When political journalist and “Meet the Press” host Tim Russert died suddenly on Friday, the public’s initial shock was followed by natural questions. A man as vital and energetic as Russert, chunky but vigorous, dropping dead of a heart attack at age 58 — presumably while under the kind of watchful, state-of-the-art health care that those of his stature receive? If it can happen to him, is anybody safe?
An autopsy soon found evidence of a fresh blockage in one of his coronary arteries, the blood vessels that course down the outside of the heart and provide this critical muscle with blood and oxygen.
In a tribute to Russert on MSNBC, Matt Lauer interviewed Russert’s personal physician, Dr. Michael Newman, who explained that while Russert was known to have coronary artery disease, aka “heart disease,” he had never had any symptoms, and he was being treated for the risk factors of high blood pressure and cholesterol. Russert’s struggle with being overweight was no secret, but he wasn’t having any problem keeping up with his busy primary schedule. And according to Dr. Newman, Russert had completed a sophisticated stress test on April 29 that showed “excellent cardiac function at a very high level of exercise, and no evidence of coronary insufficiency.”
It all wasn’t adding up to Matt Lauer or puzzled viewers, as Lauer interjected, “Let me just stop you there doctor, ’cause that is what I think so many people find so shocking: a stress test back at the end of April showing, as you said, no signs of diminished cardiac function, so how does this happen just a couple of months later?”
The answer lies in two common misconceptions: that a negative stress test is a clean bill of health; and a view of atherosclerosis that’s dominated by the clogged-pipe theory, where the biggest blockages cause the biggest problems.
Stress tests can’t detect small blockages
Coronary artery disease is the narrowing of the arteries to the heart due to a build up of atherosclerosis. A stress test of any kind, be it your basic treadmill test or the more complicated type Russert had, only detects blockages that are big enough to limit the flow of blood around them. Blood can squeeze past smaller atherosclerotic blockages relatively unimpeded, but when the artery gets narrowed by more than 70 percent, the blood flow starts to drop off.
Heart muscle downstream from a high-grade blockage typically does fine with that limited blood flow if the heart is resting. But as we exercise and the heart begins to rev up, the heart muscle demands more blood than can be delivered, and the oxygen-stressed heart does things that we can detect on an electrical tracing of the heart (EKG), or by looking at the heart with ultrasound (echocardiogram) or radioactive tracers.
So a negative stress test is always good news, but it doesn’t mean that your coronary arteries are clean.
Dr. Tim Henry, a cardiologist and director of research for the Minneapolis Heart Institute, is familiar with stress tests and the false sense of security they can sometimes give patients. To Dr. Henry, a normal stress test means “you don’t have to get something fixed [opened with an angiogram and stent]. It doesn’t mean you don’t have coronary disease, and it doesn’t mean you’re not at risk [of having a heart attack]. It’s really hard for people to get that.”
Small blockages can cause big problems
So stress tests only detect big blockages, and that’s the problem with them. It may seem counterintuitive, but it’s the smaller blockages that most often cause the biggest problems. It’s the small blockages that are most likely to cause the kind of sudden, no-warning heart attack that killed Russert.
Dr. Henry knows the numbers. “The main issue is that fifty percent of myocardial infarctions occur in people who, if you were to look a month before, had less than fifty percent blockages,” Henry explained. “The reason people have heart attacks is because they’re having plaque rupture, so called ‘vulnerable plaques,’ ” he continued.
Plaques are the medical term for collections of atherosclerosis, speed bumps if you will, that can develop inside an artery. The idea of the smallest plaques being the most dangerous is counterintuitive because when it comes to atherosclerosis, we’ve been using the wrong metaphor.
Atherosclerosis as inflammation
Atherosclerosis is not a passive plumbing problem; it’s not “too much cholesterol in the pipes and they get all clogged up.” The arteries aren’t clogged, per se, they’re inflamed. Damaged and scoured by the likes of high blood pressure, caustic cigarette compounds, unstable saturated fats, etc., the inner lining of the artery becomes scarred with what we call atherosclerosis: a collection of cholesterol, fat, irritated white blood cells, and scar tissue.
For a variety of reasons, smaller lumps of atherosclerosis — those that take up 30 to 40 percent of the blood-vessel space — are the most unstable. If they become too unstable, they rip open and form a rough spot inside the blood vessel, and within minutes a blood clot forms.
This little clotting trick is what keeps us from bleeding to death when we cut ourselves — the severed, damaged ends of the tiny blood vessel you clipped with a kitchen knife attracts a clot. The hole is plugged. But in this case, the trick has gone awry. Suddenly a coronary artery that was only minimally occluded is now 100 percent blocked: 30 percent by atherosclerosis, and 70 percent by the blood clot sticking to it. No blood flow means death to the heart muscle that’s downstream — a heart attack, a myocardial infarction. Mortally wounded heart muscle often flips into an arrhythmia—a very fast, quivering heartbeat that doesn’t move blood. The victim drops dead.
Presumably this is what happened to Russert. He had a small area of atherosclerosis that wasn’t big enough to show up on the radar of his stress test, nor during exercise. Per Dr. Newman, Russert took the aggressive, enthusiastic approach he had for journalism to the treadmill, and in fact, he had exercised that morning. But a little plaque ruptured, attracted a clot, resulting in a heart attack.
What makes a plaque rupture?
We know what processes contribute to atherosclerotic buildup within blood vessels, but we’re not sure of what makes a plaque unstable. Russert had his risk factors addressed except for his weight, but it still happened. According to Dr. Henry, “Known cardiac risk factors — the things that we know about like smoking, diabetes, hypertension, hyperlipidemia and family history — still don’t account for all of the risk, but inflammation is another one to consider.”
Inflammation is what one feels in the first few days of a cold, when the nose is fiery red and painful. The immune system is revved up by the cold virus, and there is a war going on. Damage to the inner lining of the blood vessels causes inflammation, too, and an inflamed, irritated plaque is vulnerable to rupture. Soothing all that damage is one of the key ways in which cholesterol drugs called “statins” (Lipitor, Zocor, Crestor etc.) seems to prevent heart attacks.
“Not only do the statins work by lowering your cholesterol,” Dr. Henry pointed out, “but one of the key ways they work is by plaque stabilization, making it less likely to rupture.”
Like Lipitor, aspirin has anti-inflammatory effects, but the critical role aspirin plays in reducing heart attacks is its ability to prevent a blood clot from forming on a ruptured plaque.
Ruptured plaques, fractured gussets
Dr. Alan Bank, medical director of research at the St. Paul Heart Clinic, has written a couple of papers on the mechanism of plaque rupture.
“We have a really unique theory, an interesting theory, that I personally believe is true and explains the process,” Bank told me. “The theory says that the reason plaques rupture is because they go through this fatigue process, or fatigue failure, which is the same thing that the 35-W bridge did, the same reason why airplane wings crack.”
It’s a theory more commonly studied in mechanical engineering, but Bank and colleagues at the University of Minnesota used computer models to study what happens to a cholesterol plaque when it’s exposed to low levels of cyclic stress. Remember, with every heartbeat (about 35 to 40 million times each year) a blood pressure wave comes careening down each artery.
“Over time, if you have certain kind of geometry in the plaque, because the plaque material is of a different stiffness than the rest of the wall, then you set up a focus of stress concentration, and it keeps hammering on one little area where the stress is focused,” Bank told me. “And then you end up with a little tiny crack and it progresses over time.”
“And in fatigue failure, like the Minnesota bridge, you don’t get a warning. The final end failure occurs catastrophically, and without warning usually.”
But why wouldn’t the biggest blockages attract the highest amount of stress? Don’t the biggest boulders in the river make the most turbulence?
“There are a bunch of reasons for that, mechanical reasons,” Bank noted. “The 20 to 30 percent lesions are more often softer plaques, where the material is less stiff — and when you have less stiff material next to stiffer material, you have more stress.”
No warning? So what’s a person to do?
The death of Tim Russert set off two emotions: mourning for the loss of such a talent, and a helpless feeling from anyone with concerns about heart disease. If it can happen to someone with the best of care, under a watchful eye, what about the rest of us?
There are two ways to know for sure if you have blockages in the coronary arteries. A positive stress test is highly suggestive but not proof positive, and a negative test isn’t an “all-clear” either. A coronary angiogram has long been the standard for evaluating coronary artery disease. It involves threading a small catheter up through an artery in the groin, then threading it up into the coronary arteries and using dye to take X-ray pictures of the blood vessels. Although it’s done routinely in specialty hospitals, a coronary angiogram is still a highly technical routine with slight but real risks — stroke or heart attack, for example. Because of those risks and because of cost, the test is reserved for those patients who doctors think are highly likely to have heart disease.
For years, this standard coronary angiogram was the only way to definitively diagnose coronary artery disease, but now CT coronary angiogram has arrived. Able to detect both small and large blockages with the precision of a standard angiogram but without its invasiveness and cost, a CT angiogram (performed in a CAT scanner in the radiology area) may well be the next step for those patients with normal stress tests but considerable risk factors.
It still comes down to risk factors
As confusing as all of this can be, from a clinical perspective Drs. Bank and Henry see the message in Tim Russert’s death in a similar way. A negative stress is good news but no guarantee, and treating risk factors aggressively is the key.
“Everyone should be aware that heart disease is still the most common cause of death in the country, and that it can come on suddenly,” Dr. Henry told me.
“And what can they do to prevent it? Number one, everyone can be aware of their risk factors and treat them. Number two, if you have known coronary disease, you need to take your aspirin and have all your risk factors completely under control.”
Dr. Craig Bowron is a Twin Cities internist and writer who reports on medical topics for MinnPost. He has contributed to The Rake, City Pages, Star Tribune, Pioneer Press and Minnesota Public Radio. He can be reached at cbowron [at] minnpost [dot] com.