Another view on unnecessary heart surgery. - Dr. Walt

President Bush’s unnecessary heart surgery

Monday, 12 August 2013 Dr. Walt Larimore

Former president George W. Bush, widely regarded as a model of physical fitness, received a coronary artery stent last week. Few facts are known about the case, but what is known suggests to me, and many others, that the procedure may have been both unnecessary and potentially harmful – not only for Mr. Bush, but for society, in general, and Medicare, in particular.First, some very important background: Before he underwent his annual physical, Mr. Bush reportedly had no symptoms. Quite the opposite: His exercise tolerance was astonishing for his age, 67. Just before his physical exam, he rode a mountain bike more than 30 miles in the heat on a bike ride for veterans injured in the wars in Iraq and Afghanistan. I would count that as one intense cardiac stress test. By all reports, Mr. Bush was completely asymptomatic. But then, he went for one of those fancy (and very expensive) executive physicals. It was then that things began to unwind.Here’s an explanation of what happend that was published in the Washington Post. It is written by Vinay Prasad, MD, who is chief fellow of medical oncology at the National Cancer Institute and the National Institutes of Health, and Adam Cifu, MD, who is a professor of medicine at the University of Chicago.

If Mr. Bush had visited a general internist (or family physician) practicing sound, evidence-based care, he would not have had cardiac testing. Instead, the doctor would have had conducted age-appropriate cancer screening. For the former president, this would include only colon cancer screening. It no longer would include even prostate-specific antigen testing for cancer. The doctor would have screened for cholesterol, checked for hypertension and made sure the patient was up to date on age-appropriate vaccinations, including those for pneumococcal pneumonia and shingles. Presumably Mr. Bush got these things, and he got the cardiac test as well.

What value does a stress test add for an otherwise healthy 67-year-old?No study has shown that this examination improves outcomes. The trials that have been done for so-called routine stress testing examined higher-risk patients. They found that performing stress tests on people at high risk of cardiovascular disease may detect blockages but does not improve symptoms or survival. Routine stress testing does, however, increase the use of procedures such as coronary stenting.

Unfortunately, Mr. Bush, like many VIPs, may be paying the price of these in-depth investigations. His stress test revealed an abnormality, prompting another test: a CT angiogram. This study showed a blockage, which was stented open during an invasive procedure. It is worth noting that at least two large randomized trials show that stenting these sorts of lesions does not improve survival. Because Mr. Bush had no symptoms, it is impossible that he felt better after these procedures.

Instead, George W. Bush will have to take two blood thinners, aspirin and Plavix, for at least a month and probably a year. (The amount of time a blood thinner is needed depends on the type of stent placed). While he takes these medications, he will have a higher risk of bleeding complications with no real benefit.

Although this may seem like an issue important only to the former president, consider the following: Although the price of excessive screening of so-called VIPs is usually paid for privately, follow-up tests, only “necessary” because of the initial unnecessary screening test, are usually paid for by Medicare, further stressing our health-care system. The media coverage of interventions like Mr. Bush’s also leads patients to pressure their own doctors for unwarranted and excessive care.

My good friend (and internationally-recognized lipidologist [expert in cholesterol and other blood fats]), Thomas Dayspring, MD, has written a more detailed editorial, “Commentary regarding the angioplasty and stent of President George W. Bush,” for medical professionals. I encourage my health professional readers to read Tom’s commentary in detail. Here’s a small excerpt:

George W. Bush underwent stent placement because during a routine physical a stress test (which is rarely indicated in an asymptomatic person) revealed an abnormality that led to a CT-angiogram test (which is rarely indicated in an asymptomatic person) that led to a coronary angiogram test (which is rarely indicated in an asymptomatic person) that as usual led to a stent (which is rarely indicated in an asymptomatic person).

Why was an angiogram done on an asymptomatic person?

There is a bit of a history here – all public knowledge. During his second year in office during a yearly physical at Bethesda his physician did a routine coronary calcium level which was 4 (trivial). Even though his LDL-C was fine (~100 mg/dL superb by 2001 standards), they started him on a statin and as one would suspect, a low fat diet. It is well known what a super exercise routine Mr. Bush pursues (then and now): secret service men cannot keep up with him on jogs or bike rides.

Now we find out that he suddenly needed a stent?

Well do not clogged pipes; I mean arteries – need plumbers to fix them? And is it not dietary fat and cholesterol that clogs the arteries?

Earlier in the year Dr. Dayspring posted a commentary in which he answered his own questions. In the editorial, “Coronary Artery Disease as Clogged Pipes A Misconceptual Model,” Dr. Dayspring writes that his commentary, “… was provoked by a perspective authored by Michael Rothberg of the Cleveland Clinic which was published in Circulation Cardiovascular Quality Outcomes (2013;6:129-132) entitled ‘Coronary Artery Disease as Clogged Pipes: A Misconceptual Model‘.” Dr. Dayspring writes, “It is a brilliant piece and needs to be read by all health professionals, including Mr. Bush’s physicians.” Here are some of the many highlights verbatim from that perspective:

1. Although the image of coronary arteries as kitchen pipes clogged with fat is simple, familiar, and evocative, it is also wrong.
2. The clogged pipe analogy implies cholesterol plaques in the arterial walls slowly encroach on the lumen, causing silent ischemia first, then angina, and eventually infarction. Diagnosis begins with physiologic stress testing, looking for supply–demand mismatch, and progresses to angiography to find blockages. Treatments based on this theory include both coronary bypass and angioplasty, the latter often explained to patients as a Roto-Rooter.
3. Results of such revascularization procedures are visually striking and, in stable disease, may lead to the erroneous conclusion that the plumbing problem has been fixed and the risk of myocardial infarction ameliorated.
4. Although high-grade stenoses can cause chronic angina, most cardiac events occur at lesions that appeared mild on previous angiography —- Before rupture, these plaques often do not limit flow and may be invisible to angiography and stress tests. They are therefore not amenable to percutaneous coronary intervention (PCI).
5. Local interventions can only relieve symptoms; they cannot prevent future myocardial infarctions. Indeed, at least 12 randomized trials conducted between 1987 and 2007 and involving >5 000 patients have found no reduction in myocardial infarction attributable to angioplasty in any of its forms. Despite this overwhelming evidence, the plumbing model, complete with blockages that can be fixed, continues to be used to explain stable coronary disease to patients, who understandably assume that PCI will prevent heart attacks. Cardiologists also cling to the belief that for patients with stable coronary disease, an open artery is beneficial, and the approach to stable coronary artery disease continues to be a search for ischemia. Not surprisingly, a substantial minority of cardiologists also believe that elective angioplasty and stenting can prevent heart attacks.
6. The plumbing model—in which dietary fat or cholesterol is slowly deposited in arterial walls, leading to blockages—also perpetuates misconceptions about fat consumption. Although atheromatous plaques contain lipids, they are not composed of fat directly from the diet.
7. Recommended limiting total dietary fat to 30% of calories and saturated fat to 10% on the basis of the caloric density of fat and the association of saturated fat with coronary heart disease across countries. The interpretation of this evidence was selective. — low-fat diets became synonymous with heart-healthy diets and gave birth to a generation of low-fat, high-sugar substitutes. — More recent observational studies do not support the use of low-fat diets. Subsequent studies have also found no link between saturated fat and heart disease
8. In these diets, fat is simply replaced by sugar. More recently, the AHA recommended that people limit their intake now appears to contribute to obesity, hypertension, and subsequently coronary heart disease. However, patients and many doctors have not gotten this message. The AHA’s heart-healthy label still appears on a number of low-fat, high-sugar foods, including fruit juices and sugary cereals. —- patients continue to believe that dietary fat, especially the saturated fat found in cheese and bacon, is the cause of heart disease.
9. The 2011 American College of Cardiology Foundation/AHA/Society for Cardiovascular Angiography and Interventions guideline for PCI — “evaluation of 61 trials of PCI conducted over several decades shows that despite improvements in PCI technology and pharmacotherapy, PCI has not been demonstrated to reduce the risk of death or [myocardial infarction] in patients without recent [acute coronary syndrome] — clinicians and investigators, working from an outdated conceptual model, have mistakenly focused on improving the technology for keeping open flow-limiting lesions, believing that better stents would eventually yield a mortality benefit in stable disease. The inflammatory disease model makes clear that such attempts are doomed to fail because vulnerable plaques cannot be identified or stented before rupture.
10. Clearly, the current consent process in regard to PCI for stable angina is deeply flawed because most patients do not correctly understand the benefits of the procedure they are about to undergo, and many do not have angina.
11. It is difficult to admit that in the past we got it wrong and performed what now appear to have been unnecessary procedures.

Dr. Dayspring adds:

Has anyone watched the expert doctors on many TV channels commentating on Mr. Bush?

Many seem to be unaware of the concepts outlined above. A physician expert on NBC in Manhattan commented in clueless fashion that Mr. Bush’s only prayer – and that of the asymptomatic American public looking to avoid a fatal heart attack – is to restrict dietary fat ever lower. Is she aware of the recently published in the New England Journal of Medicine (the LOOK AHEAD trial) where a low fat diet/exercise regimen caused weight loss in obese T2DM (type 2 Diabetes Mellitus) patients but the trial was stopped for futility because there was no reduction in clinical CV events? Is she aware of the complete absence of clinical trials showing any benefit from a low-fat diet on any hard CV endpoint? Is she not aware that dietary cholesterol plays almost no role in atherosclerosis – that the problem is endogenously produced cholesterol?

So unless the former President was suddenly having angina-type symptoms (which has not been mentioned in any reports – and it is doubtful to me that he was as I do not see how he could be doing his intense daily exercise regimen) – there is precious little evidence that his new stent will make a damn bit of difference.

We have any number of modern trials showing aggressive medical management is just as good at reducing subsequent CV morbidity and mortality as is a “plumbing” procedure.
What Mr. Bush really needed was an intensive biomarker search to define what lipid, lipoprotein, metabolic (including insulin resistance), genetic, inflammatory, and coagulation, etc., abnormalities he has. Only then could specific nutritional and therapeutic advice be sanely offered.

If insulin resistance issues are present he needs to consult enlightened nutritionists (and cardiologists) who understand that considering the low-fat diet (and angioplasty and stents in asymptomatic individuals) to be the cure all for every case of atherosclerosis is akin to following the leech and blistering therapies of the past.

For more opinions on the inappropriateness of the workup please see this article in Heart.org.
I’ll be interested in the comments of readers.
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Read the complete article here.

Listen to Dr. William Blanchet podcast on Bush's stent here.

An incredible teaching opportunity on the basics of heart disease - Mandrola

The George W Bush stent case: An incredible teaching opportunity on the basics of heart disease

John Mandrola, MD August 11, 2013

 

The wrist artery hardly had time to seal. (Surely it was a radial.) The controversy came that fast.
The drumbeat of naysayers seemed to start only minutes after a prideful press release announced that George W Bush had undergone successful cardiac stent placement. The ever-quotable cardiologist from Cleveland Clinic, Dr. Steven Nissen, said, “This is really American medicine at its worst.” Dr. David L Brown, from Stony Brook University, and author of an important 2012 study on stents, added that GWB was “now the poster child for the inappropriate use of stenting.”

How could this be? It must be a good thing to uncover and treat heart problems before damage occurs. What do you mean he shouldn’t have had a blockage ‘fixed’ with a stent? Blockages are bad; let’s get them cleaned up. A clear artery is better than an obstructed one, right?

These common sense notions and the intense debate surrounding GWB’s stent offers us an incredible teaching moment for heart disease. It’s hard to believe our number one killer could be this misunderstood. But it is. Both doctors and patients struggle with the basics of atherosclerosis (hardening of the arteries).

This is big. Hidden in the nuances of the GWB case are important messages about the process of atherosclerosis and the significance of the vulnerable plaque. I believe advancing the knowledge of basic atherosclerosis would go far in correcting much of the over-treatment in cardiology today. The false expectations of screening stress tests and the surprise over the lack of benefit of stenting non-symptomatic disease illustrates the wide swath of misinformation out there.

My aim is to use this controversy to spread the facts and fundamentals about atherosclerosis and heart disease.

Consider this question as you read: If you had the choice between two types of blockages in one of the three main coronary arteries (the arteries that supply the heart), which would you choose: Choice A is a thick smooth 80% blockage. Choice B is a thin-walled 10% blockage.

The GWB story:
A former president of the United States gets careful medical attention. In the course of this quite careful care, a significant coronary blockage was discovered. Like many patients with heart disease, Mr. Bush had no symptoms. He did not report chest pain, shortness of breath or dizziness. He is known to be an avid cyclist, a mountain biker even. I don’t know the former president, but I know mountain bikers. He likely demanded a lot from his heart at times. GWB is also special in that it’s hard to quantify the inflammation of 8-years in the White House. (You writers know how much criticism inflames; imagine half the free world thinking badly of you.)

The controversy in this case centers on two issues: First, why did a non-symptomatic patient get an exercise study in the first place? Second, why was a stent used to treat a blockage that was not causing symptoms?

Lack of benefit for stents in stable coronary artery disease:
Let’s begin with the second issue and work backwards. To understand the stent debate, we need to start with the aptly named COURAGE trial, published in 2007 in the New England Journal of Medicine. Researchers screened many thousands of patients to come up with about 2300 study subjects with significant coronary artery disease–similar to the former president’s. COURAGE studied two treatment strategies: about 1100 patients were randomized to optimal medical therapy and another 1100 had optimal medical therapy plus a stent placed in any blockage greater than 70%. Researchers made sure both groups had intense medical therapy, including regularly scheduled nurse-managed visits, free medicines, and dietary and exercise counseling. They then followed patients for five years and compared hard outcomes. COURAGE got its acronym because it was felt courageous to leave patients with major blockages on medicine alone. Prevailing wisdom held that major blockages needed to be stented. (But you know how prevailing wisdom often turns out.)

COURAGE investigators showed that adding a stent to optimal medical therapy and lifestyle changes made no difference in the risk of death, heart attack or stroke. Criticism of COURAGE was robust. The trial enrolled mostly white male patients and bare metal (not drug-eluting) stents were used. Some said the intensity of medical therapy was unrealistic in the real world. (A highly relevant criticism in this era of lean healthcare delivery.) Applicability of COURAGE was also called into question as the investigators had to screen many thousands of patients to get down to 2300 subjects.
These findings, however, turned out to be no fluke. In 2012, a meta-analyses of 8 similar stent trials (JAMA –IM), including 7229 patients, confirmed the lack of benefit for stents in patients with stable coronary artery disease.

It was settled then; stents should only be used in symptomatic patients, like those having heart attacks, chest pain, arrhythmia, or in those with weak hearts and congestive heart failure. Using stents pre-emptively did not work to prevent heart attacks, strokes or death. For the record, when angioplasty (the precursor of stents) was used in asymptomatic patients, it did not prevent heart attack, stroke or death either.

The explanation: Consider basic atherosclerosis.
Coronary artery disease stems from diffuse disease of the blood vessel wall. (We call the inner lining of the blood vessel the endothelium.) Wrong thinking holds that blood vessels are inert pipes that carry blood to organs. So, if a blockage exists, squish it open and voila, it’s fixed. This is total nonsense. The blood vessel wall, the blood itself, and their interaction are wildly active in a biologic sense. (I hate the word dynamic, so let’s just say the endothelial-blood interface is far from static.) Sticky platelets, irritable endothelium, the two together–this is heart disease.

Think of the things that can happen in a blood vessel: One possibility is that overtime a slow-growing thick-walled plaque accumulates cholesterol and fat. The growth may enlarge enough to obstruct blood flow to the heart (or any organ). These ‘stable’ blockages can cause angina—a short supply of nutrients at times of high demand. Though impressive to look at, because of the degree of obstruction, these plaques are less of a problem. We say they are less vulnerable to rupture. What’s more, not only are these thick stable plaques unlikely to rupture, but the downstream heart muscle gets accustomed to periods of low nutrients–ischemia. We say that part of the heart is pre-conditioned for ischemia. (I’ll come back to that.)

Another (more worrisome) thing that happens in blood vessels can occur in the earlier phases of heart disease. It’s these younger, less developed, more thin-walled and non-obstructive plaques that cause heart attacks, strokes and sudden death. These are the vulnerable plaques. Because vulnerable plaques don’t obstruct blood flow and rarely have calcium in them, they are neither symptomatic nor detectable by stress testing, coronary CT or heart catheterization. Innocuously termed “lumen irregularities,” these areas of disease are where the danger lies. Here’s why: the thin-walled plaque is more likely to fissure. A tiny crack exposes the inside of the plaque to components of the blood. What happens to your skin when you cut it? It bleeds, and then a clot forms. That’s okay on you arm, but clot formation in the inside of a blood vessel leads to abrupt occlusion of the vessel—a heart attack or stroke. And sudden death due to arrhythmia can occur in this scenario because the supplied heart muscle is not used to low nutrient levels. Non-pre-conditioned heart muscle is electrically irritable. Plaque rupture is why people can die suddenly the day after a normal stress test.
And there’s more. Non-obstructive, possibly vulnerable, plaques occur throughout the three major coronary arteries. Yes, there may be one bad 80% blockage, an eyesore that captures the attention of the cardiologist, but when there is one bad blockage, there are often many other much more vulnerable plaques. So the problem with the major blockage is not just the restriction of downstream blood flow, but rather, it’s a marker for diffuse atherosclerosis. That’s one reason why stents don’t prevent heart attacks or death. The stent treats the blockage least likely to cause the calamity.
But that’s not the only problem with stents. Another issue is that stents create their own disease. The metal cage inside a blood vessel can act as a source of clots. This means patients with stents must take drugs that block platelet function. These “blood thinners” increase the risk of bleeding. The duration of anti-platelet treatment varies depending on patient and stent characteristics, but is often long-term. Stopping an anti-platelet drug shortly after a stent, say in the event of trauma or surgery, greatly increases the risk of abrupt stent closure and heart attack. So stents aren’t free; they come with significant long-term tradeoffs.

The role of Inflammation:
Coronary artery disease equals atherosclerosis. It is a diffuse process involving inflammation in the blood vessel wall. The things that cause atherosclerosis are well-known, and work through chronic inflammation. Smoking is especially terrible. It causes long-term plaque accumulation, increases in platelet stickiness and irritation of the blood vessel wall. Smoking cessation results in near immediate decreases in vulnerable plaque rupture. It’s why you see so many fewer heart attacks with smoking bans; removing exposure from smoke has an immediately soothing effect on blood vessels. High blood pressure exerts its effects on the blood vessel via physics. Imagine 100,000 daily pulses of blood through a soft flexible blood vessel versus a stiff non-complaint hypertensive one. Stiff pipes are more apt to crack. Diabetes wreaks havoc in many ways. Insulin is a real baddie for blood vessels. As a growth factor, insulin causes deposition of fat in plaques. As an inflammation mediator, insulin contributes to the irritability of plaques. You don’t want high insulin levels; this is why a low-calorie diet devoid of simple sugars is so effective. Ask the healthy 90 year-old farmer from Indiana, how much food from packages he eats. Stress takes a toll over time as well. We know chronic angst, unhappiness and anger all associate with heart disease. The common denominator here is also inflammation. When you are inflamed emotionally, so are your platelets and endothelium. Genetics plays a strong role too. We inherit eye color, personality, intelligence, aerobic prowess and so on. We also inherit susceptibility to arterial disease.

I hope you can see why treating and preventing heart disease is not just about squishing low-vulnerability plaques. You can understand why the COURAGE trial showed that adding stents to optimal medical therapy did not lower the risk of heart attack or death. And, if the plaques most likely to kill are not obstructive, you can also understand the limits of stress testing.

Effective treatment of heart disease:
Although we are not close to knowing which of the many thin-walled 10% coronary plaques are vulnerable, we still have a lot that we can do. Note the pronoun, we.
stat
Heart disease therapy means addressing a diffuse disease. It means reducing both the number of plaques and their vulnerability. Ultimately, this is about lowering inflammation. First comes lifestyle. Remember the four legs of the table of health: good food, good exercise, good sleep and good attitudes. Eating less insulin-spiking sugar, inflammatory trans-fats and fewer calories lowers inflammation. The emerging understanding of the importance of gut bacteria gives credence to the saying, we are what we eat. Nutrition is not complicated: eat real food when you are hungry. Exercising every day that you eat soothes the mind, conditions the heart and keeps the body from accumulating fat. Our bodies are beautiful; it’s tragic when humans don’t use their bodies. Getting high quality sleep lowers inflammation. You don’t need me to tell you how good it feels to sleep well. Finally, I’d bet every bike I own that compassion, grace and optimism soothe the vulnerable plaque.

After lifestyle comes medical therapy. Statin drugs don’t prevent heart attacks, strokes and death by lowering cholesterol; that’s just something us humans can easily measure. Statin drugs improve outcomes in patients with established heart disease by reducing inflammation at the arterial wall/blood interface. Beta-blockers and ACE-inhibitors (and ARBs) aren’t just simple blood pressure lowering agents. They have important activity on the neuro-hormonal milieu of the diseased heart and blood vessel. And simple aspirin therapy goes a long way in preventing platelets from accumulating on vulnerable plaques. Science confirms that these classes of drugs lower event rates in patients with established heart disease or those at high-risk of heart disease. I call them the big four heart medications. (BTW: they are all generic!)

Heart disease treatment, however, remains a team sport. Doctors can’t do it alone. Right now, there’s far too much emphasis on treating a diffuse disease with focal therapies. Stents may improve blood flow; bypass surgery may provide a brief reprieve; ICDs offer some protection to selected patients, but it will always be about lowering inflammation. There’s no pill or stent or ICD for that.

JMM
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Read the complete article here.

The angioplasty and stent of President George W. Bush - Dayspring

Commentary regarding the angioplasty and stent of President George W. Bush           

By: Thomas Dayspring, MD, FACP, FNLA, NCMP

  

Commentary from Thomas Dayspring MD, FACP, FNLA regarding the angioplasty and stent of President George W. Bush 

George W. Bush underwent stent placement because during a routine physical a stress test (which is rarely indicated in an asymptomatic person) revealed an abnormality that led to a CT-angiogram test (which is rarely indicated in an asymptomatic person) that led to a coronary angiogram test (which is rarely indicated in an asymptomatic person) that as usual led to a stent (which is rarely indicated in an asymptomatic person). Why was an angiogram done on an asymptomatic person? Did the test show early marked ST depression that suggested a main stem lesion? There is a bit of a history here – all public knowledge. During his second year in office during a yearly physical at Bethesda his physician did a routine coronary calcium level which was 4 (trivial). Even though his LDL-C was fine (~100 mg/dL superb by 2001 standards) they started him on a statin and as one would suspect, a low fat diet. It is well known what a super exercise routine Mr. Bush pursues (then and now): secret service men cannot keep up with him on jogs or bike rides. Now we find out that he suddenly needed a stent. Well do not clogged pipes; I mean arteries – need plumbers to fix them? And is it not dietary fat and cholesterol that clogs the arteries? For more opinions on the inappropriateness of the workup please see  http://www.theheart.org/article/1567069.do

 

Earlier in the year I posted a commentary on LecturePad.org regarding “Clogged Arteries.” (click here to review) That posting was provoked by a perspective authored by Michael Rothberg of the Cleveland Clinic which was published in Circulation Cardiovascular Quality Outcomes. (Circ Cardiovasc Qual Outcomes. 2013;6:129-132) entitled Coronary Artery Disease as Clogged Pipes A Misconceptual Model. It is a brilliant piece and needs to be read by all providers including Mr. Bush’s physicians. Here are some of the many highlights verbatim from that perspective ....

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Read the complete article here.

I also recommend The Doc's Opinion on President Bush here.

Listen to podcast by Dr. William Blanchet here.