The Doctor Weighs In

William Bestermann, MD

The intensive glucose lowering arm of the ACCORD trial was just shut down because of an increased number of deaths in that portion of the study.  That finding has created a great deal of confusion on the long-held belief that aggressive treatment of blood sugar should protect patients from vascular events and death.  That belief, like many that prevailed in the practice of medicine, made perfect sense.  Virtually all of the bad things that happen to diabetics are the result of vascular disease.  Blindness, kidney failure, and nerve injury are the result of small vessel disease.  Heart attack, stroke and amputation are the result of large vessel disease.  For a long time, we have known that lower sugar reduces the damage to small vessels.  Very aggressive care should therefore lower heart attacks and strokes due to large vessel disease.

Glucose lowering-per se-does not prevent heart attack, stroke, or death.  I think the ACCORD trial did establish that fact, but this finding is now commonplace in vascular medicine.  Let not your heart be troubled.  There is a place for aggressive glucose control in optimal medical therapy for disease of the large vessels.  We have learned that certain drugs lower the risk factor, but do not protect the patient from events or death.  ACCORD is no different.  Treating hypertension  prevents heart attack and stroke.  Alpha blockers lower blood pressure.  Alpha blockers are inferior to other treatments in preventing events.  Rosiglitazone lowers blood sugar.  Rosiglitazone is associated with increased cardiovascular events.  The very first trial that looked at glucose lowering using tolbutamide was shut down early because of an increased death rate.  For decades estrogen was prescribed for its cardioprotective effects.  That practice ended when a controlled clinical trial showed that estrogens combined with progesterone were associated with increased numbers of heart attacks.  We have known for decades that higher HDL lowers vascular risk-yet a clinical trial for a medication that dramatically raised HDL had to be shut down because of increased events.  In fact, our whole system functions as if bypass surgery and angioplasty are the ultimate answer in heart attack prevention.  These treatments do nothing to prevent heart attack in the stable patient.  There is therefore, a long list of treatments that make sense but when subjected to clinical trials offer no benefit or actually cause harm.

The ACCORD trial was not a vascular trial but a sugar trial.  The trial was designed to test the hypothesis that lowering the sugar, taking precedence above all other considerations would lower events.  The interventions section from the ACCORD protocol states: “Both the intensive and the standard therapy groups will utilize all currently available glucose-lowering therapies.  The two treatment groups will have different glycemic targets and will have different thresholds of glycemic control at which therapeutic changes will be considered.

To achieve these glycemic targets, participants  will require self-management education and dietary and lifestyle interventions, as well as pharmacologic therapy.  They will also require different drug choices and treatment intensities.  For example, within 6 months of randomization, most intensive group participants will likely be on 3 or more injections of insulin a day in addition to two or 3 oral agents.  Conversely, standard therapy participants are less likely to be on insulin, will be on less than or equal to 2 injections per day if insulin is used, and will be taking fewer oral agents.  Moreover, the frequency with which self-management behavior is applied and participants are contacted will vary between the two levels of glycemic control.”  Later, in the Dietary and Lifestyle Interventions section there is the following guidance for investigators: “All participants will be provided with the same dietary and lifestyle recommendations to optimize their glucose control.  These will include : a) advice that blood glucose control may be more critical than weight control in reducing the risk of complications of diabetes.”
The investigators could use metformin, thiazolidinediones (TZDs), insulins, sulfonylureas, exanatide, and acarbose.  

There have been serious questions raised in the past about the adverse effects of certain drugs for diabetes on vascular events and survival.  These questions have been raised for rosiglitazone and sulfonylureas.  Diabetes is itself a weight-related illness.  Most type 2 diabetics have blood pressure and cholesterol problems that are both made worse by increased weight.  All diabetic treatments except for metformin, exanatide, and acarbose are associated with weight gain.  If you compare twice daily insulin with metformin and a single long-acting insulin shot, the metformin-insulin people gain no weight and the twice daily insulin patients gain an average of 10 pounds in one year.  This is no small matter in a weight-driven illness.  The ACCORD trial allowed a number of medical interventions that would be expected to produce weight gain.

On the very same day that the intensive glucose-lowering arm of ACCORD was shut down, the Steno-2 investigators reported their 13 year follow-up for aggressive treatment of high-risk type 2 diabetic patients.  They found that early intensive intervention with multiple drug combinations and behavior modification leads to reduced rates of death and cardiovascular disorders.  There was a 20% absolute risk reduction in the primary end-point of  all-cause mortality.  There was also a 13% absolute risk reduction for cardiovascular death.   In Steno-2, cholesterol, hypertension, glucose were all treated in an intensive and structured way.  The conservatively treated patients in the Steno-2 trial had a 50% death rate over 13 years-a shocking mortality rate.

The big difference in the glucose management compared with ACCORD was that Steno-2 provided an evidence-based protocol consistent with best practice.  Overweight diabetics in Steno 2 were given metformin.  Gliclazide was added to the medical therapy of obese patients who did not achieve goal glucose reduction.  If the glicazide-metformin combination did not result in reduction of A1c to 7.0, then gliclazide was dropped and long-acting insulin added to the metformin.  This is a critical difference.

The insulin-metformin regimen does not cause weight gain.  Metformin is the only diabetic drug with powerful evidence of reduction of incidence of myocardial infarction (39%) and all cause mortality (42%) compared with diet and exercise.  Pioglitazone has some evidence of a less potent effect in this regard.  If metformin fails, it is because the patient is not making enough insulin and so simply replacing the insulin that the patient cannot make should result in preservation of the protective effects of metformin regarding heart attack and death.  Steno 2 seems to bear that out.

Metformin is a drug that has powerful vascular effects on a par with a statin or ACE inhibitor.  Metformin is associated with modest weight loss, decreased total cholesterol, decreased triglycerides, decreased LDL cholesterol, improved endothelial function (increased ability of the artery to dilate) and positive effects on the increased tendency to clot formation found in diabetics.  Metformin cuts to the center of the metabolic syndrome and diabetes by upregulating AMPK-its only site of action.  A study abstract that has just been published by David Lefer’s group shows that a single dose of metformin reduces myocardial infarction size in lab animals by 50% by upregulating AMPK and nitric oxide activity.  A single dose of statin does the same thing.  These are powerful effects.  The National Registry of Myocardial Infarction showed that  the patient entering an emergency room with a heart attack was one third as likely to develop CHF or die if a statin was started in the ER and continued during the hospitalization.  These effects are due most likely to a reduction in myocardial infarction size.

These two studies, ACCORD and Steno 2 teach us a great deal about the way that we should manage the epidemic of type 2 diabetes.  It is not about the sugar.  Simply driving the sugar lower may well be harmful.  The Institute of Medicine in 2001 recommended evidence-based protocols consistent with best practices in the treatment of chronic conditions.  Steno 2 fits that recommendation and ACCORD clearly does not.  Steno 2 should provide us with the model of the future- that is a coordinated-integrated attack on global cardiovascular risk using medications that have been shown to reduce the risk of heart attack and death.  ACCORD has shown us that aggressive care using any modality that lowers the risk factor may be dangerous and a premium should be placed on medications that have been shown to reduce events and death.  The ADA treatment guidelines say that metformin should be started at diagnosis in the absence of contraindication and these results underscore that recommendation.  Long-acting insulin should be used sooner as in Steno 2 rather than later.  

Over a 10-year period in South Carolina ending in 2007, I personally treated 450 type 2 diabetic patients with an average age of 65 and multiple comorbidities.  By using metformin, a self-adjusted long-acting insulin shot and the South Beach diet, I was able to maintain an A1c in that patient population that ranged from 6.8-7.0 over a the entire 10-year period.  These patients did very well with nothing approaching a 50% mortality.  Most of these patients had hypertension and cholesterol problems.  They were treated in a systematic protocol-driven manner.  Pharmaceutical interventions were chosen using the following cascade of priorities. 

1. event reduction
2. effect on weight
3. beneficial effects on other risk factors
4. effects on endothelial function and arterial structure
5. convenience
6. side effect profile
7. reduction of insulin resistance

The basic protocol used looked like this:

Most of these drugs are now available at Walmart for $4 a month.  Most of the patients actually lost weight and kept it off.  The patients could be seen at a reasonable rate of speed and for relatively little cost.  Aggressive diabetes management can be an important part of vascular risk reduction.

The last message anyone should take away from the ACCORD shut-down is that aggressive treatment is a bad idea.  Evidence of event reduction is king and other treatments should only be used when the patient cannot take the evidence-based therapy.

Dr. Bestermann leads the Center for Cardiovascular and Diabetes Management at the Holston Medical Group in Kingsport TN. He is a regular contributor to The Doctor Weighs In.

"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?

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.

Brian Klepper

OK, I'll admit it. I love reading the obituaries. They recount the marvelous achievements as well as, occasionally, the equally glaring flaws, of people we knew or, more often, didn't know.  I can't help being astonished, shocked, delighted, repulsed. Who knew all that was lurking under there?

There's a good one in Saturday's New York Times that's relevant to this blog.  Epidemiologist Ralph S. Paffenbarger Jr., MD, DrPH, ScD died at 84, ironically of heart failure. Dr. Paffenbarger became nationally influential for his work describing the relationship between exercise and longevity and for promoting vigorous activity to prevent heart disease. He was a professor at both Harvard and Stanford, and in 1987 he became President of the American Epidemiological Society. He helped write the exercise recommendations for the US Surgeon General's Report on Physical Activity and Health, published in 1996.

It's clear from the article as well as the Wikipedia entry that he had an active, inquiring, engaged mind. One simple but important insight early in his career was that the sedentary drivers on London's double-decker buses had higher coronary risks than the more active conductors. Later, during the 1960's, he established a  study - it's still running - that looked at the effects of exercise on 17,000 male Harvard graduates, ages 30 to 70. Here's a paragraph from the obit:

By the 1970s, the study’s preliminary findings suggested that men burning 2,000 or more calories a week faced a substantially lower risk of death from heart disease than their more sedentary peers. Indeed, in 1984, Dr. Paffenbarger concluded that, among 640 men in the study who had died of cardiovascular disease, the death rate for the most sedentary was nearly twice that for the most active. By the ’90s, the study refined that figure, finding that regular exercise reduced coronary death rates by 25 percent to 33 percent.

Maybe most interestingly, Dr. Paffenbarger actively translated his work's meaning into his own life. A sedentary 45 year old, he started running and was hooked by the second week. He said, “I found it invigorating. I could consider my thoughts and conflicts, I could prepare letters, ponder problems, prepare talks.” It eventually became a 50 mile a week habit. He became a marathoner, competing in 151 marathons, as well as ultra-marathons like the grueling 100 mile mountainous Western States Endurance run.

But most importantly, he nailed down for the rest of us incontrovertible evidence of a simple life truth. Nothing's certain, but if we're active, we improve our chances to live better longer.

Here's to you and a well-lived life, Dr. Paffenbarger!

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 chronic conditions:

“The current systems cannot do the job. Trying harder will not work.  Changing systems of care will.”

This document is the medical equivalent of the infantry journal articles written by Patton and Eisenhower.  It is a call to action and change, yet little in practice has changed since it was published in 2001.  Why?  The Chief of Infantry is alive and well.  Paradigm change has dramatic consequences and, for the leaders of the old order, the changes are negative.

The consequences of the utter failure of leadership in this case are exactly the same as a frontal assault: thousands of dead and disabled as a monument to our inaction.  Heart attack and stroke accounted for roughly 800,000 deaths in 2003. Many of these deaths were premature and avoidable. The bodies may not lie in heaps before a trench-line, but they mean the same thing: a failure to bring the full benefit of new technology to those we have promised to protect. 

There is a very real price to be paid for our failure to translate our new scientific knowledge about vascular disease into practice.  The Steno II trial compared optimal medical care (that is, drug therapy) in type 2 diabetes to usual care, and reduced the number of vascular events by half.  Only a small percentage of the study's patients had to be treated more aggressively to prevent a heart attack or a stroke.

The type 2 diabetic has a lifetime risk of dying from a vascular event of 65-80%.   Each risk factor - glucose, pressure, and cholesterol - treated to goal using the right medication reduces the risk of a vascular event by half.  Only 7% of type 2 diabetics have all three risk factors simultaneously to goal. 

Our failure to provide more aggressive risk factor management in these patients obviously is very damaging to their health.  The economic cost is equally painful.  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. In stable angina patients, optimal medical therapy was just as good in preventing a heart attack in a stable angina patient as optimal medical therapy plus a stent—for one third of the cost.

If current trends are any indication, medicine, the insurance industry and government will be slow to lead on transformation.  Patients and businesses that pay the bills must demand better or continue to receive medical care that is not what it could be.

Dr. Bestermann is medical director of the Vascular Medicine Center at the Holston Medical Group in Kingsport, Tennessee.

by Bill Bestermann, MD

The medication rosiglitazone or Avandia has been the subject of a great deal of controversy in recent months and there have been a couple of entries here on this topic :  Truth and consequences:  The sad tale of Avandia, GSK, the FDA, and medical research, Avandia, GlaxoSmithKline and bullying; or, how did we get into this mess? , and Avandia, the FDA, and the assault on science

Dr. Stephen Nissen and John Buse have been the objects of personal attacks described here at TDWI. The discussion does bring up a larger issue that often becomes blurred in the complexity of caring for patients.

Virtually everything that happens to a diabetic patient is vascular. Most people understand that the heart attacks, strokes and amputations are related to disease of the large arteries, but the blindness, nerve damage and kidney failure seen in adult onset diabetics are vascular as well. I actually became a diabetologist because of my interest in preventing adverse vascular events through optimal medical care. When I first started with this, I thought it would be about high cholesterol and high blood pressure. Very quickly, I realized that type 2 diabetics were the highest risk patients.

So it is that the pressing question in type 2 diabetes becomes:

“What are the interventions that treat the arterial disease present in all diabetics and particularly which interventions can show evidence of reducing the incidence of these devastating vascular events.”

There are many treatments for the type 2 diabetic that lower blood sugar and small vessel complications. There are few medications with evidence of benefit in lowering heart attack and stroke when compared with diet and exercise.

There have been any number of interventions aimed at patients at high risk for vascular events that make perfect sense, but do not pan out when subjected to the test of clinical trials. For example, women who are pre-menopausal are virtually bullet-proof when it comes to risk for vascular events. The menopause is associated with dramatic reductions is estrogen levels and so it must be true that estrogen is the protective agent. Therefore, giving estrogen in a pill will not only control menopausal symptoms but will protect post-menopausal women from heart attack and stroke. Brilliant reasoning-but clinical trials showed no protection. How much cost and how many side-effects have been endured for no benefit?

Similarly, HDL or good cholesterol is a topic of great interest in vascular medicine. Patients with high HDL levels have fewer cardiovascular events but HDL levels have been notoriously difficult to improve. Recently, a very promising new drug caused HDL levels to rise dramatically but the trials involving this compound were stopped because of excess vascular events.

In the treatment of cardiovascular risk factors, evidence of event reduction (reduction of adverse clinical outcomes, such as heart attacks and strokes) is king. When comparing vascular treatments, the lowering of the surrogate target of blood sugar, blood pressure, or cholesterol is necessary, but not sufficient. The real target is event reduction.

Drs. Nissen and Buse are not only justified in raising concerns about increased vascular events, they are ethically obligated to do so. This only underscores the vital importance of event outcomes studies for any medication used to reduce vascular events. Generally speaking, if you have a choice between a risk factor medication that has evidence of heart attack and stroke reduction and one that does not, take the medication with evidence of event reduction. 

Dr. Bestermann is medical director of the Vascular Medicine Center at the Holston Medical Group in Kingsport, Tennessee.

This is Dr. Bill Bestermann's first post as one of the TDWI writers (A Big Welcome, Bill!).   Dr. Bestermann makes it clear that there is a long way to go, baby, before the diagnosis and treatment of heart disease in women gets to where it should be...hey! ladies, let's WISE up!  Here you go:

The evidence has become irrefutable that life-style change and medications aimed at vascular risk factors outperform bypass surgery and stenting in prevention of heart attack. Not only that, but non-invasive strategies have positive benefits on the entire vasculature that prevent stroke, nerve damage, eye damage, kidney damage and amputation.

Women are different

These differences may be even more important for females. For some time now, there has been discussion of women being different in the manifestation of vascular disease. Women are generally smaller in stature and so would have smaller vessels. They are protected by hormonal factors and experience fewer vascular events prior to the menopause. Now it seems that women really are quite different in how they deposit atherosclerotic plaque and that this difference is important in their diagnosis and treatment.

Men are more likely to develop focal stenoses in addition to more diffuse disease. These localized narrowings may interfere with flow and lead to the classic anginal symptom of chest pain relieved by rest. Women, on the other hand have more diffuse disease that does not cause a vascular narrowing as often. Therefore, their pains are more atypical, may not be related to exertion at all, and may indicate a tendency to increased vascular reactivity and spasm. Women develop plaque and their plaque burden may be quite high, but their deposition of cholesterol is concentric, symmetrical and diffuse with the result that the vessel appears “small”.

The WISE Study

The recent WISE (Women’s Ischemia Syndrome Evaluation) Study sponsored by the National Institute of Health-National Heart Lung and Blood Institute underscores these differences. Even today, the cardiac catheterization is considered the “gold standard” when testing for the severity of heart artery disease. A woman with chest pain who has a cardiac catheterization that is normal is considered “cleared” as far as coronary disease goes and told that there is some other cause such as stress, depression, or gastrointestinal disease.

In the WISE Study 673 women had cardiac catheterizations done for the evaluation of possible coronary artery disease. 45% of these women had persistent chest pain. Women with no coronary obstruction and no chest pain had a very low rate of coronary events. Women with recurrent chest pain and normal coronary arteries had a significant 20% six-years risk of developing heart attack, cardiovascular death, stroke or congestive heart failure. This reflects the fact that plaque in women is deposited in a symmetrical fashion along the length of the artery making it appear small. In this high-risk group, only 9% of women were on lipid lowering therapy and 14% on antihypertensive treatment one year after the catheterization. Obviously, for these patients medical therapy is their only hope and they are receiving the benefit of this treatment far less often than should be the case.

The Takeaway Message

The takeaway message is that the current method of evaluating coronary arteries in standard practice may give the patient a false sense of security if there is no blockage found. There is no way that a stress test or catheterization can adequatly reassure us that that patient is low risk. The woman with persistent chest pain should be evaluated with other modalities. If coronary intravascular ultrasound is available at the time of the catheterization then that is very helpful. If not, calcium scoring correlates directly with the amount of plaque in an artery. The calcium score coupled with the Framingham risk score is a practical way to get a much better idea of the risk in a stable patient

The data indicating a need to improve risk assessment and risk factor management in these patients is clear. Still the system continues to function much as it has for over three decades. This may be the best example of how actual practice lags changes in knowledge and technology. The pace of change in how we deal with these patients has been so slow that it is hard to explain. There is always a resistance to the new way and in this case perverse financial incentives aggravate the situation.

So, what should we do?

Patients (that means you) and payors (health plans, governmental agencies, and employers) are going to have to insist that they receive the benefits of the new science before we see improved care at reduced cost.

Bill Bestermann, MD

Photo from USA Today, by Jeff Mitchell, Getty ImagesAccording to a front page story in USA Today, there has been a “mind-boggling” increase in the number of people who are severely obese (aka morbid obesity). A study, published in the journal Public Health, by RAND Corporation researcher Roland Sturm, documents that there are 2.6 million more people with a body mass index of 40 or higher than there were just five years ago. Overall almost 25% of people are now considered obese, up from 20% in 2000. A staggering 66% of people in the US are either overweight or obese.

To help us visualize what this means, USA Today published a chart to accompany the article. Here is what it takes to be obese or severely obese:

Height                    Obese                    Severely Obese

5 foot 4                             174                                             232

5 foot 10                          209                                              278

George Blackburn, associate director of nutrition at Harvard Medical School is quoted as saying the increase in the percent of severely obese people is a catastrophe.

All this fat is not going to melt away without effort — effort on the part of individuals, communities, and society as a whole. For Americans to lose all that weight and get physically fit will require both personal and collective responsibility.

We need more bike paths; attractive, easy to use stairwells; safe neighborhoods; availability of inexpensive healthy foods; PE in schools; exercise breaks at work; and, in general, an American lifestyle that makes it easier to do the right thing for our health and well-being, than the wrong.

Failure to make significant changes in our work and family lives will indeed lead to a health catastrophe – more and more childhood and adult obesity, epidemics of diabetes, heart disease, high blood pressure and abnormal lipids and other obesity-linked diseases.

So, let’s get on with it…let’s work together to get the lifestyles we want and need.  I really hope I am not writing about severe obesity levels of 30% in 2012.

Pat Salber

A bit of history

· In 1991 the NIH started two large studies, called the Women’s Health Initiative, or WHI. One study looked at postmenopausal women taking estrogen plus progestins (Prempro) for control of hot flashes and night sweats. The other study looked at postmenopausal women who have had a hysterectomy and were taking estrogen (Premarin) for control of these symptoms.

· In 2002 one WHI study was halted, because the women taking Prempro had more heart attacks than the ones who did not. At the time, this caused great confusion among women, an great surprise among physicians. No wonder: A 1985 Harvard study (the Nurses Health Study) showed that hormone use lowered heart attack risk by 50%. Several other studies, albeit smaller, showed cardiac and cholesterol profile benefits.

· As if to confirm the bad results of the first WHI study, the second one, of women taking Premarin, was halted in 2004 because of increased incidence of strokes.

A second look

A recent reanalysis of combined data of both WHI studies (a total of 27,347 women) has recently been published (JAMA, vol. 297, pp. 1465-1477, 2007). The basic finding can be summarized with the old adage: timing is all.

· Women who started taking hormones within 10 years after reaching menopause had an 11% lower risk of heart attacks.

· Women who started taking hormones within 10-19 years after reaching menopause had a 22% higher risk of heart attacks.

· Women who started taking the hormones 20 or more years after menopause had a 71% higher risk.

· All women taking hormone therapy had a slight increase of breast cancer risk.

The news is actually better than it looks. Most women who use hormonal therapy do it within 5-10 years of reaching menopause; so in terms of absolute numbers most women can safely use the hormones.

To take or not to take, that is the question

.

· The risk of breast cancer is slight, and there is no additional risk if you limit the hormone treatment to 4 years.

· There is evidence, from the WHI studies and from other studies, that hormonal therapy reduces osteoporosis and the incidence of hip fractures.

· Changes in lifestyle, like diet and exercise, have a much stronger beneficial effect on cardiac risk and osteoporosis than hormonal therapy. It is also much more pleasant, and it is risk-free.

· In the final analysis, you will have to decide if your symptoms are severe enough to justify hormonal therapy.

Caveat emptor

The new analysis did not make hormone therapy kosher for prevention of cardiac disease. For that, the best modality, as I mentioned, is a healthy diet plus physical activity. And if drugs are indicated, there are far more effective ones the estrogen.

Why the conflicting results?

There is an apparent paradox here: same studies, same set of data, yet the original analyses were so alarming that they caused both trials to be halted.

The answer is quite enlightening in terms of trial design, and in terms of public understanding of the complexity of clinical trials.

The mean age of women entering the WHI trials was 63. Women reach menopause by and large between the ages of 45 and 55, with a mean age of about 50. Therefore, most women in the study received the hormone therapy, on average, 13 years after reaching menopause. That put them at a higher risk of cardiac disease. In fact, of the 27,347 participants in the WHI studies, only 3425 women were under age 55. The beneficial effects that the drug had on the younger women were simply swamped by the deleterious effects it had on the older women, who made up the large majority (87.5%) of the study population. Only the subsequent analysis of the timing of therapy with respect to the onset of menopause could have uncovered this fact.

Dov Michaeli, MD, Ph.D

Every once in a while a medical research study is published that significantly alters clinical practice. The paper on percutaneous coronary intervention (PCI) in patients with stable coronary artery disease, published in the prestigious New England Journal of Medicine on March 26, 2007, is one such study.  The results show that PCI plus optimal medical management (lifestyle changes and drugs) are no more effective than optimal medical management alone at preventing heart attacks and death in individuals with stable coronary artery disease.

 In the NY Times’ story about the study, Steven E. Nissen, MD, President of the American College of Cardiology, describes the study as a blockbuster. And, indeed it could lead to some folks’ blocks being busted (particularly stent companies, such as Boston Scientific and the Cordis Cardiology division of Johnson and Johnson, as well as invasive cardiologists who perform these procedures).

The name of the study is COURAGE, an apt description for a study that is likely to be attacked vigorously by people who stand to lose in the high stakes arena of invasive cardiology. COURAGE stands for “Clinical Outcomes Utilizing Revascularization and Aggressive Drug Evaluation.”

Understanding plaque

In order to understand what these researchers were trying to determine, it is important to understand a bit about what causes heart attacks. Years ago, we used to think heart attacks were caused because one or more blood vessels supplying the heart became progressively more narrowed by ath