The Doctor Weighs In

By Pat Salber

When I was a practicing Emergency Physician, I always used to volunteer to work Super Bowl Sunday. Two reasons: 1) I could care less about football, and 2) It is the one day of the year when no one, and I mean no one, comes to the ER. Whole families on their second week of a cold show up on Christmas Eve. Folks drop by to have their skin rashes checked out on Thanksgiving Day. New Years Eve and New Years Day – busy, busy, busy. But Super Bowl Sunday, while the Super Bowl is on, is dead quiet.

If you talk to emergency physicians, they all have stories about the guy who got chest pain during the first quarter, but held out, sweating and breathing hard, until the game was over. By the time this fellow actually showed up in the ED, his heart muscle had been starved for oxygen for quite some time and the damage was worse than it would have been if he had shut off the TV and dialed 911.

Turns out, according to a study presented at last year’s American College of Emergency Physicians’ 37^th annual scientific session, that some guys (and it is mostly guys), do delay seeking emergency care if they are watching a game. Dr. David Jerrard of the University of Maryland Medical Center in Baltimore and colleagues tracked ER visits over a three year period during and immediately after 800 postseason professional football games, major league baseball games, or Division l college football or basketball games. They found that on the days that games were televised, more men were seen in the 4 hours following the event than were seen during the same 4-hour period on nongame days.

An internet report on the study published on Daily News Central quoted Dr. Jerrard as saying, “Men should not risk their health by putting off going to the emergency room because they want to see the final results of a football game. It could be the last game they ever see."

A more recent article, titled “Super Bowl Could Be Heart Health Hazard,” describes the results of another research study. The investigators looked at cardiac events in Germany (greater Munich area) during the World Cup competition in Germany in the summer of 2006. They analyzed results from 4,279 patients. The results showed that cardiac emergencies were more than double the norm on the seven days when the German team played – it was triple for men. The effect was the strongest for people with known heart disease. Ok, this study looked at soccer fans soccer…I believe we can extrapolate the results to American football fans as well...are they any less rabid?

Considering the learnings of these two studies together, leads me to make two recommendations:

• If you have known heart disease, be sure you take your cardiac meds (including aspirin if prescribed) and have your nitroglycerin handy.
• If you get chest pain (or any other serious symptoms) during the game, get yourself to the ER.

Chances are the game is going to be on all of the TV sets in the hospital anyway so you probably won’t miss much. Besides, you can always record it or watch the recaps on ESPN. I am willing to bet that if your problem turns out to be serious, you probably won’t really care who won or lost the game anyway.

by Bill Bestermann, MD

I recently recorded “New Measurements Such as the Coronary Calcium Score Can Determine the Risk for Heart Attack” with Dr. George Lundberg at the American Heart Association Annual Scientific Sessions in Orlando. I want to thank my colleagues at “The Doctor Weighs In” for making this possible for me. The invitation to submit the editorial came directly from a blog entitled "New Technology to Determine Risk of Heart Attack" that I had written in this space that was posted in October 2007 and I would refer you to that piece for more detail on this topic. The video editorials are all very brief and present the idea in its most condensed form. You can access this video editorial at The Doctor Weighs In Video Editorials.

The knowledge surrounding unstable plaque continues to move forward rapidly. Recent studies of the coronary arteries using intravascular ultrasound examination of all three major vessels at the time of acute myocardial show multiple plaque ruptures. On average, patients had two active lesions with some patients having as many as 6 recent plaque ruptures. On coronary angioscopy, vulnerable arterial surfaces appear yellow and these lesions are very widely distributed in the coronary artery system leading to the concept of pan-coronary arteritis or multifocal plaque rupture.

A study of 48 thrombi in 50 ruptured coronary plaques in 30 patients showed that healing was slow and clot was persistent. When patients were re-examined at 13 months, 35 of the 48 thrombi were still present and only 23 of the ruptured plaques were healed. As these plaques healed there was a progression of fixed stenosis. The serum CRP was lower in the healed plaque rupture patients than in those whose arterial injuries had not healed. All of this supports the concept of a diffuse and dynamic process that is best approached with optimal medical therapy.

Keywords: coronary, angioscopy, plaques, stenosis, calcium score, arteritis, measurements, pan-coronary.

By Dov Michaeli MD, Ph.D

Stem cell research is hot, and getting hotter. Big deal, you might think. This esoteric topic may be important for some scientists, or maybe a few politicians—but what’s in it for me? Let me tell you right off: a lot more than you can imagine. Just consider the statistics, and do the math of your odds requiring one day stem cell therapy.

Heart disease:

• Almost 1 out of every 2.4 deaths in the USA result from cardiovascular disease, or CVD.
• Since 1900, CVD has been the leading cause of death in every year but one - 1918. In that year, the main cause of death was the Spanish Flu pandemic.
• About every 29 seconds an American will suffer a coronary event.
• About every 60 seconds, someone dies from one.
• At least 250,000 people die of heart attacks each year before they reach a hospital.
• It is a myth that heart disease is a man's disease. In fact, cardiovascular diseases are the number one killer of women (and men). These diseases currently claim the lives of more than a half a million females every year - more than the next 16 causes of death put together.

Diabetes (type 2):

· As of 2005, 20.8 million people—7.0% of the population—had diabetes; According to recent CDC figures, there are approximately 798,000 new cases of type 2 diabetes annually in USA, most are Type 2 diabetes.

· According to the WHO figures, there were 173 million cases of type 2 diabetes worldwide in 2002.

· Type 2 diabetes confers a two to four-fold greater risk of coronary heart disease among men and a three to five-fold increased risk among women.

· Diabetes also magnifies the effect of raised cholesterol levels, raised blood pressure, smoking and obesity and so influences coronary heart disease risk indirectly.

· Number of deaths with diabetes as underlying cause of death climbed form 34,500 in 1980 to 62,000 in 1996—an increase of over 44% in 16 years.

· Diabetics use medical resources at a higher rate than average nationwide. Diagnosed diabetics constitute about seven percent of the total population, but diabetes costs account for about 13-14% of all health care expenditures. Diabetes treatment costs about $113 billion a year - more than three and a half times as much as the care for non-diabetic patients.

Alzheimer’s disease:

· There are now more than 5 million people in the United States living with Alzheimer’s. This number includes 4.9 million people over the age of 65 and between 200,000 and 500,000 people under age 65 with early onset Alzheimer's disease and other dementias. This is a 10 percent increase from the previous prevalence nationwide estimate of 4.5 million.

· Every 72 seconds, someone develops Alzheimer’s.

· Without a cure or effective treatments to delay the onset or progression of the Alzheimer's, the prevalence could soar to 7.7 million people with the disease by 2030. By mid-century, the number of people with Alzheimer's is expected to grow to as many as 16 million, more than the current total population of New York City, Los Angeles, Chicago and Houston combined.

· As the prevalence impact of Alzheimer's grows, so does the cost to the nation. The direct and indirect costs of Alzheimer's and other dementias amount to more than $148 billion annually, which is more than the annual sales of any retailer in the world excluding Wal-Mart.

Parkinson’s disease

· There are about 1.1 million people in the U.S. diagnosed with Parkinson’s disease. This is a rate of about 360/ 100,000 people. The rate for people over 65 is about 3%.

· The most detailed report on the economic impact of PD was prepared in 1998 for the Parkinson's Disease Foundation. This study estimated the per-individual yearly cost of PD in 1997 at $24,041 ($24,425 in 1998). Based on a prevalence of one million affected individuals, the total economic burden was calculated at $24 billion.

So there you have it. I listed only four diseases that may be amenable to stem cell therapy. The reason I included the costs of these diseases is to highlight the cost to you, in the form of health-care insurance and direct costs, before you die.

What is a stem cell?

Just think of it as the stem of a plant, which gives rise to the branches and leaves. The developing embryo is formed by a few cells that have the potential to develop into any of the body’s almost 200 cell types. We call such cells ‘pluripotential’, and when their origin is from an embryo they are called ‘embryonic pluripotential cells’. It turns out that every fully formed tissue-- be it blood, neurons, heart—maintains a small reservoir of pluripotential cells, albeit less “pluri” than the embryonic ones, because they are destined to develop into only one or a few specific tissues. This is biology’s form of insurance, in case a certain tissue is in need of repair or regeneration. Alas, in the course of evolution we lost our capacity to regenerate new heart muscle or new brain cells, although the cells are still there, dormant.

The big debate the country went through was over the use of cells derived from a (discarded) blastula (an early stage of embryonic development, consisting of a spherical layer of around 128 cells surrounding a central fluid-filled cavity). Some people saw it as tantamount to murder; others saw the tilting of the moral balance in favor of a discarded agglomeration of 128 cells over the suffering of millions of living people as incomprehensible, if not unconscionable.

The new discovery: genetically manufactured stem cells

Last week Shinya Yamanaka of the University of Kyoto reported that his team has created pluripotent cells from human skin cells, or fibroblasts. On the same day, a team of researchers led by James Thompson at the University of Wisconsin, Madison, reported the same. Do you get the sense that there must have been a fierce race underway to reach this goal? You are absolutely right. Here is what happened.

Last year Yamanaka discovered that introducing four proteins called transcription factors into mouse skin cells ‘reprogrammed’ the cells into embryo-like state. There are thousands of different transcription factors in every cell nucleus, and their function is to regulate gene expression. The discovery that only four transcription factors can induce such a profound change in the character of a cell is astounding. But this was in mouse, and there are basic differences between human and mouse cells. Yamanaka knew that his publication would trigger an intense race to accomplish the same feat in human cells. He worked 16 hour a day, seven days a week, and reported last week that the same four factors produced the same results in humans. The cells were taken from the face of a 36-year-old Caucasian woman. He repeated the exercise with cells from joint fluid from a 69-year-old man with similar results.

Back in Madison James Thompson read Yamanaka’s mouse experiment with more than passing interest. After all, he was the discoverer of the method to propagate human embryonic stem cells. He immediately set out to repeat Yamanaka’s experiments in human cells, with two differences. The first was the source of the skin cells: he obtained them from foreskin, which is fertile ground for a lot of internet jokes but is otherwise of no import. The other difference is important; he used four transforming factors, but only two of the ones used by Yamanaka. He avoided one factor, c-myc, because it is associated with cancer. The fact that he could use different transforming factors suggests that in the future, scientists will have great latitude in the formation of ‘induced pluripotent stem (iPS) cells’, maybe of different traits and capabilities.

The future is bright

These were the first two teams to reach the finish line. Many more are still racing. With researchers crowding into the field rapid advancements are certain. As several scientists ecstatically stated, this is a paradigm shift in reprogramming cells, and will relatively soon result in patient-specific pluripotent cell therapy. Many obstacles remain, but all are surmountable; the big breakthrough has been accomplished. The grim statistics of heart disease, diabetes, neurological diseases, and probably cancer, will become a lot less menacing.

Dov Michaeli MD, Ph.D is in the biotech industry

By Dov Michaeli MD, Ph.D

Phew…that was something. We ate and we ate, and drank and drank—I thought we are going to burst. Literally. I hope everybody in our Thanksgiving party (over 30 people) survived intact. Being a doctor, and a worrier, the thoughts of what could go wrong were never quite banished by the pleasures of gluttony. What dangers were going through my mind?

The burst stomach

Have you ever seen a snake swallowing a whole turkey? You can actually see the poor creature traveling through the long intestines of the tubular glutton. Well, a burst stomach is extremely rare, and happens only in rare conditions where the brain center controlling hunger and satiety is malfunctioning. Normal stomach capacity is about 8 cups, although it can range form 4 to 12, according to Dr. Edward Saltzman of Tufts Medical School, quoted in a New York Times article on the hazards of Thanksgiving. But for us regular gluttons, there are more common dangers lurking in stuffing our faces.

Heart attacks

This is probably the most serious problem of serious overeating. Here is what happens:

A normal meal of about 1500 calories sits in the stomach 1-3 hours, depending on the amount of fat in the diet; fat slows down stomach emptying. How is this night different from all other nights? The average American consumed yesterday 4500 calories and 229 grams of fat, according to the Calorie Control Council (full disclosure: they represent the makers of low-calorie foods). The average time to empty this humongous amount of fatty food is 8 hours. This in itself can cause only a sensation of fullness (loosen your belts) and flatulence (leave the room, please). But what goes on in your physiology is more serious: in order for the stomach and intestines to perform their job, they get an increased supply of blood coursing through the arteries and veins that supply them. This blood is diverted from vital organs such as the heart (vital for all of us) and the brain (less vital for some people I know). Now if instead of 1-3 hours the blood has to take an 8 hour detour, and a lot more blood diverted, to boot, and you can see the stress the heart and the brain are undergoing. In fact, if the blood supply to the heart is marginal to begin with, this massive diversion of blood volume will tip the balance and result in a heart attack.

To add insult to injury, the high fat content in a typical Thanksgiving meal results in a massive influx of lipids and triglycerides into the blood. This situation, called hyperlipidemia and hypertriglyceridemia, causes an increase in platelet aggregation. Those tiny cells, when sticking together to form a platelet clot, can cause blockage of the coronary precipitating, yes you guessed it, a heart attack. The combination of reduced volume of blood flow to the heart, and the increase in blood coagulability is more than additive; the risk is not 1+1=2, it is more like 1+1=10.

The gall of it all

In order to absorb dietary fat our digestive system needs to break it up into microscopically small particles. This is accomplished by the bile, a juice flowing from the gallbladder. Sometimes, the solids in the bile precipitate out and form gallstones. They can then occlude the bile duct, the narrow outlet from the gallbladder to the small intestine. When there is a lot fat in the diet, the hormone chlecystokinin signals that a large amount of bile is required. But if the bile duct is occluded the bile backs up, and the result is excrutiating abdominal pain that may mimic the pain of a heart attack.

What about the brain?

Here the consequences can be just as serious. The reason we feel drowsy after a heavy meal is that blood supply to the brain is reduced. This in itself never killed anybody. But add to this the amount of alcohol we consume with the meal—and put us behind the wheel, and you can see why the accident rate is sky high and Highway Patrol is out in force on Thanksgiving Day.

Before you rush to your computers to berate me for omitting your favorite culprit or theory, here is one subject you shouldn’t bother about: the urban legend that the amino acid tryptophan is the culprit of the meal-induced drowsiness. Tryptophan is indeed the precursor of melatonin, the sleep-inducing hormone. But the amounts required to increase significantly the level of melatonin are much higher than even the most outrageously gluttonous feast can provide.

Now that I told you how badly we behaved yesterday, did I restrain myself? As they say in New York, fuggeddaboudit; I stuffed my face and enjoyed every calorie of it. Today, though, starts the hard task of atoning for my sins. But I enjoyed it while it lasted. I hope you did too.

Dov Michaeli MD, Ph.D is in the biotech industry.

By Dov Michaeli MD, Ph.D

Have you heard the one about the boy who ran through the kitchen into the backyard and dropped dead? No, this is not a bad joke. It is a real case report published in the 80’s. Imagine, if you will: a young boy with known allergy to fish running through the kitchen while his mother is boiling some fish stock. He inhales a few molecules of the fish protein that dissolved in the cooking vapor, and dies within minutes! To put things in perspective: we are not talking here about toxins, that can kill at microgram concentrations (millionth of a gram), and not even nanogram concentrations (billionth of a gram), but picograms (trillionth of a gram). This is probably as potent a killer as they come.

Anaphylactic shock

The cause of this deadly attack is known only in general terms. People who are allergic have a certain immunoglobulin, called IgE, at above normal concentrations. These antibodies, like all other types of antibodies, are specific to certain antigens, or allergens. One of the most common is house-dust, another common group of allergens comes from pollens of a variety of grasses and flowers. But there are literally hundreds and thousands of other allergens, some of them extremely rare. Whatever the specific allergen, the IgE destined to bind with it will do just that—and will in turn bind to a receptor, the IgE receptor, on a cell called mast cell. These cells line up blood vessels, primarily small veins and capillaries. Once the complex of IgE/allergen binds to the IgE receptor—all hell breaks loose. The mast cell releases its stores of histamine, which in turn causes the runny nose, the hives, or the asthma attack. But some people, mostly people who have allergies, but also some who haven’t had any known allergies, will react in a much more violent type of reaction—the anaphylactic type. In this reaction the histamine release by the mast cells is vastly more massive than in the run of the mill allergic reaction. This causes increased permeability of the blood vessels and a flood of blood plasma rushing out into the surrounding tissues. The end result: difficulty breathing, profound hypotension (low blood pressure), slowdown in heart rate or even cardiac arrest, reduced supply of blood to the brain, the kidneys and all other organs—leading to a generalized failure of all body systems. Pretty scary stuff.

What makes these people vulnerable?

This is a question that occupied the best minds in allergy research for decades—but with little or no results. Until now, that is.

In a publication in Nature Immunology Online Kirk M. Druey and his colleagues of the National Institute of Allergy and Infectious Diseases (NIAID) report that a protein in mice known as RGS13 suppresses allergic reactions, including the severe, life-threatening reaction of anaphylaxis. RGS13 is one of a large group of regulator of G protein signaling (RGS) proteins that act as traffic lights for signaling networks within cells. Though the biochemical actions of most RGS proteins in laboratory tests are known, their physiological functions in the body are still a mystery. Therefore, the current findings may have broader implications for many different biological processes, such as metabolism, cancer progression, cardiac function and others.

RGS13 is known to inhibit cellular responses induced by G-protein-coupled receptors (GPCR), which are the most abundant cell surface receptors in the body. It is also known that these receptors are the targets of approximately 60 percent of therapeutic drugs for various diseases. Since RGS13 is expressed in mast cells, Dr. Druey and his NIAID colleagues decided to explore the role of RGS13 in mouse models of anaphylaxis. Through genetic engineering, they made a group of mice deficient in the RGS13 gene. Normal mice served as the control group. To test for systemic anaphylaxis, they injected the allergen, IgE antibody and a blue dye directly into the veins of the mice. The organs of RGS13-deficient mice showed an anaphylactic response that was twice as large as that of the normal mice.The results indicate that RGS13 suppresses the anaphylactic response in mice, whereas RGS13 deficiency and abnormal RGS13 expression and function contribute to increased mast cell activity, which occurs during an allergic response, including anaphylaxis.

Surprise, surprise

The study is also important because for the first time, researchers have shown that RGS13 inhibits the activity of PI3 kinase (PI3K), an enzyme involved in many biological processes, including those involved in cancer and diabetes. Therefore, the research has implications for numerous other diseases and medical conditions in addition to allergies.

Which brings me to the larger point I never tire of making: The beauty and excitement of scientific research is in its total and utter unpredictability.

Once the researchers confirm their mouse findings in humans (highly likely), they could use this knowledge to synthesize drugs that would mimic the action of RGS13, thereby treating people prone to extreme allergic reactions. But they could also design drugs that would inhibit RGS13, for the treatment of diabetes and several cancers.

Could anybody ask for a more bountiful harvest of scientific results? And for the policy mavens among us: can you find a return on investment that would come even close?

Dov Michaeli MD, Ph.D is in the biotech industry

By Dov Michaeli MD, Ph.D

In 2005, a team of investigators at the Center for Disease Control and Prevention, or CDC, published a paper that shook the foundations of our long-held beliefs; they found that death rates due to overweight (BMI 25-30) and obesity (BMI >30) were actually lower than death rates due to underweight. The paper came under withering criticism by scientists and nutritionists who had been preaching the gospel of weight control. “Libertarian” organizations funded by the food industry, such as “Food Freedom”, piled on with glee. Their basic message: you can’t trust those scientists; just let the consumer beware (and, I presume, let Darwin and the forces of the “free” market weed out those who did not).

The most serious criticism of the study was that it was not even a prospective study, let alone a controlled one. It had a retrospective design, the least reliable of epidemiological studies. Furthermore, it relied on death certificate reports, notoriously inaccurate and many times misleading. Just as one example, a patient dying of a heart attack would normally have his cause of death listed as myocardial infarction, without mention of the underlying type 2 diabetes. It also flew in the face of a huge body of literature showing excess mortality due to obesity and its link to type 2 diabetes and its cardiac and kidney complications, as well as some of the biggest cancer killers such as colon, breast, esophageal, uterine, ovarian, kidney and pancreas—all obesity related cancers. I might add that recently prostate cancer was added to the list.

In a paper published in the Nov 7 issue of JAMA, the authors of the 2005 study went back to the same data bases they had used, in order to determine which causes of death are associated with underweight and which are associated with overweight and obesity.

The envelope, please…

The group with normal weight (BMI 20-25) were considered the baseline and the groups over or below this range were compared to them.

The diseases associated with overweight and obesity were not surprising; the usual suspects were identified, again: heart disease, kidney disease, type 2 diabetes and cancers related to excess weight.

What is intriguing is the relationship of underweight (BMI less than 18.5) to disease; to my knowledge, this kind of information has not been available before this study was published. These people suffered excessive mortality rates from acute and chronic respiratory disease, injury, as well as some cancers that are not related to excess weight, and miscellaneous other diseases (Alzheimer’s, Parkinson’s).

Critique

The study is revealing, especially in its identification of underweight as not healthy. Jewish and Italian mothers, please stand up and say in unison: I TOLD YOU SO.

What could explain the lower rate of mortality associated with overweight than that associated with underweight? No answer is offered by the survey, but what comes to mind is that modern medicine is simply too good at warding off death. We can now keep patients with heart disease and kidney disease alive with all kinds of wonderful drugs and procedures. Even colon and breast cancers, major killers in the not-too-distant past, are now more like chronic diseases, thanks to early detection, chemo- and biological therapy. And bear in mind: the study measured death rates only; it did not attempt to measure the prevalence of disease that has not resulted in death during the study period. 

What could explain the underweight association with disease? A study of this kind cannot establish causality, but one can speculate (especially when not subjected to the jaundiced eyes of peer reviewers). Two things come to mind: muscle mass and immunity. BMI below 18.5 almost by definition means that some of the lost weight comes from loss of muscle. One of the most important muscles, when it comes to infectious diseases, is the diaphragm. When this muscle is weak, respiration is weak, lungs are not ventilated completely, and before long pneumonia ensues. Bedridden patients, elderly people, patients with AIDS, cachectic (wasted) patients with advanced cancer—all are susceptible to respiratory infections. In fact, this is the most common cause of death in such patients. Likewise, low nutritional status is associated with defective immunity to infectious diseases. But, as I said, this is sheer speculation.

What about the validity of the study as a whole? None of the deficiencies that plagued the original paper, namely retrospective design and reliance on death certificates, have been cured. The methodology is identical, the data base is identical—the only difference is that here we get an analysis of the diseases associated with out- of- the- normal body weights.

Dr, Flegal, the senior author of the study, was quite cautious in her assessment of the study . According to Dr. Flegal, "The take-home message is that the relationship between fat and mortality is more complicated than we tend to think." On the other hand, experts like Walter Willett, professor of epidemiology and nutrition at the Harvard School of Public Health, "dismissed the findings as fundamentally flawed, saying [that] an overwhelming body of evidence has documented the risks of being either overweight or obese." He called the findings "rubbish."

Well, well, I wouldn’t go that far. The study did contribute some valuable information on underweight and its relationship to disease. And it provoked controversy—which is great; this is how science is done and how progress is made.

"Most heart attacks in women are preventable," is the headline of an article posted on NBC.com.  The article describes a study, published in the Archives of Internal Medicine, that was done by the researchers at the Karoinska Institute in Sweden.  Dr. Agneta Akesson and colleagues looked at the diet and lifestyle patterns of almost 25,000 postmenopausal women.  At the time of enrollment none of the women had heart disease, diabetes or cancer.

The researchers asked the women to fill out "food frequency" questionnaires to identify how often they ate 96 different foods.  The researchers analyzed the data and found four major dietary patterns:

• Healthy - vegetables, fruits, and legumes
• Western/Swedish - red meat, processed meat, poultry, rice, pasta, eggs, fried potatoes, and fish
• Alcohol - wine, beer and some snacks
• Sweets - sweet baked goods, candy, chocolate, jam, and ice cream

Other information collected included family history of heart disease, education level, physical activity, and body measurements.

The women were followed for an average of 6 years.  During that time, 308 women had heart attacks.  The investigators found that two of the dietary patterns (healthy and alcohol) were associated with a decreased risk of heart attack.  Women who drank less than a quarter ounce of alcohol daily (that is just a splash in the bottom of your glass) and ate lots of veggies, fruit, whole grains, legumes, and fish had a 57% lower risk of having a first heart attack.  That is a whopping big difference.

If women added three other healthy lifestyle habits into the mix (not smoking, being physically active, and avoiding too much weight gain), they had a 92% lower risk of heart attack.  In other words, most heart attacks in women are preventable by making healthy lifestyle choices.

Now, it is one thing to say, eat healthy, drink in moderation, exercise and maintain a healthy weight.  It is quite another thing to actually do all of those things over the course of an entire lifetime.  On the other hand, if you look at the amount of money the US (and, indeed, the entire world) spends to treat cardiovascular disease, I believe you would find there is enough there to buy each and every person a personal cook and a personal trainer (I believe this is the secret to Oprah's weight loss and maintenance).

I say this tongue in cheek, but it does make the point that we aren't spending our "health" care dollars on the right things.  We spend generously to fix disease, but we are very stingy when it comes to funding health.   It is time to get this right.  There aren't enough dollars in any treasury to treat all of the heart disease we are going to see as a result of the global epidemic of obesity and physical inactivity.  This must be  a top priority of policy makers and health reformers.  Studies, like the Karolinska study, should be used to promote changes in public policy - such as healthy school foods, ensuring that all neighborhoods have access to fresh fruits and vegetables and that they have safe places where kids and adults can move their bodies (without worrying about getting shot in the process).

Every politician, health reformer, and policy wonk ought to know about this study and others that prove that healthy lifestyles mean fewer heart (expensive) attacks - not just in women, but in men as well.  The bottom line is most heart attacks are preventable!

by Bill Bestermann, MD

In my last post, I discussed the untimely death of Wake Forest Basketball coach Skip Prosser and the relationship of vulnerable plaque to sudden cardiac death and myocardial infarction. Only 14% of heart attacks are caused by a fixed artery blockage of 70% or greater. For 70% of heart attack patients, the blockage in the coronary artery is less than 50% (non-obstructive). A non-obstructive plaque causes no symptoms and usually would not produce a positive stress test. Since the 50% blockage typically causes no symptoms, for 70% of myocardial infarction patients, the heart attack or sudden death is their first symptom.

We try to overcome this by using the Framingham risk score, assigning points for risk factors including HDL cholesterol, systolic blood pressure, age, total cholesterol, and smoking status. This is useful, and helps to identify some high-risk patients, but still we frequently miss people who go on to infarction. Our current system, based on risk scores, stress tests, coronary angiography, bypasses and stents has simply failed to identify too many patients with substantial risk.

Since the vast majority of heart attacks are not occurring at sites of fixed stenosis but rather at the site of a vulnerable plaque rupture, the question becomes-how do we identify these high-risk patients and treat them aggressively. Patients who have established atherosclerotic arterial disease at any site should be treated as if they have coronary artery disease. Arterial disease is a diffuse process and any blockage anywhere indicates that most of the arteries are involved with atherosclerotic plaque. There is a dramatic correlation between type 2 diabetes and arterial disease. The same holds true for patients with kidney damage. Both of these patient classes should be treated with the same level of aggression as the patient with established vascular disease. Patients with a high Framingham Risk Score should be aggressively managed. The risk factor management targets for these patients are lower than those we normally are aiming for. The blood pressure should be less than 130 systolic (top number). The LDL cholesterol should be less than 70. The hemoglobin A1c should be under 6.5.

There are many patients at risk who fit none of these categories and currently they are not being treated aggressively enough. Patients with strong family histories but low to intermediate risk scores are an example. Some people have intermediate risk scores but in actuality are very high risk—how do we identify them? Since the fundamental risk is the extent of plaque in the artery—specifically the amount of unstable plaque—the ideal way to identify high-risk patients would be to develop a methodology that allows us to identify patients with unstable plaque. The higher the amount of unstable plaque, the higher the risk.

The gold standard for directly examining the amount of plaque in the artery is coronary catheterization using intravascular ultrasound technology. This is an invasive technique that carries some risk and substantial expense. It is not routinely used even in patients having a heart catheterization. It is impractical for intermediate risk screening.

More studies are now available to help us understand the role of coronary artery calcium scoring. The American College of Cardiology and the American Heart Association have just published an expert consensus document on this technology. Atherosclerotic plaques are dynamic deposits in the arterial wall that go through progressive and predictable stages. Plaque “instability and rupture can be followed by calcification, perhaps to provide stability to an unstable plaque.” The authors state: “Radiographically detected coronary calcium can provide an estimate of total coronary plaque burden. The authors go on to provide a further rationale for the use of this technology: “Patients who have calcified plaque are also more likely to have non-calcified or “soft-plaque” that is prone to rupture and acute coronary thrombosis….coronary artery calcium scoring may be able to globally define a patient’s CHD (coronary heart disease) event risk by virtue of it’s strong association with total coronary atherosclerotic disease burden, as shown by correlation with pathologic specimens. Perhap even more convincing is the following:

“ Pathology studies have shown that the extent of coronary calcium within plaques tends to be related to healed plaque ruptures.” We cannot identify the vulnerable plaque but we can quantify ruptured plaque history which tells us his risk for future plaque rupture and thrombotic obstruction. We cannot identify the vulnerable plaque, but we can identify the “vulnerable patient.”

Even more impressive, when we combine the Framingham Risk Score and the Coronary Calcium Score, we have a system that is able to predict coronary risk in a very robust fashion as shown in the figure below. Any patient with a coronary calcium score over 100 should be considered to have coronary disease and should have risk factors reduced to those same aggressive targets.

Women are a special case here and for them this technology may be even more important. Women are less likely to form focal narrowings in the arteries and so they are even more likely to have an infarction with a non-obstructive plaque (narrowing less than 50%) Women tend to deposit their plaque in a concentric, symmetrical fashion up and down the artery. In fact, women with recurrent chest pain and a normal heart catheterization still have a 20% six-year risk of sudden death, myocardial infarction, stroke or congestive heart failure (WISE study). For this reason, I would not consider any woman’s cardiac workup to be complete until she had a calcium score. Too many women are told they have nothing to worry about after a normal heart catherterization. The woman with recurrent chest pain is still often high risk and in need of aggressive risk-factor management.

Here is the really amazing part. In spite of the extensive literature on the new science of risk assessment and the importance of vulnerable plaque, almost no insurance companies pay for the calcium score. In our group practice, we offer this test for $249.00. When you consider the information to be gained from the study, that seems very reasonable. This technology should be much more widely applied to identify high-risk patients and we should press the payors to allow this test in intermediate-risk patients.

Bill Bestermann

The Wake Forest University School of Medicine is my alma mater and earlier in the week I came upon our quarterly alumni magazine.  I was at first struck by the wonderful cover photo and then chagrined as it began to dawn on me what the picture meant.

You can see this warm, engaging man relating to the students at a Wake Forest basketball game and the love these young people felt for him is plainly seen in their happy expressions.  The photo speaks volumes about head basketball coach Skip Prosser.  It is a painfully tragic scene because the coach came in after a jog this summer and died suddenly at the age of 56.  The great game was the life he lived.

Athletic Director Ron Wellman said “Prosser’s life wasn’t about championships—although he won the ACC regular season championship in 2003—but about relationships and friends.  ‘Skip tried to know everyone.  Once you met him, you considered him a friend and he considered you a friend.  On campus, he seemed to be everywhere.  When he said hi, that made your day.”  Somehow, looking at this haunting picture, that is believable.

Events like this weigh heavily on my heart because most of them could be avoided.  Medical science has advanced to the point that the number of sudden deaths related to heart attack could be dramatically reduced.  Leading cardiologists like Peter Libby, Erling Falk, and Steven Nissen have helped us to understand that a heart attack does not come from a fixed blockage.  Myocardial infarction and cardiac sudden death almost always are the result of a ruptured vulnerable plaque.  A 1995 article by Erling Falk documents that only 14% of heart attacks occur at a point in the artery where the obstruction exceeds 70%.  Seventy percent of myocardial infarctions occur where the fixed obstruction is 50% or less.  Since a 50% blockage seldom produces symptoms, for 70% of patients, the heart attack is the first symptom.  Unfortunately, for many patients the first symptom is fatal.

In fact, the new science of arterial disease goes back nearly twenty years. The Falk article summarized findings from 4 previous studies.  The summation of the data from those studies helped us understand that chronic obstruction is not the cause of a heart attack, most heart attacks occur when a newer, less obstructive plaque ruptures.  The unstable plaque contains LDL cholesterol or “bad” cholesterol.  That LDL cholesterol is oxidized—chemically changed—in the wall of the artery and then it is recognized as foreign by the body.  The human body deals with foreign material by attacking it with white cells or pus cells.  The unstable plaque is a microabscess or a tiny boil in the wall of the artery.  When that boil ruptures, a toxic, inflamed gruel with the consistency of toothpaste comes in contact with the blood in the artery and sets off the clotting process.  If the clot partially blocks the artery, unstable angina or an acute coronary syndrome is the result.  If it totally blocks the artery, myocardial infarction is the result.  The blocked artery causes death of the heart muscle downstream.

Only a few heart attacks occur as the result of severe chronic obstruction of the artery because the more obstructive plaques are much more stable.  They have been present longer.  The body reacts to those lesions by producing a thick cap over the cholesterol plaque and the inflammation produced by the white cells (pus) causes scar tissue formation.  The inflamed cholesterol is bound up and rupture is more difficult.

This scientific understanding ties the new critical facts of arterial disease together.  It explains the fact that the anticoagulant aspirin cuts the risk of heart attack by a third.  It helps us understand why the clot dissolver TPA (tissue plasmin activator) aborts the heart attack process.  It helps us understand why statins have power beyond cholesterol lowering in that they dramatically reduce inflammation and quickly stabilize plaque to prevent rupture.  Other medications like ACE inhibitors for blood pressure and metformin for diabetes have beneficial effects on the metabolism of the arterial wall to improve arterial function and diminish plaque instability.  The highest risk patients---type 2 diabetics—have an 80% life-time risk of heart attack or stroke.  Treating pressure, glucose, and cholesterol to aggressive goals lowers the risk by roughly half for each risk factor.  Dr. Steven Nissen and others have shown that aggressive lowering of the LDL cholesterol with statin therapy stabilizes the plaque and actually reverses the buildup of LDL cholesterol and pus in the wall of the artery.  So, we really have a very solid understanding of how arterial disease works and the ability to produce a tremendous  reduction in the risk of heart attack with medical treatment.

It is somehow ironic that one of the first two articles of the four cited in the Falk study came from Wake Forest.  Dr. WC Little and his team wrote in Circulation in 1988:

”Acute myocardial infarction is usually produced by the sudden total occlusion of a coronary artery by thrombus (clot), usually occurring at the site of an atherosclerotic lesion.  Our study indicates that the lesion that will be the site of the thrombotic occlusion frequently is not severe when evaluated by coronary angiography weeks to years before the infarct in patients with mild-to-moderate coronary artery disease; thus, coronary angiography was not able to accurately predict the time or location of the subsequent myocardial infarction.  (my italics) In the majority (66%) of patients in this study, the myocardial infarction occurred because of the occlusion of a coronary artery that did not contain an obstructive (more than 50% diameter narrowing stenosis) on a previously performed coronary angiogram.  A high-grade stenosis (more than 79% diameter narrowing) was initially present in the infarct related artery in only one patient.  Furthermore, the myocardial infarction did not  occur because of occlusion of the previously patent artery with the most severe stenosis in two thirds of the patients.”

Dr. Little and his colleagues went on to conclude:

“Because it was difficult to predict the site of the subsequent occlusion in our patients from the initial coronary angiogram, coronary bypass surgery or angioplasty appropriately directed only at the angiographically significant lesions initially present in almost all our patients would not have been effective in preventing the majority of myocardial infarctions.  This does not indicate that arteries that do not have obstructive lesions should be bypassed or dilated.  Instead, effective therapy to prevent myocardial infarction may need to be directed at the entire coronary tree, not just at obstructive lesions.  Such therapy to prevent myocardial infarctions might rationally include avoiding smoking, reducing serum cholesterol, administering agents that alter platelet function…(my italics)"

In 1988, Dr. Little was saying that bypass surgery and angioplasty did not prevent heart attack in stable patients and could not be expected to prevent heart attack in stable patients.  He predicted the results of the COURAGE trial (New England Journal-2007) nearly 20 years ago.  The COURAGE trial compared optimal medical therapy with optimal medical therapy plus appropriate stenting in patients with angina, most of whom had two and three vessel coronary disease.  There was no difference in heart attack or sudden cardiac death in the two groups after 5 years of therapy.  In other words, the stent added nothing but pain relief.  Additionally, in the COURAGE trial, 70% of the patients were pain-free at 5 years on medical therapy alone.

The new science of vascular disease tells us that we are doing too many catheterizations, bypasses, and stents.  We are doing a miserably inadequate job of identifying high-risk patients like Skip Prosser and providing optimal management for all risk factors.  We have known or should have known that for almost 20 years.  Let us call it what it is—a failure of leadership.  How many good men like Skip Prosser have to go down before we get this right?

By Dov Michaeli MD, Ph.D

In a September 6 posting (Bipoar Diagnosis in Children: another epidemic?) I posited that because of the fuzzy definition of this and other psychiatric disorders, physicians tend to take an expansive view of the disorder, for a variety of reasons (not the least of which is monetary)—resulting in a forty (40!) fold increase in diagnosis in eight years, from 1994-1995 to 2002-2003. One week later, the New York Times of September 13 published an excellent op-ed by Sally Satel, a psychiatrist and resident scholar at the American Enterprise Institute and co-author of “One Nation Under Therapy”, which deals with the same problem.

“ We still don't know how much of this increase represents long-overdue care of mentally ill youth and how much comes from facile labeling of youngsters who are merely irritable and moody”.

Dr. Satel point out that Part of the confusion stems from the lack of a discrete definition of juvenile bipolar illness in the diagnostic manual. But there is a deeper problem: despite the great progress being made in neuroscience, we still don't have a clear picture of the brain mechanisms underlying bipolar illness -- or most other mental illnesses . ”

Fair enough. To borrow a baseball metaphor (I can’t believe I am using it) we are at the beginning of the first inning; we barely scratched the surface of this enormously complex organ, and understand even less how it works and why it malfunctions. So yes, we cannot define a disease with the same accuracy as we define, say, a myocardial infarction or a bacterial infection. But surely we could do better. Even in the days when the pathophysiology underlying a heart attack was not known, the symptoms were clearly defined and diagnosis was made quite reliably.

Part of the problem of relying on symptoms to define a disease is that many patients meet several diagnostic definitions at once. Roughly half of children with a diagnosis of ADHD, for example, also have symptoms that fit the definition of bipolar disorder. Do these patients actually suffer more than one illness, or do they just appear to? Conversely, very diverse patients often qualify for the same diagnosis. Children with depression, anxiety, irritability, moodiness or plain exuberant personality can all fit the diagnosis of ADHD.

What’s to be done?

Earlier this summer, the American Psychiatric Association announced that a 27-member panel will update its official diagnostic handbook, the Diagnostic and Statistical Manual of Mental Disorders. The fifth edition, which is scheduled to come out in 2012, is likely to add new mental illnesses and refine some existing ones. Dr. Satel proposes to define each disease as a continuum, allowing the physician to make a more refined and more nuanced diagnosis. Excellent idea! But I would say: not enough. I would add to each diagnosis several illustrative case studies, maybe in the form of an accompanying workbook. Such case studies could describe the classical presentations of a given disorder as well as its extremes, both mild and severe. This would illustrate the breadth of a diagnosis, and hopefully avoid much of the confusion that is common today.

The current state of psychiatric diagnoses reminds me of the Talmudic proverb, “the breach invites the thief”, by which it meant that the lack of clear definition and boundaries invites all sorts of bad behavior. Hopefully, the new Manual will close that breach.

Dov Michaeli MD, Ph.D is in the Biotech industry.

Brian Klepper

This week TDWI is delighted to take our turn hosting Health Care Wonk Review, a collection that highlights some of health policy's best observers. The quality of these 14 posts is very high, and well worth your time.

As HWR has gained visibility and popularity, the number of submissions has risen. We couldn't publish them all, so chose the ones we thought were must-reads across industry sectors. (Apologies to those we didn't include this time.)

Before we begin, a quick announcement. Envision Solutions, LLC and Trusted.MD Network have launched the second annual global survey of healthcare bloggers.  The companies are producing this poll to shed additional light on why people blog about health-related subjects.  Click on the link to learn about and take the survey.  The study will close on October 15.

Now onto the show!

Physician Temper Tantrums. Over at Managed Care Matters, Joe Paduda picks a scab and elicits a (deliciously) minor furor. He argues that when payors use the results of claims data analysis to encourage patients to see better performing doctors, they are well within their rights as purchasers. He also notes (and I agree) that when doctors reject out-of-hand claims data as inherently flawed and inappropriate to provide quality analysis, they may not appreciate the progress in the available tools and methods, and may be simply defensive. Actually, he says "their actions look more childish than professional from here." A provocative piece.

No Docs in This Box. Retail medical clinics are popping up all over as an inexpensive alternative to a full-blown practice or the ER. Traditional providers are crying foul, but InsureBlog's Bob Vineyard suggests this is the pot calling the kettle black.

Abusing The Orphan Drug Law To Rip Off Customers. In a damning indictment of a drug company's business practices, David Williams at the Health Business Blog discusses Questcor Pharmaceuticals announcement about “a new strategy and business model for H.P. Acthar Gel(R).”

What Are The Real Savings In Medical Tourism. MedTripInfo's Michael Horowitz analyzes the probable total savings for a hip replacement obtained overseas. They're substantial.

Medical Justice League of America. The Sentinel Effect's Richard Eskow describes a new group that provides "gag order" forms to dissuade patients from reviewing their docs online, and also promises to "relentlessly" fight med mal lawsuits." The situation he relates would be hilarious if it weren't so lopsided and scary.

Make Sure Your Online SaaS Vendors Are Appliance Capable. The Healthcare IT Guy, Shahid Shah, provides sage advice on why you should not depend on "software in a cloud" without a backup plan. With big outages from Microsoft, Skype, eBay, and PayPal recently making headlines, it is wise to make sure you're protected. A fascinating and smart look at the pitfalls and realities of letting other companies be responsible for your mission-critical IT functions.

What The Lumenati Are Saying May Surprise You.  The ever-entertaining Matthew Holt is making the final dash toward hosting the Health 2.0 conference, where the discussion will focus on a significant portion of market-based reform, and the players will be none of the usual suspects. Meanwhile, back at The Health Care Blog, he ticks off some surprisingly lucid health care insights from the most unexpected sources.

Mitt Romney's Health Plan - A Foot In Each Canoe.  Over at Health Care Policy and Marketplace Review, Bob Laszewski wryly observes that conservative Presidential candidate Mitt Romney would like to have it both ways. He gloats over the Massachusetts reform he helped to engineer while assuring his political base that it wouldn't work elsewhere. (It's also not yet clear that it is going to work in Massachusetts.) It's a delightful bit of political dissonance, seen through the clarity of Bob's highly polished health policy lens.

BiPolar Diagnosis in Children: Another Epidemic? Here at The Doctor Weighs In, the erudite Dov Michaeli recounts a recent review article from the Archives of General Psychiatry. Between 1994-1995 and 2002-2003, an 8 year period, the rate of bi-polar diagnoses in children increased 40 fold! He lists a range of possible explanations for the epidemic, but settles, gloomily and cynically, on money. By explicating an immense but relatively obscure problem, he lays bare a pervasive trend that's corroding our health system. A must read!

Conflicted View on the Pitfalls of Government-Sponsored Comparative Effectiveness Research. In a withering analysis, Roy Poses at Healthcare Renewal rebuts a recent commentary by WSJ Editorial darling Scott Gottlieb. Dr. Gottlieb disparaged government-sponsored research as biased against costly drugs, while ignoring similar and more odious flaws in private sector research practices. AND Dr. Gottlieb conveniently neglects to disclose that he's associated with the biotechnology sector. Superb.

To Hell and Beyond: Dave Holland's Terrible Story. At Workers' Comp Insider, Julie Ferguson points to a particularly gruesome work-related accident by way of reminding us that these incidents are still all too common. Julie's perspective is particularly poignant, because it is also a reminder that what lies beneath the day-to-day work  of the people who write for and read this review is the vital goal of preventing and managing the suffering that is too often a part of life.

Katrina: Two Years Later Are Health Systems Better Prepared?  On the second anniversary of Hurricane Katrina, NewsHour correspondent Tom Bearden asks a coastal area provider if the health systems are now better prepared. The short answer is "No," according to the  interview excerpted by Jane Hiebert-White on Health Affairs Blog.

Cookbook Medicine Saves Lives.   A pretty good cook (I can vouch for her!) as well as a physician, The Doctor Weighs In's Pat Salber relates the substance of a July 23 article in the Archives of Internal Medicine. She describes a new heart failure guideline that improves outcomes when followed by clinicians, and details the range and depths of those improvements. She concludes with a quote from  the lead author, telling us that if these protocols were followed in hospitals across the country, they would result in 40,000 fewer deaths and 1.4 million fewer hospital days annually. Keeping in mind that this is just one condition in the vast complex of health care, it is a deeply compelling point.

Reform's Tougher Problem. I've been a bedouin lately, wandering from oasis to oasis, grateful for the chance to publish on Pat Salber's The Doctor Weighs In, Bob Laszewski's Health Care Policy and Marketplace Review, and on Matthew Holt's Health Care Blog. This post, placed on Matt's site, summarizes what I've learned working for several years on the reform problem. I now believe that meaningful change can only occur through the leadership of the non-health care business community, the one group with more power and influence than the financially conflicted health care sector. Non-health care's business leaders will pursue this effort, not because they care about health care or social justice, but because health care's impending instability will threaten the stability of their own econonic environments.

Thanks again to Health Wonk Review for letting us host, and thank you for stopping by.

By Dov Michaeli MD, Ph.D

The sometimes acrimonious debate over the use of human embryonic stem cells usually follows this outline:

Con : We respect all life, however primordial. The blastocyst is a potential human being and deserves all the ethical considerations of a living human.

Pro : The blastocyst is just an agglomeration of cells formed within one week of fertilization of the egg, still undifferentiated into organs such as a heart, GI tract or nervous system. There is nothing “human” about it. And in any event, these embryos are destined to be discarded by the fertility clinic.

Against the theoretical/ theological argument of respect for potential life, the promise of curing  presently incurable diseases is real, not theoretical, and the beneficiaries are live, suffering human beings, not cells in a dish with a vanishingly small potential of becoming a human embryo.

Con: We cannot play God and decide who should live and who should die. However small the potential of the potential for life—it is still there. And in any event, the potential for using embryonic stem cells for therapeutic purposes is theoretical at best. So far, not one therapy or potential therapy has been scientifically demonstrated.

The last argument has just been demolished

The online edition of the August 26, 2007 Nature Biotechnology published an article by scientists from the University of Washington and from Geron Corporation. They created a myocardial infarction in rats that mimicked the human variety in every significant detail. They then transplanted cardiomyocytes (heart muscle cells) derived from human embryonic stem cells into the infarcted or dead heart tissue and observed that:

· The heart was partially revascularized.

· Heart failure was reversed.

· Contractile function of the heart was restored to pre-infarction level.

What now?

• This experiment will need to be replicated, preferably by another research group. If the results of the repeat experiment confirm these spectacular results it will be tried in humans, whether in the U.S. or elsewhere.
• Could similar experiments with neuronal cells be far behind? In fact, some are already ongoing.

And the societal ramifications?

The somewhat esoteric, academic/ethical/moral debate will assume a much higher degree of intensity: every patient with heart failure or myocardial infarction will have a real life interest in the issue; for many it will be literally an issue of life and death. And the caregivers and families of Alzheimer's disease patients? And spinal cord injury patients? And cancer patients? For all of them and their families it will be an overriding political issue. We are talking about many millions of voters with a personal interest in the issue. Who ever thought that science might one day be the cause of a political earthquake?

Interestingly, the ones with the sharpest appreciation of this development are not politicians or government bureaucrats, but Wall Street investors who put their money where their mouth is. Here is Tobin Smith, one of the most insightful among them:

“ OUR TAKE: The implications of this study are mind boggling -- I mean simply breathtaking. This is the futuristic stuff that gives us the reason to buy GERN on pullbacks”.

Now, I wouldn’t rush out and buy Geron stock; it will be many years before they realize one dollar of profit. But the advance reported in this study is indeed breathtaking.

Dov Michaeli MD, Ph.D works in the Biotech industry.

By William Bestermann MD

Half of health care's $2 trillion dollars is spent on five chronic conditions. Three of those conditions - vascular diabetes, coronary disease and congestive heart failure - are interrelated in their causation. If we simply applied what we have already learned, we could eliminate enormous suffering and significantly reduce the cost of these conditions.

Many professionals in positions of leadership today were educated in the 60s, opposed the Vietnam War, and viewed military intelligence as an oxymoron. But my oldest son, a West Point graduate, has taught me lessons that have changed my life and are relevant to the major conundrum facing medical practice today.

West Point places a primary stress on technical adaptation.  These young cadets are taught “Tactics Lag Technology.”  That is to say if the officer applies tactics appropriate to the last war in the face of more deadly weaponry in the current war, he will likely be responsible for the deaths of hundreds if not thousands of his personal friends, team mates, and countrymen.  Military officers, in their movement upward in rank and responsibility, learn of our own new technical capabilities, those of potential enemies, and how to integrate these into best military practices to minimize casualties while increasing the likelihood of success of the mission.  This is a central focus in military culture.

First, a bit of military history

These cultural attributes of the modern American military officer did not just drop out of the sky.  West Point cadets study the American Civil War in some detail.  That conflict saw the beginning of dramatic technical change including railroads, rifles in large number, and trenches that transformed warfare forever.  Prior to the War Between the States, for thousands of years, generals managed the attacking force in the same way.  The defenders would line up over a broad front, in ranks perhaps two or three deep, over a couple of miles depending on the size of the force. The attacking force would assemble in front of them in full uniform with color guards and regimental bands playing marching music.  Then the attackers would march to within effective range of their weapons.  As the Civil War began, most units were armed with muskets and the effective range was 40 yards.   So the Union and Confederate units would march to within 40 yards, fire one volley or perhaps several followed by a bayonet charge.  The carnage was not terrible and the loser was the one who lost his nerve and abandoned the field.  

As the war progressed, both sides replaced muskets with rifles and the defenders dug trenches.  As the Confederates prepared for Pickett’s charge at Gettysburg, the Union troops were behind a stone wall defense and armed with rifles.  Nearly a mile of open field lay between the opposing forces.  The Southern Commander Robert E Lee had ordered the charge, but Corps Commander Longstreet objected, simply knowing by observing the situation that the mission was impossible.  General Lee ordered him to charge the Union force in spite of the objection and Pickett’s Division was cut to pieces in a matter of minutes.

The following spring, US Grant had assumed command of all Union armies.  He was determined to end the war by capturing Richmond and crossed the Rapahannock River to begin what became the Overland Campaign.  In battle after battle, the Union forces charged entrenched confederates, with the same resulting horror the Confederates suffered at Gettysburg.  General Grant suffered 60,000 casualties in the month of May 1864 alone.  The puzzle of the rifle and the trench never was solved in the Civil War.

Amazingly, when WWI started 50 years later, tactics had still changed very little, though the technology of war had changed dramatically.  The forces involved had tanks, airplanes, machine guns, repeating rifles, mortars, breech loading artillery, trenches, and barbed wire at their disposal.  The method of attack had not changed.  The frontal assault was still the order of the day.  The British suffered 60,000 casualties on the first day of the Somme offensive.  The generals still did not get the message and over the new few months 500,000 promising young men were shot down in that single campaign.  WWI ended and the puzzle of the repeating rifle, trench and machine gun was still not solved.

The wrath of the status quo

The terrible carnage of WWI broke the spirit of Europe and there are still residual cultural effects on that continent.  In the aftermath, the promising young American officers Dwight Eisenhower and George Patton wrote infantry journal articles describing a new kind of attack that would later be called “blitzkrieg” or lightning war.  In this assault, all of the heavy weapons of the attacking force would be combined in units actually making the assault.  All of the tanks, artillery, bombers, machine guns, mortars and mechanized infantry would be thrown at the weakest point in the enemy line. They would break through, and turn left and right to “roll up” the force in the trench.  History has shown this to be a brilliant disruptive innovation in warfare and frontal assaults no longer occur.

How did the senior army leadership respond?  The Chief of Infantry called Eisenhower in and told him that his articles did not represent sound infantry doctrine and that if he wrote any more articles of that nature he would be court-martialed.  Billy Mitchell actually was court-martialed for advocating similar valid innovative disruptions in the army air corps.  Thank goodness the innovations advocated by Eisenhower, Patton, and Mitchell were adopted and played a critical role in WWII.

The change from frontal attacks to the attack of supreme violence aimed at a point is a very dramatic example of paradigm change.  The whole dynamic of combat changed from a defense that could not be overcome to an attack that could not be resisted.  The officers directing the blitzkrieg assault were not more diligent, more industrious, smarter, brighter or more dedicated than their predecessors.  No, they were not superior in any way-they had simply used a new system, a new application that was more effective.

So what does all of this have to do with medicine?  

You might think “How could these people be so blind? We would never do such a thing.”

Think again!  The science around medical practice in the treatment of atherosclerotic vascular disease has utterly changed.  The evidence that demands a change in paradigm has become irrefutable.  The technology of vascular medicine has progressed at a pace fully equal to that seen in the military.  The old attack on vascular lesions in stable patients aimed at fixed narrowings – bypasses and stents – are as thoroughly discredited as frontal assaults in the face of machine fire. (More on this in another post.)

The Institute of Medicine is the medical arm of the National Academy of Sciences.  The IOM membership is composed of 1,400 of the best minds in medicine.  In its 2001 report, “Crossing the Quality Chasm,” the IOM summarized what was needed to treat c