Goodbye, Mr. Russert

Tim Russert died suddenly today. I admired his journalism, his ability to press questions that has become so rare. He didn’t seem to suffer from the “two-side-ism” that has become so common in today’s journalism; he realized that some issues don’t have two valid opposing views. But others will eulogize him. I’d like to talk about why he died.

Of course, we don’t know very much at this point. What we do know is that it was sudden.

There are a number of reasons for someone to suddenly drop dead, the most common having to do with the cardiovascular system. Pulmonary embolism and massive stroke can sometimes present as sudden death. A common cause, though, is a clinical entity known as “sudden cardiac death” (SCD) .

Sudden cardiac death is very common, killing around 300,000 Americans every year. Most of these people are found to have underlying coronary artery disease. Other causes include hypertrophic cardiomyopathy (seen in young people), and various inherited heart rhythm disturbances, such as long QT syndrome.

Sudden cardiac death, by definition, happens quickly. The person experiences little warning, goes down, and dies. There is no lingering. Still, the proximity and availability of emergency care can make a difference. Automated external defibrillators (AEDs) are becoming more common, and can save lives if used immediately.

Most SCD is due to underlying coronary artery disease. How does this lead to sudden death?

Usually, SCD is caused by a fatal arrhythmia, or disturbance in the normal beating pattern of the heart. This can happen for many reasons—previous damage to the electrical system from heart attacks, electrolyte disturbances, drugs and medications, and structural heart problems such as dilated cardiomyopathy.

It is very difficult to save someone from SCD—they must be very lucky and have sophisticated help nearby. So, like most things medical, prevention is very important.

Since most SCD is associated with coronary artery disease (CAD), identification and treatment of underlying CAD can save lives. There are many online tools available to help you evaluate your own risk.

Risk is divided into two categories: fixed, and modifiable. An example of a fixed risk factor is family history. If your father had a heart attack at thirty, you are at increased risk and there’s nothing you can do to change that fact.

The most important modifiable risk factors are high blood pressure, high cholesterol, diabetes (sort of), and cigarette smoking.

We know quite a bit about treating heart disease. A complete evaluation by a primary care physician in an invaluable tool in reducing your risk of heart disease and many other illnesses.

On my old blog I compiled a list of things you should ask your doctor:

  1. What is my blood pressure? Is it OK?
  2. Have I been checked for diabetes?
  3. How is my cholesterol? Is that OK?
  4. Am I due for any vaccinations?
  5. Do I need any cancer screening, such as PSA, colonoscopy, mammogram, pap smear?
  6. How is my weight? What is my body mass index (BMI)?
  7. Here is my medication list–does it match yours?
  8. What is my overall cardiac risk? (e.g. see this link, or this one).
  9. How do I quit smoking?

Tim Russert was a relatively young man, at the height of a remarkable career. Many people who die suddenly leave behind family and friends with no chance to plan for their own deaths. Despite what some of the modern shamans out there might say, my job as an internist focuses very strongly on primary and secondary prevention. Stop by and see me some time.


  1. Egaeus

    I actually first heard about this in a doctor’s office. I’m not a big fan of TV news, but Tim Russert has always struck me as a decent journalist, much better than the hacks on Faux News.

    And you’ll be pleased (or worried?) to know that I thought about you today. While rereading the literature sent to me by the retinal specialist I visited today, I noticed that they listed the Christian Ophthamological Society as one of their affiliations. They’re a creepy group. I was less than thrilled, especially since there was a chance that someone with, in my opinion, a tenuous grasp of reality would be lasering my retinas. I couldn’t help but wonder, “What would PalMD do?”

    I ended up letting the religious guy laser my retinas, as it did turn out that I was in the first stages of potentially going blind from a retinal detachment (hooray myopia). The guy who was assisting, who shared my disbelief, assured me that despite his deep religious convictions, HlbMD knew what he was doing.

  2. Since you touched on this, it isn’t too much off topic (I hope.) I saw the report from the ACCORD study showing an increased risk of mortality from cardiovascular events with more aggressive diabetic control. It seems that, at some point, the side effects of the medication outweigh the benefits. What’s the professional take on this?

  3. Ian Tindale

    Whew, that’s a relief. It only affects Americans.

  4. Russert had a fractured ankle during the winter and was on crutches for a prolonged period. He just returned from Ital, where he had taken several long flights. He was obese and he had a history (publicly reported) of cardiovascular disease. My money is not on SCD but rather a likely embolus.

  5. According to wikipedia,

    “An autopsy, performed on the day of his death, determined that his history of diabetes mellitus and coronary artery disease led to sudden cardiac death. The immediate cause of death was an occlusive coronary thrombus.[25][1] On the special reports program, Russert’s friend Dr. Michael Newman stated that the autopsy showed coronary artery disease in the left anterior descending artery, and a fresh blood clot was visible on one of these plaques.”

  6. natural cynic

    I heard one report say that Russert had a negative stress test at the end of April this year. Confirmation?

    And Bill [and PalMD], the ADVANCE study – a larger study from Australia – reported this year [most recently at the San Francisco Meeting of the American Diabetes Assn last week] showed that there was no higher cardiovascular risk with tighter control in Type 2 diabetics. The same findings were the result of the American VA study also reported in the SF meeting. The main takeaway message is the control over blood pressure and hyperlipidemia are crucial while blood glucose control may not be.
    See here for blog, and here

  7. NC, I address some of that in the post referenced above.

    Diabetics not infrequently have false negative stress tests, especially if they have balanced triple vessel disease.

    Also, not all AMIs are from critically stenosed arteries. Arteries with non-critical stenosis may still have an unstable plaque that can rupture, causing an acute occlusion.

  8. Clarissa

    If I had a doctor who as an atheist, and disrespected my beliefs, that would make me nervous too.

    I have met some arrogant pricks working in hospitals…I have not notice that they are especially good doctors because of their self importance.

  9. If we are going to speculate, I would put in low NO as a long term complicating factor, and perhaps as an acute precipitating factor.

    Diabetes is associated with low NO. Hyperglycemia is a major compensatory factor to not enough mitochondria. Mitochondria make ATP using O2, if there are not enough mitochondria more ATP needs to be made via glycolysis which requires 19 times more glucose for the same ATP production. NO is what determines the number of mitochondria that one has. Not enough NO results in not enough mitochondria which then requires hyperglycemia to cope with. Hyperglycemia then generates superoxide which can then exacerbate the low NO.

    I think the trade-off of hyperglycemia and ATP production is what caused the increased mortality in that study due to “tighter” blood glucose control. Too much glucose in the blood does cause chronic problems, but too little glucose in the extravascular space (where it really matters, next to the cells that are taking it up) is worse. Most tissues don’t get glucose from the bulk blood but from the plasma flowing through the extravascular tissue where the glucose level is lower (because intervening cells consume it). It is extremely difficult to measure glucose levels there, but that is where it is most important.

    Low NO also causes osteoporosis. The fundamental regulation of bone stiffness is via bone strain causing the release of NO which causes deposition of bone mineral where the NO level is highest.

    NO is a major factor that regulates acute vasodilation. NO activates sGC which generates cGMP which causes the smooth muscles of the arteries to relax. NO is also what regulated O2 consumption by mitochondria. Under conditions of hypoxia, mitochondria generate superoxide which pulls down the NO level, and disinhibits cytochrome c oxidase which pulls down O2 levels allowing more O2 to diffuse to the hypoxic site. If NO/NOx status is compromised, then that vasodilation may be impaired. An acute blockage causes local hypoxia which can cause local high superoxide and local low NO levels causing local vasoconstriction or vasospasm. Hemoglobin is the normal sink of NO, so hemoglobin tied up in a clot may serve as a sink of NO and cause local constriction at the clot site.

    There are a number of mechanisms by which hypoxia causes NO production from nitrite. Nitrite is broadly protective against damage due to ischemia in animal models.

    NO inhibits the cytochrome P450 enzymes, one of which is responsible for the generation of vitamin K, (Cytochrome P450-2C9) which is a major clotting factor. Usual treatment for excessive coagulation is warfarin (yes, the same warfarin that is used as rat poison) which is a pretty specific inhibitor of that enzyme. NO is also a factor that makes the inside surfaces of blood vessels less sticky.

    He had just flown back from Italy, which means he had been exposed to low O2 (aircraft are not pressurized to one atmosphere but to a lower pressure), which may have increased superoxide production. Air in aircraft typically has a slightly higher level of ozone depending on the altitude the plane is flying at and how good the catalysts are that the aircraft is using to destroy the ozone. Ozone destroys NO and induces oxidative stress. The nasal passages produce a lot of NO, so that the air that reaches your lungs has a couple hundred ppb NO when it reaches them. That NO is reduced by contaminants in the air, particularly particulates but also by cold air, by dry air and by air with a lower O2 level.

    Any kind of travel is always a disruption to one’s normal routines, different food, different time schedule, different activity levels, different sleep levels. Balancing insulin requirements when everything else is changing has to be more difficult. The normal stress response is to lower NO levels.

    From what has been reported it sounds like a plaque rupture which is very hard to predict. Atherosclerotic plaques are complex things that form on some arteries. They are usually composed of mostly of lipid and fibrotic tissue and to some extent infiltrated by macrophages. What usually causes an acute rupture is when the macrophages release proteases which dissolve the fibrotic tissue too fast and it gives way. One of the things that cause macrophages to do that is superoxide. That normally accompanies inflammation where it is necessary to clear out what ever protein gunk is at the site of inflammation that needs to be cleared out. NO tends to reduce inflammation by inhibiting NFkB. I think the chronic systemic inflammation associated with all of the degenerative diseases is due to low NO.

  10. I just came across a pretty good and fairly extensive review of the physiology and risk factors for diabetes, pre-diabetes, and cardiovascular diseases, extremely relevant to Mr. Russert’s case.

    I haven’t read the whole thing carefully yet, and can’t really address the non-NO stuff in it, but they do have a pretty nice discussion (starting on c19) on the involvement of NO. I think their discussion of peroxynitrite is a little overblown, superoxide is an anion and is confined by lipid membranes, so the site of NO destruction is inside the structures that make superoxide (mitochondria and microsomes) because the superoxide is vectorally produced to the inside. Superoxide can’t get out, but NO can get in. Peroxynitrite can’t get out either, but NO2 from peroxynitrite can.

    They do mention that supplemental antioxidants don’t seem to work and suggest trying to find things that suppress free radical formation farther up stream. That is actually what NO does. If you have enough NO, then at the site of superoxide formation it forms peroxynitrite which regulates the formation of superoxide. If you don’t have enough NO, the site of peroxynitrite formation is different and it causes diffuse damage rather than precise regulation.

  11. I admired his journalism, his ability to press questions that has become so rare. He didn’t seem to suffer from the “two-side-ism” that has become so common in today’s journalism; he realized that some issues don’t have two valid opposing views.

    This description bears little resemblence to the Tim Russert that actually existed in the real world. For better eulogies of Tim Russert, please see here, here, here, here and here. Russert also was responsible for one of the most dishonest and absurd public debates in recent political history (see more here and here).

    To head off criticism, it is irrelevent to me that Tim Russert was a nice man in his private life. He is a public figure know for his public work as a journalist. If an engineer designed a bridge and it fell down, if a shipright built a ship and it sank, if a contractor built a house and it collapsed, they would not be remembered fondly for their personal warmth or caring. They would be condemned for their incompetance and idoicy.

    De mortuis aut bene aut nihil mendacium est.

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