, when you have atherosclerosis, although you may not feel it, your blood vessels do not function as well as they could. So it may reduce, subtly, your quality of life, as well.
Zipes: If they are symptomatic — palpitations, chest pain, shortness of breath, dizzy spell, blackout spell, go see a doctor. No. 2, routine evaluations of individuals after the age of 50 is a very reasonable thing to do. Early presentation of heart disease could be picked up at that time. If he had significant coronary disease, as apparently he had, very aggressive treatment with statins, ACE inhibitors, aspirin, beta-blockers, are indicated.
Patterson: No. 1: Have a dialogue with your physician about your risk and whether you’re at high risk or not. No. 2: Identify those things under your power to control and to change those that you can. No. 3: Make those changes as part of a lifestyle commitment and not as a diet you fall on and off of; it really needs to be a lifestyle commitment. No. 4: Understand that cardiovascular disease is the No. 1 cause of death and disability in our society, so it’s something you really can’t afford to ignore.
What would you want women to keep in mind, because it’s the No. 1 killer of women as well?
Patterson: My comments to women are these. The No. 1 disease women are afraid of is breast cancer, but the No. 1 cause of death in women is heart disease. The second point to make is symptoms of heart disease are frequently much more subtle in women and much more difficult to diagnose, so women shouldn’t allow themselves to be judged by the same standards as men in terms of whether or not they’re having symptoms of heart disease or whether or not they’re at risk for heart disease.
Ostfeld: Women are approximately six to seven times more likely to die from heart disease than they are from breast cancer. Clearly, you do not want either, but it highlights how critically important it is for women to take their heart health very seriously as well.
What else would you want to add?
Ostfeld: If someone looking for a magic bullet to protect themselves from heart disease, the closest thing we have to that is exercise. It is healthy for us in so many ways. I would encourage people, under the guidance of their physician, to structure an exercise plan that works for you.
Patterson: Heart disease is the No. 1 cause of death and disability in our society. We’ve done a great job reducing the amount of heart disease in the United States over the past several decades, but it’s still the No. 1 health problem that we face. And we’ve got a long way to go to get to the point of a) being able to diagnose problems like vulnerable plaque and b) being able to reduce the risk of heart disease to zero. And those are the two goals that really stand at the forefront of cardiovascular care.
Zipes: Stress the importance of having a defibrillator available and to use it promptly. One of the things I’ve advocated for some time is that youngsters in high school or even younger be taught how to use a defibrillator and then to have them as available as fire extinguishers.
It’s something someone that young could master?
Zipes: Without question; absolutely. There are studies, actually, showing that grade-school kids can learn how to use a defibrillator. I’ve advocated that like you learn driving or typing or whatever; this ought to be part of public health education.
Editor’s note: Zipes spoke with WebMD before Russert’s doctor, Michael Newman, MD, told CNN’s Larry King that Russert had been treated with a defibrillator three times after collapsing at NBC and before arriving at hospital. Newman wasn’t sure why defibrillation didn’t save Russert, but he told King that successful defibrillation may be harder in large people with large hearts.
WebMD Medical News: ” Tim Russert Dies of Heart Attack.”
Cam Patterson, MD, chief, division of cardiology, University of North Carolina at Chapel Hill.
Robert Ostfeld, MD, MSc, cardiologist, Montefiore Medical Center, in New York.
Douglas Zipes, MD, past president, American College of Cardiology; distinguished professor of medicine, Indiana University.