If you’ve had a coronary stent implanted or undergone bypass surgery, it is common to wonder about the status of the stent or the bypass grafts or the coronary arteries that maybe had a 50 or 60% blockage and were left alone.
This is especially likely if there was little or no warning that you had really severely blocked coronary arteries.
After all, you are thinking: “doesn’t it make sense to monitor these things and stay on top of them; be proactive?”
It certainly seems reasonable on the surface, and for many years, routine stress testing of patients without symptoms on an annual basis, was the norm.
However, this practice is much more likely to cause harm than to benefit patients and is recognized by the American College of Cardiology as one of 5 things that patients and physicians should question as part of the “Choosing Wisely” campaign (see here).
“Performing stress cardiac imaging or advanced non-invasive imaging in patients without symptoms on a serial or scheduled pattern (e.g., every one to two years or at a heart procedure anniversary) rarely results in any meaningful change in patient management. This practice may, in fact, lead to unnecessary invasive procedures and excess radiation exposure without any proven impact on patients’ outcomes.”
Studies have shown that stress testing less than two years after a coronary stent, very rarely change management.
The American College of Cardiology, American Society of Echocardiography and the American Society of Nuclear Medicine are all in agreement that stress testing less than two years after a coronary procedure is “inappropriate,” and more than two years after the procedure is “uncertain.”
Why Do Cardiologists Order These Tests If They Are Inappropriate?
There are 3 reasons, and they are representative of the major factors driving all over-testing in medicine.
Financial. Cardiologists frequently benefit from stress tests they order in multiple ways. First, they may own the nuclear camera used in the test and the more stress tests performed in their office, the more money they will make from the technical remuneration for the procedure. The cardiologist also frequently interprets the test results and receives a professional fee for both supervising and interpreting the nuclear images. Finally, if the test is abnormal, the cardiologist may then recommend additional testing, which he may perform (cardiac catheterization, stent) or interpret (coronary CT angiogram).
Defensive medicine. It is not uncommon for cardiologists to be sued for NOT performing a test or procedure when the patient’s outcome is bad. On the other hand, I have never heard of a cardiologist being sued for DOING an inappropriate stress test.
Keeping the customer happy. Too often patients feel that if their doctor is performing frequent tests on them, he is being vigilant, proactive and “staying on top of things.” They don’t realize the down sides to the extra testing and the lack of benefit.
Not uncommonly, patients switching to me from another cardiologist indicate that they have been getting an annual stress test and are disappointed to hear that I am not recommending one.
They may think that I’m lazy or not up on the latest techniques in cardiology. Usually in this situation I have to spend a fair amount of time trying to teach them about the possible downsides of over-testing.
In the case of stress nuclear testing, harm comes from two sources:
Radiation. Stress nuclear tests typically utilize the radio tracer Technetium-99 and result in a radiation dose of around 15 mSv. This is about 10 times the radiation from a typical coronary calcium scan. A chest x-ray gives 0.02 mSV and the annual background radiation in the US is 3 mSv.
False positives. Nuclear imaging is very susceptible to images which appear to show abnormalities of blood flow, which in reality are just due to soft tissue (breast, diaphragm, fat) interposed between the heart and the camera. These can be interpreted as due to a heart attack or blocked coronary artery when everything is actually fine with the artery. False positives then lead to additional testing such as a cardiac catheterization, which carries risks of bleeding, heart attack, stroke and death.
One important point to remember is that coronary stenting has not been shown to reduce heart attacks or prolong survival outside the setting of an acute heart attack. Therefore , if you’ve already had a cardiac catheterization that either resulted in bypass surgery or a stent of one artery, it is highly unlikely that a subsequent catheterization/further procedures will lower your heart attack or dying risk.
Certainly, if you have a change in symptoms that suggest that your coronary artery disease has progressed, this is an appropriate reason to consider stress testing. Such symptoms include shortness of breath on exertion and chest discomfort, especially if it occurs during activity. Diabetics often don’t have symptoms that warn them of a problem, therefore, we should consider stress testing more frequently and at a lower threshold for them.
For most people, however, more is not always better when it comes to cardiac testing and, in many circumstances, can be worse.
Why is death from coronary heart disease declining in the US at the same time that obesity and diabetes rates are climbing?
Two editorials recently published in The Lancet show the widely varying opinions on the optimal diet for controlling obesity , diabetes and coronary heart disease that experts on nutrition, diabetes and heart disease hold.
The first paper contains what I would consider the saturated fat “traditionalist” viewpoint. This is a modification of the misguided concept that was foisted on the American public in the 1980s and resulted in the widespread consumption of industrially produced trans-fats and high sugar junk food that was considered heart healthy.
The traditionalists have shifted from condemning all fats to vilifying only saturated and trans fats. They would like to explain at least part of the reduction in coronary heart mortality as due to lower saturated fat consumption and the accompanying lowering of LDL (“bad”) cholesterol.
The SFA traditionalists fortunately are in decline and more and more in the last five years, prominent thinkers, researchers and scientists working on the connection between diet and the heart believe saturated fats are neutral but sugar and refined carbohydrates are harmful in the diet.
Darius Mozzafarian, a highly respected cardiologist and epidemiologist, who is dean of the School of Nutrition Science and Policy at Tufts, wrote the second editorial and is what I would term a saturated fatty acid (SFA) progressive.
He makes the following points which are extremely important to understand and which I have covered in previous posts. I’ve included his supporting references which can be accessed here.
Fat Doesn’t Make You Fat, Refined Starches And Sugar Do
"Foods rich in refined starches and sugars—not fats—seem to be the primary culprits for weight gain and, in turn, risk of type 2 diabetes. To blame dietary fats, or even all calories, is incorrect
Although any calorie is energetically equivalent for short-term weight loss, a food's long-term obesogenicity is modified by its complex effects on satiety, glucose–insulin responses, hepatic fat synthesis, adipocyte function, brain craving, the microbiome, and even metabolic expenditure Thus, foods rich in rapidly digestible, low-fibre carbohydrates promote long-term weight gain, whereas fruits, non-starchy vegetables, nuts, yoghurt, fish, and whole grains reduce long-term weight gain.1, 2, 3
Overall, increases in refined starches, sugars, and other ultraprocessed foods; advances in food industry marketing; decreasing physical activity and increasing urbanisation in developing nations; and possibly maternal–fetal influences and reduced sleep may be the main drivers of obesity and diabetes worldwide".
There Are Many Different Kinds of Saturated Fats With Markedly Different Health Effects: It Makes No Sense to Lump Them All Together
"SFAs are heterogeneous, ranging from six to 24 carbon atoms and having dissimilar biology. For example, palmitic acid (16:0) exhibits in vitro adverse metabolic effects, whereas medium-chain (6:0–12:0), odd-chain (15:0, 17:0), and very-long-chain (20:0–24:0) SFAs might have metabolic benefits.4 This biological and metabolic diversity belies the wisdom of grouping of SFAs based on a single common chemical characteristic—the absence of double bonds. Even for any single SFA, physiological effects are complex: eg, compared with carbohydrate, 16:0 raises blood LDL cholesterol, while simultaneously raising HDL cholesterol, reducing triglyceride-rich lipoproteins and remnants, and having no appreciable effect on apolipoprotein B, 5 the most salient LDL-related characteristic. Based on triglyceride-lowering effects, 16:0 could also reduce apolipoprotein CIII, an important modifier of cardiovascular effects of LDL and HDL cholesterol. SFAs also reduce concentrations of lipoprotein(a) ,6 an independent risk factor for coronary heart disease."
The Effects of Dietary Saturated Fats Depend on Complex Interactions With The Other Ingredients in Food
"Dietary SFAs are also obtained from diverse foods, including cheese, grain-based desserts, dairy desserts, chicken, processed meats, unprocessed red meat, milk, yoghurt, butter, vegetable oils, and nuts. Each food has, in addition to SFAs, many other ingredients and characteristics that modify the health effects of that food and perhaps even its fats. Judging the long-term health effects of foods or diets based on macronutrient composition is unsound, often creating paradoxical food choices and product formulations. Endogenous metabolism of SFAs provide further caution against oversimplified inference: for example, 14:0 and 16:0 in blood and tissues, where they are most relevant, are often synthesised endogenously from dietary carbohydrate and correlate more with intake of dietary starches and sugars than with intake of meats and dairy.4"
Dietary Saturated Fat Should Not Be a Target for Health Promotion
"These complexities clarify why total dietary SFA intake has little health effect or relevance as a target. Judging a food or an individual's diet as harmful because it contains more SFAs, or beneficial because it contains less, is intrinsically flawed. A wealth of high-quality cohort data show largely neutral cardiovascular and metabolic effects of overall SFA intake.7 Among meats, those highest in processing and sodium, rather than SFAs, are most strongly linked to coronary heart disease.7Conversely, higher intake of all red meats, irrespective of SFA content, increases risk of weight gain and type 2 diabetes; the risk of the latter may be linked to the iron content of meats.2, 8 Cheese, a leading source of SFAs, is actually linked to no difference in or reduced risk of coronary heart disease and type 2 diabetes.9, 10 Notably, based on correlations of SFA-rich food with other unhealthy lifestyle factors, residual confounding in these cohorts would lead to upward bias, causing overestimation of harms, not neutral effects or benefits. To summarise, these lines of evidence—no influence on apolipoprotein B, reductions in triglyceride-rich lipoproteins and lipoprotein(a), no relation of overall intake with coronary heart disease, and no observed cardiovascular harm for most major food sources—provide powerful and consistent evidence for absence of appreciable harms of SFAs."
Dietary Saturated Fats May Raise LDL cholesterol But This Is Not Important: Overall Effects On Obesity and Atherosclerosis Are What Matters
"a common mistake made by SFA traditionalists is to consider only slices of data—for example, effects of SFAs on LDL cholesterol but not their other complex effects on lipids and lipoproteins; selected ecological trends; and expedient nutrient contrasts. Reductions in blood cholesterol concentrations in Western countries are invoked, yet without systematic quantification of whether such declines are explained by changes in dietary SFAs. For example, whereas blood total cholesterol fell similarly in the USA and France between 1980 and 2000, changes in dietary fats explain only about 20% of the decline in the US and virtually none of that which occurred in France.11Changes in dietary fats11 simply cannot explain most of the reductions in blood cholesterol in Western countries—even less so in view of the increasing prevalence of obesity. Medication use also can explain only a small part of the observed global trends in blood cholesterol and blood pressure. Whether decreases in these parameters are caused by changes in fetal nutrition, the microbiome, or other unknown pathways remains unclear, thus highlighting a crucial and greatly underappreciated area for further investigation."
Dietary Saturated Fats Are Neutral For Coronary heart Disease Risk
Finally, SFA traditionalists often compare the effects of SFAs only with those of vegetable polyunsaturated fats, one of the healthiest macronutrients. Total SFAs, carbohydrate, protein, and monounsaturated fat each seem to be relatively neutral for coronary heart disease risk, likely due to the biological heterogeneity of nutrients and foods within these macronutrient categories.7Comparisons of any of these broad macronutrient categories with healthy vegetable fats would show harm,12 so why isolate SFAs? Indeed, compared with refined carbohydrates, SFAs seem to be beneficial.7
The overall evidence suggests that total SFAs are mostly neutral for health—neither a major nutrient of concern, nor a health-promoting priority for increased intake.
Focusing On Reducing Saturated Fats Leads To Unhealthy Dietary Choices
"Continued focus on modifying intake of SFAs as a single group is misleading—for instance, US schools ban whole milk but allow sugar-sweetened skim milk; industry promotes low-fat foods filled with refined grains and sugars; and policy makers censure healthy nut-rich snacks because of SFA content.13 "
It is extremely hard to change most people’s opinions on dietary fat.
My patients have been hearing the SFA traditionalist dogma for decades and thus it has become entrenched in their minds.
When I present to them the new progressive and science-based approach to fat and saturated fat some find it so mind boggling that they become skeptical of the skeptical cardiologist!
Hopefully, in the next few years, the progressive SFA recommendations will become the norm and maybe , some day in the not too distant future, the inexplicable recommendations for low-fat or non fat dairy will disappear.
As more data accumulates we may become SFA enthusiasts!
For another viewpoint (?from an SFA enthusiast) and a detailed description of both editorials see Axel Sigurdsson’s excellent post here.
These members of the “calcium club” are portrayed as unbiased self-less promoters of the prevention of heart attacks and sudden death, fighting an uphill battle against the evil procedure and money-driven forces who push coronary stents-greedy interventional cardiologists and the device, hospital and insurance industries.
A constant theme in the documentary is that CAC scanning should be to the heart what mammography is to the breast. It should be done on all patients over a certain age and should be covered by insurance.
As a non-invasive cardiologist with a strong interest in prevention, I am definitely a strong proponent of CAC scans in the right population. As the skeptical cardiologist, however, I find flaws with the mammography comparison.
Let’s review some of the established science regarding CAC scans.
What Is A CAC Scan?
The CAC scan utilizes computed tomography (CT) X-rays, without the need for intravenous contrast, to generate a three-dimensional picture of the heart. Because calcium is very apparent on CT scans, and because we can visualize the arteries on the surface of the heart that supply blood to the heart (the coronary arteries), the CAC scan can detect and quantify calcium in the coronary arteries with great accuracy and reproducibility.
A preventive cardiologist, Dr. Arthur Agatson, who is interviewed in the film (and who is also the creator of the South Beach Diet, a low carbohydrate, high fat diet), developed a method for counting up the amount of calcium in the coronary arteries (the Agatson or calcium score).
Calcium only develops in the coronary arteries when there is atherosclerotic plaque. The more plaque in the arteries, the more calcium.
What Is The Risk Of A High CAC Score
Multiple observational studies have shown that a high versus low calcium score is indicative of high risk for heart attack and death.
For example, a large study published in 2008 (the MESA study), followed 6,814 individuals for 3.8 years. Compared with patients with a CAC score of 0, patients with a CAC score of 101-300 had a 7.7 fold increase risk of a coronary event (heart attack). CAC score of >300 conferred almost a tenfold increase risk.
Based on data from 5 large studies and almost 15,000 patients, we can put patients with CAC score in very low to high risk categories for cardiac events over the next 10 years.
What Is The Value Of A Zero Calcium Score?
Just as important as identifying patients with advanced or premature atherosclerosis who should be getting intensive therapy for prevention of cardiac events, is identifying those patients who may not warrant therapy.
A CAC score of zero puts a patient in an extremely low risk category. A recent study, with the provocative title of:
A 15-Year Warranty Period for Asymptomatic Individuals Without Coronary Artery Calcium
…demonstrated that a zero calcium score confers this low risk of cardiac events for up to 15 years.
Thus, many patients, who are considered intermediate risk based on standard risk factors, do not have significant plaque by CAC score and may not need otherwise indicated statin therapy.
The comparison of mammography to CAC scanning is appropriate in that both have created considerable controversy and are at the epicenter of discussions on the value of mass screenings in the prevention of life-threatening disease.
In contrast to CAC, mammography has been widely accepted and promoted by most professional organizations. In recent years, however, the value of mammography for all women over the age of 40 has been questioned.
In 1980, a randomized controlled trial of screening mammography and physical examination of breasts in 89, 835 women, aged 40 to 59, was initiated in Canada. It was called the Canadian National Breast Screening Study.
The findings published last year were:
Annual mammography in women aged 40-59 does not reduce mortality from breast cancer beyond that of physical examination or usual care when adjuvant therapy for breast cancer is freely available. Overall, 22% (106/484) of screen detected invasive breast cancers were over-diagnosed, representing one over-diagnosed breast cancer for every 424 women who received mammography screening in the trial.
Downsides of breast cancer mammography screening include:
-Over-diagnosis: finding and treating breast cancer that would not have been a threat to the patient.
-False positives: the test identifies a possible cancer which is not subsequently confirmed. False positives lead to breast biopsies, which are not needed and often cause needless anxiety and stress.
Is CAC Screening The Cardiac Equivalent Of Mammography?
CAC scans differ fundamentally from mammography because atherosclerosis is a continuous and diffuse arterial process, whereas breast cancer is (most often) localized, and either present or not.
The development of atherosclerosis starts with fatty streaks in multiple arterial beds fairly early in life, followed by progressive plaque development with progressive build up of calcium in the plaques.
Thus, the CAC score ranges continuously from zero up to several thousand.
The calcium score is not subject to false positives-if calcium is detected, atherosclerotic plaque is present.
A mammogram is either abnormal, suggesting cancer and requiring a biopsy, or it is normal. There is no continuous grading of risk.
The second fundamental difference in the two disease processes is that atherosclerosis can kill suddenly without warning.
As pointed out in numerous examples in The Widowmaker, an individual can seem fit and hearty one minute, and be dead the next, from a heart attack caused by a lethal abnormal rhythm.
Breast cancer deaths on the other hand, occur slowly after diagnosis, and are generally predictable.
Nuclear Stress Tests are the Mammography of the Heart
If we are looking for a cardiac test that has characteristics similar to mammography, the nuclear stress test is much closer than CAC.
With a nuclear stress test we are using a radio tracer injected intravenously, which subsequently traverses the coronary arteries into the heart muscle. Subsequent imaging of the photons emitted by the radio tracer allows assessment of the status of blood flow down the coronary arteries.
The test is designed to identify coronary arteries with flow limiting blockages (usually >70% blocked), caused by atherosclerotic plaques. Such blockages are more likely to be causing symptoms and therefore more likely to require treatment with coronary stents or bypass surgery.
Like mammography, then, nuclear stress tests are either abnormal or normal, and when abnormal they can be falsely abnormal.
Nuclear stress tests have a very high incidence of false positives. These false positives result in invasive catheterization procedures to more directly image the arteries, and may result in inappropriate coronary stenting or bypass procedures with associated risks.
It is because of the high risk of false positives and attendant harm that in the last decade, all cardiac societies recommend against the routine use of stress testing in asymptomatic patients.
As pointed out in the Widowmaker, there is no data which suggest that stress testing improves outcomes for cardiac patients.
Stress tests by design tell us nothing about the noncritical build up of atherosclerotic plaque. You can have a normal stress test and have a huge burden of plaque in your arteries.
It is this silent build up of atherosclerosis, with sudden rupture of plaque, which results in sudden death in most cardiac patients.
What Is The Breast Cancer Equivalent Of CAC?
A CAC of the breast would identify abnormal cells as soon as they began on the presumably multi-year road to becoming a full flown cancer.
To be fully equivalent to the CAC, the breast CAC would have to have a proven treatment that could be instituted once a certain stage of cell transformation had been reached.
For atherosclerosis, that treatment is statin drugs, which are recommended for those with high risk CAC scores.
For breast cancer, the treatment of choice is mastectomy.
Would Widespread Institution of CAC Screening Save Millions of Lives?
For mammograms based on a review of all the evidence, the US PTF concluded:
Over a 10-year period, screening 10,000 women ages 50 to 59 years will result in 8 (95% confidence interval [CI], 2 to 17) fewer breast cancer deaths, and screening 10,000 women ages 60 to 69 years will result in 21 (95% CI, 11 to 32) fewer deaths.
To scientifically determine how many lives are saved by CAC screening, we would need an extremely large randomized controlled trial lasting for at least 6 years.
Individuals with low or intermediate risk from standard risk factors for atherosclerosis would receive a standard approach to management or would undergo CAC screening with treatment determined by calcium score.
Such trials have been proposed but to date have not been funded by the NIH thus we may not have a definite answer for a long time.
Should CAC Scans Be Covered Like Mammography?
I am very conflicted on this question.
On one hand I do believe that appropriate use of CAC scans prevents heart attacks and sudden death. How many, remains to be seen. As we saw for mammography, only large scale randomized trials will tell us for sure who will benefit and how much.
On the other hand, I can see potential for abuse, and in the wrong hands, excessive downstream invasive testing, which will minimize the benefits of early detection.
If CAC scans are covered by insurance and used widely, they could become a method for unscrupulous cardiology centers and doctors to proceed to unnecessary testing that would ultimately increase the amount of inappropriate coronary stenting.
Indeed, it is quite ironic that the major theme of The Widowmaker, that of the medical-industrial stent complex suppressing CAC scan usage, is quite illogical, for widespread, injudicious use of CAC scanning would be a boon for stent inserters and makers.
The inappropriate use of CAC scan information is limited currently because most of the doctors ordering them are primarily interested in prevention, not in generating more testing and procedures.
The other limit on its use is cost. For 99% of my patients the $125 for a CAC scan at my hospital is not a limiting factor.
On the other hand, in a less affluent population, this would be a large and limiting expense; the poor would be getting a lesser standard of care.
The cases of patients in The Widowmaker who feel like a CAC scan saved their lives are very similar to those of breast cancer patients who feel mammography saved theirs.
These patients often become passionate advocates for a specific test based on their own experience. The Widowmaker, in fact, was funded by David Bobbett, an Irish millionaire who discovered that he had an extremely high calcium score and now feels like everyone should get the test.
Bobbett is convinced that the test saved his life, but all anecdotal patient stories about CAC scans “saving their life” have to be taken with a grain of salt.
After this (far too long) discussion I have to conclude that although they share many features, CAC scans are not the mammography of the heart.
The documentary, The Widowmaker (available on Netflix streaming) should definitely be watched by everyone.
It presents some great information on dying suddenly from heart attacks in an entertaining way.
It makes two important points: coronary stents don’t prevent heart attacks and coronary scans can identify advanced coronary artery disease before heart attacks happen.
I am in total agreement with these two points and have made them several times in previous posts (here and here).
The film is a work of advocacy, however, and twists the truth to prove its underlying theory: that greedy doctors and hospitals are choosing to “push” expensive coronary stents that do no good until you are having a heart attack. Also, that doctors and hospitals are also somehow suppressing the use of coronary calcium scans, which could prevent millions of heart attacks and deaths.
Creating black and white heroes and villains in documentaries makes for riveting entertainment, but often at the cost of sacrificing the truth.
Let’s look at the villains that The Widowmaker presents.
First up is Julio Palmatz. Dr. Palmatz is a vascular radiologist who invented, along with Dr. Shatz, one of the three primary stents that ultimately gained widespread clinical usage. The Widowmaker implies that Palmatz was THE stent developer, and follows Julio as he revisits the garage in Texas where he developed prototypes for the slotted tube stent.
At this point in the movie, it would be understandable if you thought Julio was going to be one of the heroes. He seems very personable as he describes the inspiration for his stent design and points out the area in the garage where his work bench stood.
However, the documentary wants, ultimately, to portray Palmatz as greedy, unconcerned about patient welfare, and in the pocket of wealthy investors.
He has done well financially because the patent on his coronary stent was eventually sold to Johnson and Johnson for millions (and he is interviewed on the grounds of his Napa Valley vineyard).
A recent scholarly analysis of the process of the development of stents differs with this portrayal of Palmatz:
“We found that the first coronary artery stents emerged from three teams: Julio Palmaz and Richard Schatz, Cesare Gianturco and Gary Roubin, and Ulrich Sigwart. First, these individual physician-inventors saw the need for coronary artery stents in their clinical practice. In response, they developed prototypes with the support of academic medical centers leading to early validation studies. Larger companies entered afterwards with engineering support. Patents became paramount once the technology diffused. The case of coronary stents suggests that innovation policy should focus on supporting early physician-inventors at academic centers.”
Although stents ultimately have become over-utilized, they represent a tremendous invention and contribution to cardiac care.
In the setting of acute heart attacks, stents are clearly life saving and thousands of patients have had their clinical angina or claudication greatly relieved when stents are utilized appropriately for blocked coronary and peripheral arteries.
Consequently, Palmatz and many of the other interventional cardiologists who developed and performed early studies on coronary stents are widely considered heroes by the vast majority of knowledgeable cardiologists.
There is no evidence that they have colluded with industry to inappropriately promote stents or to suppress utilization of methods for early diagnosis and prevention of coronary artery disease.
The documentary then switches to characterizing the world of cardiology after stents were approved by the FDA in the early 90s.
There clearly was (and is) an irrational exuberance about stents and some of this sprang from excellent reimbursement for doing the procedures.
The focus moves to Mt. Sinai Hospital in Manhattan, and arguably the busiest interventional cardiologist in the world, Samir Sharmin.
The movie implies that Mt. Sinai was going broke until it began performing lots of catheterization and stent procedures. Sharmin who does over 1500 interventions per year and apparently earns over 3 million dollars per year is interviewed and filmed performing a stent procedure.
The average viewer likely gathers from the context of the interview with Sharmin, that he is only doing these procedures to make money.
At various points during the movie, Dr. Steven Nissen, past president of the American College of Cardiology, is interviewed and referred to as “America’s top cardiologist.”
In my opinion, Nissen has been an outstanding, independent voice of reason in the world of cardiology. During the interview, he makes the very valid points that coronary calcium scans have not been embraced for routine usage because there are no outcomes data.
At one point he says, “I don’t like medical cults” in reference to those who support more widespread coronary calcium scans.
The movie leaves the uninformed viewer thinking that Nissen is part of a cabal blocking coronary calcium scans, perhaps due to his connections with industry or an inappropriate resentment of the “calcium club” pushing the scans.
Nothing could be further from the truth. I think Nissen is one of the few prominent cardiologists who are not subject to major bias of one type or another and I strongly respect his opinions.
The movie also attempts to portray the editor of Circulation, a major cardiology journal supported by the American Heart Association as inappropriately withdrawing a paper that would have endorsed coronary calcium scanning. It’s not possible to really tell what the truth is about this withdrawal, but this is a very minor episode in the history of coronary calcium scanning.
Ultimately, The Widowmaker fails its audience in presenting the truth because it desperately wants to convince us that there is a connection between the promotion of coronary stents and the failure of coronary calcium scans to be accepted by guidelines and covered by insurance.
There is no such connection. Many interventional cardiologists are enthusiastic promoters of prevention and aggressive use of coronary calcium scans. I have seen no evidence of greedy interventionists trying to suppress coronary scans.
In Part II of this analysis, I will take a look at the “heroes” of The Widowmaker, the inventors and promoters of coronary calcium scans, and we will see if they are truly heroic.
I’ve just finished watching a documentary on Netflix called The Widowmaker which alternately had me fascinated, disgusted, bored, excited, and angry.
This movie is about the treatment of coronary artery disease and what we can do about the large number of people who drop dead from heart attacks, some 4 million in the last 30 years.
The documentary, as all medical documentaries tend to do, simplifies, dumbs down and hyperbolizes a very important medical condition. Despite that it makes some really important points and I’m going to recommend it to all my patients.
At the very least it gets people thinking about their risk of dying from heart disease which remains the #1 killer of men and women in the United States.
Perhaps it will have more patients question the value of stents outside the setting of an acute heart attack. This is a good thing.
Perhaps it will stimulate individuals to be more proactive about their risk of heart attack. This is a good thing.
Take a look. Think about it. If you decide you might benefit from a coronary calcium scan of your heart let me know.
I’ll dissect this movie in detail in subsequent posts. There are a lot of inaccuracies but some fundamental and important points are made that patients need to now.
Stents do not prevent heart attacks.
Standard risk factors do not do well at predicting who will have a heart attack.
The skeptical cardiologist has heard a few cardiologist colleagues rave about the movie “Forks Over Knives” and promote the so-called “whole-foods, plant based diet.”
One of the two major physician figures in the movie is Dr. Caldwell Esselstyn, a former surgeon and now a vegan evangelist.
Esselstyn, along with T. Colin Campbell (of the completely discredited “China Study” (see here for a summary of critical analyses of that data), Dean Ornish, and Nathan Pritikin, are the leading lights of a dying effort to indict any and all fat as promoting heart disease and all the chronic diseases of western civilization.
Esselstyn, in his book, “Preventing and Reversing Heart Disease” lists the following rules:
you may not eat anything with a mother or a face (no meat, poultry, or fish)
you cannot eat dairy products
you must not consume oil of any kind
generally you cannot eat nuts or avocados
What? No Fish or Olive Oil? You Cannot Be Serious!
The best randomized controlled trials we have for diet to prevent coronary artery disease (CAD, the cause of heart attacks) have shown that supplementing diet with olive oil and nuts substantially lowers CAD.
Every observational study in nutrition has demonstrated that fish consumption is associated with lower cardiovascular disease.
Esselsstyn’s Really Bad Science
While working at the Cleveland Clinic, Esselstyn developed an interest in using a plant-based diet to treat patients with advanced CAD. He says he had an epiphany one rainy, depressing day when he was served a slab of bloody roast beef.
In his own words:
“my original intent was to have one group of patients eating a very-low fat diet and another receiving standard cardiac care and then compare how the two groups had fared after three years.”
If he had followed his original intent, and randomized patients entering the study, he could claim that he had performed a legitimate, important scientific study. Twelve of the 24 would be allocated by lottery to the Esselstyn diet and 12 to whatever was the standard recommended CAD diet at the time. Unfortunately this approach, due to a “lack of funding, was not practical.”
So instead, 24 patients were sent to him, “all suffering from advanced CAD” and began the horrifically strict dietary program he had developed based on his “logic and intuition.”
Interestingly, patients not only were put on Esselstyn’s incredibly low fat diet, but they were also given cholesterol lowering medications and were “switched to statin as soon as these became available in 1987.”
In addition, 9 of the 18 patients who stuck with the program had previously undergone coronary bypass surgery and two had undergone angioplasty of a coronary artery.
6 of the 24 original patients “could not comply with the program” and were sent back to their regular cardiologists. This gives you an idea of how difficult it was to follow this diet.
Esselsstyn’s “data” then consists of following 18 patients, 9 of whom had already undergone coronary bypass surgery, all of whom were taking statin drugs with his diet without any comparison group.
This group of 18 did well from a heart standpoint, of course. It is impossible to know if the diet had anything to with their outcome. Most of them had already undergone the “knife” or had had angioplasties that took care of their most worrisome coronary blockages. They were all taking statin drugs . They were all nonsmokers and they were all highly motivated to take good care of themselves in all lifestyle choices.
Any patients who were not intensely motivated to radically change their diet would have avoided this crazy “study” like the plague.
This “study” is merely a collection of 18 anecdotes, none of which would be worthy of publication in any current legitimate medical journal.
Three of the 18 patients have died, one from pulmonary fibrosis, one presumably from a GI bleed, and one from depression. Could these deaths be related to the diet in some way? We can’t know because there is no comparison group.
Should Anyone Eat Ultra-low Fat Diets?
It is possible that the type of vegan/ultra-low fat diets espoused by Esselstyn and his ilk have some beneficial effects on preventing CAD, but there is nothing in the scientific literature which proves it.
Scientific reviews of the effect of diet on CAD in the last 5 years have concluded that the evidence is best for the Mediterranean diet, which emphasizes fish consumption, olive oil and nuts. These reviews dismiss ultra-low fat diets because of a lack of evidence supporting them, and an inability to get people to follow them.
If you have ethical or philosophic reasons for only eating things with no mother or face, then by all means follow your conscience.
Too often, however, I find that those who choose veganism for philosophic reasons want to find health reasons to support their diet and mix the bad science and philosophy into a bland evangelical stew they recommend for all.
I remain, therefore, in favor of cioppino, paella, butter and all the glories of the omnivore that make life so rich.
I have updated this post with comments from readers and my response along with analysis of the latest “data” from Dr. Esseslstyn’s “study” at my post entitled:
No, you are not “sabotaging” your heart with statin drugs. Neither are you “wrecking” your heart.
But that title probably got your attention if you are taking a statin drug and thought that it was helping your heart.
This question is prominently displayed on the Health portion of a news website called Newsmax, that somehow interrupted my web surfing today. If you click on the banner, you will get to listen to the words of Dr. David Brownstein, “America’s most popular family physician.”
Dr. Brownstein, in my opinion, should more properly be termed “one of America’s most popular quacks, charlatans and purveyors of misinformation in order to market useless junk.”
What Brownstein says can be found on multiple similar sites across the internet which are promoting “alternative” or “natural” approaches to high cholesterol.
His claims can be summarized as follows:
statin drugs do nothing to protect you from heart attacks
statin drugs “weaken your heart,” muscles, cause fatigue and lower your sex drive, damage your kidneys and liver
statin drugs prevent the formation of cholesterol which is essential for brain, sex hormone and vitamin D production
1/2 of people with heart attacks have normal cholesterol levels
CHF is increasing in frequency and it is related to an increase in statins and consumption of sugar and refined carbohydrates
Big pharma has perpetrated the biggest fraud in medical history on the American public by brainwashing doctors, beginning in medical school, to prescribe statin drugs
These claims resonate with patients who are reluctant to take medications and who feel that “natural” approaches to prevention and treatment are superior.
Brownstein uses a combination of alarmist rhetoric and pseudoscientific jargon that appeals to those seeking alternatives.
Let’s look at his claims.
Do Statins Prevent heart Attacks?
Statins unequivocally prevent heart attacks in patients who have had heart attacks or have evidence of advanced vascular disease due to atherosclerosis. This is called secondary prevention and there are almost no cardiologists/scientists with any credibility who dispute the value of statins in secondary prevention.
The only specific study that Brownstein cites is the ASCOT-LLA study, published in 2003 which looked at ten thousand patients with hypertension, no heart disease and low or normal cholesterol levels, half of whom got 10 mg of atorvastatin and half a placebo.
This was a primary prevention study and showed such a benefit of the atorvastatin on reducing heart attack and coronary deaths that the study was stopped early, at 3.3 years at which time 154 patients receiving placebo versus 100 receiving atorvastatin had had heart attacks or died from coronary disease.
This was a highly significant reduction in events. There are several ways to look at this data and present it to patients; Brownstein implies that “Big pharma” presented the most favorable way, which is that there was a 36% reduction in relative risk.
The absolute risk of an event in the atorvastatin group was 1.7% (2.7% in the placebo group), so the absolute risk reduction was from 2.7% down to 1.7% or 1%.
To help better understand the data, we can also look at the number needed to treat (NNT). The NNT is the inverse of the absolute risk reduction. So for the ASCOT trial, the absolute risk reduction was 1%. 1 divided by 1% is 100 — 100 people would need to be treated with atorvastatin (the generic of Lipitor) over the study period to prevent one heart attack. (For more discussion on the NNT check out this blog post and this paper on its limitations)
Understandably, Pfizer, the makers of atorvastatin, prominently displayed the 36% relative risk reduction in their direct to consumer marketing campaigns (featuring Dr.Robert Jarvik (proclaiming himself a doctor in direct to consumer videos), although he was never a licensed physician (see here for interesting discussion on the controversy that ensued)).
Until, the FDA compels them to do otherwise, big pharma will project their products in the most favorable light possible.
However, it is debatable whether presenting data to patients using absolute risk reductions or NNT info plus relative risk reductions results in better choices. As Mcalister has pointed out:
“For example, many British patients with atrial fibrillation who were likely to benefit from anticoagulant therapy because of their risk profiles and their similarity to the participants in randomized trials supporting the efficacy of warfarin declined warfarin therapy when presented with the data about their absolute risks and benefits.”
ASCOT really makes a strong case for taking a statin drug to prevent heart attacks, even in those with normal or low cholesterol levels, not the opposite, as Brownstein has implied.
Do Statin Drugs “Weaken” The Heart Muscle Or Cause Heart Failure?
After criticizing the now infamous “Seven Nations Study” of Ancel Keys, which found high fat consumption in countries with high rates of heart attacks, Brownstein trots out the weakest imaginable argument for statins causing heart failure: heart failure has increased in the last decades, statin use has increased, therefore statins are causing heart failure.
Correlation does not equal causation!
There is no compelling evidence that statins cause heart failure or weaken heart muscle.
In fact, a recent review of heart failure and statins concluded that statins, while not reducing mortality in heart failure, do have favorable effects on reducing the rate of hospitalization for heart failure and increasing the strength of the heart muscle.
Statins may not be as beneficial in patients with heart failure, but they definitely don’t cause heart failure.
Much of the misinformation about heart failure and statins arises from sites like Life Extension, which promotes sales of its own preferred brand of vitamin CoQ10, ubiquinol. (According to their website, though, this is for altruistic reasons: “We at the Life Extension Foundation take a different view. Keeping our members in a youthful state of longevity is the most efficient way of maintaining the revenue stream we need to fund our scientific research projects. We had no problem reducing our margins to provide members with the clearly superior ubiquinol form of CoQ10.”)
As is typical for this slick organization (see my previous post here), the writing has the veneer of science but is all pseudoscience with references that are outdated, irrelevant or meaningless.
Statin Side Effects
I’ve written about statin side effects and the decision to take them based on analysis of risks and benefits here and here.
By far, the most common thing we see is myalgia, aching of the muscles, and this is reversible.
The bottom line is that the benefits of statins far outweigh the risks if you are at very high risk for heart attack and stroke. The risks outweigh the benefits if you are at very low risk.
Brownstone is not the only purveyor of dangerous misinformation on Newsmax’s Health website. There seems to be a concerted effort to promote quacks and charlatans and any information on this website is suspect.
A good rule of thumb if you are searching for credible health information on the web:
Avoid sites that use scare tactics and inflammatory rhetoric to induce you to stop your prescription medication and buy a health newsletter or nutraceutical.
By the way, Big Pharma has not brainwashed me.
I have no ties to industry.
I stopped taking any pharma food or money years ago.
I can tell you exactly when the pain started. I was riding my bike in Forest Park, the great urban park of St. Louis. Ordinarily, I cycle from my house to the park, cutting across the ivy-covered semi-Ivy league campus of nearby Washington University and circling its beautiful acres on a recently refinished bike path.
As I started the slow incline that parallels Skinker Avenue just West of Forest Park, a cyclist flashed past me. I could swear he said “Oh dear, oh dear. I shall be late.”
Instead of continuing straight along the bike path, the late cyclist suddenly veered to the left, following a heretofore untraveled spur that led up into the dark, impenetrable forests of the park.
At this point, the sensible, sixty-something portion of my psyche should have taken over and had me continue on the relatively straight, flat and well-traveled road that I had grown accustomed to. Alas, it was the teenage boy who took control and insisted on us taking the road less traveled.
The spur of the bike path had not been regularly maintained and there were numerous rough spots: ridges and chasms emerged with disconcerting frequency as I progressed.
The lure of exploration pulled me on. I kept my speed up as I descended a hill with the path turning sharply to the right. Suddenly an even sharper right turn emerged with a particularly uneven section of path. I lost control of the bike and landed heavily on my left side.
I felt a sudden sharp pain just to the left of my breastbone about midway in my chest.
As a cardiologist I spend a lot of time talking to people about chest pain and thinking about what is causing it.
The heart is in the chest and it is natural to believe that pain that comes from this area could be a manifestation of the dreaded heart attack. Since heart attacks are the #1 killer of both men and women and they can very quickly lead to life-threatening arrhythmias it is wise to take seriously any pain in the chest.
Three Types of Chest Pain
I was trained to sort what patient’s described to me about their chest pain into three bins: Typical anginal pain, atypical anginal pain and non cardiac pain.
Angina is doctor-speak for chest pain that is due to the heart muscle not getting enough blood (usually due to a blocked coronary artery)
Cardiologists consider any discomfort from the lower ribs up to the bottom of the neck as chest pain although patients often don’t perceive it as a pain.
Heart attack pain often feels like a pressure, a heaviness or a burning and in addition to somewhere in the anterior chest region it can manifest in the neck or jaw or one or both of the upper arms.
My chest pain was worse when I took a deep breath (pleuritic) and this almost always indicates a lung cause or inflammation in the muscle/bones/joints that are related to breathing. Furthermore, pushing on the ribs made it worse making it virtually certain that it was musculoskeletal.
A brief (well done) history and physical exam therefore would assign my chest pain to the “non cardiac” bin.
Typical anginal pain is brought on by exertion, lasts 3-15 minutes and is relieved by nitroglycerin or rest.
The probability of a patient with non cardiac chest pain having significantly blocked coronary arteries is generally lower than that of a patient with typical anginal pain. However, as this chart demonstrates, patients (generally those with significant risk factors) can have severely blocked coronary arteries and have non cardiac chest pain.
For example, I have risk factors of age (>55 years), being male, hyperlipidemia and hypertension. A cardiac catheterization done on me at the time of my non cardiac chest pain might well show significantly blocked coronary arteries. Of course, these blocked arteries would have absolutely nothing to do with my pain.
This fundamental paradox is the source of a lot of the overtesting and over treatment that occurs in cardiology. Most of the time, chest pain that prompts a patient to come to the ER or doctor’s office does not fall easily into the non cardiac category or the typical anginal category: these are the atypical anginal patients.
Additional testing is required , progressing from EKGS and cardiac enzymes to stress testing to cardiac catheterization. If there are elevation of the cardiac enzymes or abnormalities of the EKG that indicate a recent or active heart attack then a cardiac catheterization is warranted because it is very highly likely that a tightly blocked coronary artery is the cause and opening that artery will be beneficial.
However, most patients have normal cardiac enzymes and unremarkable EKGS and can end up getting catheterizations (due to either inaccurate stress tests or cardiologist’s recommendation) that they don’t need.
Once a catheterization is done, patients may then get a stenting procedure on a blocked coronary artery that wasn’t causing any problems. Not uncommonly, multiple blocked coronary arteries are found and the patient is rushed off to have a bypass operation. If the blocked arteries weren’t the cause of the patient’s chest pain (i.e. the pain was non cardiac) these procedures are likely doing more harm than good.
When To Go To ER With Chest Pain
I’ve spent thirty years fielding after hours telephone calls from patients who are having chest pain.
It is not easy to make a reliable determination of who is likely having a heart attack or other potentially dangerous cardiac problem and who is not just based on the history.
If a patient called me describing what I described above I would likely advise him to go to the ER for evaluation (although I would be pretty sure it wasn’t a heart attack: sometimes rib fractures are associated with collapsed lungs or hemorrhage into the pleural space and sometimes trauma to the chest can cause heart damage). It’s always better to err on the side of caution when were’ dealing with potentially life-threatening problems.
After office hours, the only way to get an electrocardiogram and cardiac enzymes to be sure that the chest pain is or is not a heart attack is to go to an ER. Generally, if the patient has escalated the level of concern to calling the on call cardiologist, the symptoms are worrisome.
The bottom line for me is that you only get one chance to die (You only die once (YODO)
If you’re having a heart attack at any second your heart can go into ventricular tachycardia or ventricular fibrillation and you will die within minutes.
Thus, I have to have a very low threshold for advising trips to the ER. If I’m wrong, the patient could die.
I didn’t go to the ER because I was 100% certain that my chest pain was non cardiac. I’m also a doctor and therefore a very bad patient. I survived, however, and over several weeks the pain gradually subsided.
As a result of this fall (and several other bike falls I’ve had in the last few years) I’ve re-evaluated my cycling. I’m going to stay on very well-maintained paths and slow way down when the going gets rough.
Hopefully, this will allow me to continue the cycling which I’m convinced is helping to prevent me from visiting the ER with a true heart attack!
The skeptical cardiologist was in Atlanta recently visiting his Life Coach (LCOSC). Oddly enough, the wife of the LCOSC (who I’ll call Lisa) had just undergone a coronary calcium scan and it came back with a high score. Most women her age (58 years old) have a zero score but hers came back at 208 .
What is the significance of a calcium score of 208 in this case?
The CT scan for calcium (discussed by me in more detail here) focuses entirely on quantifying the intense and very specific kind of x-ray absorption from calcium. The three-dimensional resolution of the scan is such that the coronary arteries which supply blood to the heart can be accurately located and the amount of calcium in them very accurately and reproducibly added up. Calcium is not in the arteries normally and only accumulates as atherosclerotic plaque builds up over time. The build up of fatty plaque (atherosclerosis) is the major cause of coronary artery disease (CAD, sometimes termed coronary heart disease (CHD)) which is what causes most heart attacks and most death in both men and women in the U.S.
We can enter Lisa’s numbers into the online MESA calculator to see how she compares to other white 59 year old women. The calculator tells us that 72% of her peers have a zero calcium score and a score of 208 is higher than 95% of her peers. Although the 95th percentile is a good place to be for SAT scores it is not for atherosclerosis. This means substantial amount of fatty atherosclerotic plaque has built up in the arteries and puts the individual at significantly greater risk for heart attack and stroke. A calcium score of 100-300 confers a 7.7 times increased risk compared to an individual with similar risk factors with a zero calcium score.
Most of the risk factors that we can measure to assess one’s risk of heart attack (blood pressure, diabetes, smoking) were absent in Lisa. Her cholesterol levels had risen in the last 10 years but when I entered her numbers (total cholesterol 221, HDL 68) into the ASCVD risk estimator her 10 year risk came back at 2.5%. This is considered low and no treatment of cholesterol would be advised by the new guidelines.
The only clue that her cardiologist would have that Lisa has advanced premature atherosclerosis is that her mother had coronary heart disease at an early age, something we call premature CAD. Her mom at the age of 62 suffered a heart attack and had a stent placed in one of her coronary arteries. The occurrence of significant premature CAD in a parent or sibling substantially increases the chances that a patient will have premature CAD and the earlier it occurred in the parent or sibling the higher the risk.
Some of this excess risk is transmitted by measurable risk factors such as hypertension and hyperlipidemia and some through lifestyle factors but the majority of it is through genetic factors that we haven’t fully identified.
How much of an individual’s risk for heart attack is determined by genetics versus lifestyle?
A large Swedish study found that adopted men and women with at least one biological parent with CHD were 1.5 times more likely to have CHD than adoptees without. In contrast, men and women with one adoptive parent were not at increased risk.
Since 2007 an intense project to identify genetic factors responsible for CAD has been underway at multiple academic centers. Thus far 50 genetic risk variants have been identified. According to Dr. Robert Roberts
” All of these risk variants are extremely common with more than half occurring in >50% of the general population. They increased only minimally the relative risk for coronary artery disease. The most striking finding is that 35 of the 50 risk variants act independently of known risk factors, indicating there are several pathways yet to be appreciated, contributing to the pathogenesis of coronary atherosclerosis and myocardial infarction. All of the genetic variants seem to act through atherosclerosis, except for the ABO blood groups, which show that A and B are associated with increased risk for myocardial infarction, mediated by a prolonged von Willebrand plasma half life leading to thrombosis”
How well do the standard risk factors capture the individuals risk for heart attack?
The standard approach to estimating risk fails in about 25% of individuals as it does not accurately convey the high risk of the patient with family history and it overestimates risk in many elderly individuals who have an excellent family history.
It is in these patients that testing for the actual presence of atherosclerosis, either by vascular screening or coronary calcium is helpful.
Reducing The Excess Risk of Premature CAD
For many individuals there are clear-cut lifestyle changes that can be implemented once advanced CAD is identified: cigarette smoking cessation, weight loss through combinations of diet and exercise with resulting control of diabetes, However, many patients like Lisa, are non-smokers, living a good lifestyle, eating an excellent diet with plenty of fresh fruit, vegetables, fish and healthy oils and without obesity or diabetes. There is no evidence that modifying lifestyle in this group is going to slow down an already advanced progression of atherosclerosis.
Patients like Lisa have inherited predisposition to CAD, it is not due to their lifestyle.
Lisa’s cardiologist suggested she get a copy of Dr. Esselstyn’s book “Prevent and Reverse Heart Disease”. This book, based on the author’s experience in treating 18 patients with advanced CAD espouses an ultra low fat diet. The author declares that “you may not eat anything with a face or a mother (meat/poultry/fish)” and bans full fat dairy products and all oil (“not even a drop”)
Such “plant-based diets” (codeword for vegan or vegetarianism) lack good scientific studies supporting efficacy and are extremely hard to maintain long term. There is nothing to suggest that Lisa’s long term risk of heart attack and stroke would be modified by following such a Spartan dietary regimen.
Her cardiologist did recommend two things proven to be beneficial in patients with documented advanced CAD: statins and aspirin.
Taking a statin drug will arrest the atherosclerotic process and reduce risk of heart attack and stroke by around 30% as I’ve discussed here and here.
An aspirin is now indicated since significant atherosclerosis has now been documented to be present as I’ve discussed here.
We can blame a lot of heart disease on lifestyle: poor diets and lack of exercise are huge factors leading to obesity, diabetes, hypertension and hyperlipidemia, but in many patients I see who develop heart disease at an early age, lifestyle is not the issue, it is the genetic cards that they have been dealt.
Until we develop reliable genetic methods for identifying those at high risk it makes sense to utilize methods such as vascular screening or coronary calcium to look for atherosclerosis in individuals with a family history of premature CAD.
Once advanced atherosclerosis is identified, we have extremely safe and effective medications that can help individuals like Lisa deal with the cardiovascular cards they have been dealt.
The updated AHA/ACC Cardiovascular Prevention Guidelines (CPG) which include the excessively wordy “The Treatment of Blood Cholesterol to Reduce Atherosclerotic Cardiovascular Risk in Adults Risk” were published late last year and immediately were the center of controversy.
After working with them for 9 months and using the iPhone app to calculate my patients’ 10 year risk of atherosclerotic cardiovascular disease (ASCVD, primarily heart attacks and strokes) it has become clear to me that the new guidelines will recommend statin therapy to almost all males over the age of 60 and females over the age of 70.
As critics have pointed out, this immediately adds about 10 million individuals to the 40 million or so who are currently taking statins.
Should we be starting all elderly Americans on statin drugs?
My simple answer is no. It doesn’t make sense to do this, because clearly not all elderly individuals have atherosclerosis or will ever develop its consequences of heart attack and stroke. Many have inherited the genes that allowed their parents to live free of heart disease into their 90s and will not benefit at all from long term statin therapy; they may actually suffer the expense and side effects instead.
How can we better decide who among the elderly will benefit from statin therapy?
If you have read my previous posts on searching for subclinical atherosclerosis here and here you probably know the answer. Let’s look at a specific case and apply those principles.
Robert is 69 years old. I see him because, in 2010, the posterior leaflet of his mitral valve ruptured, resulting in the mitral valve becoming severely incompetent at its job of preventing back flow from the left ventricle into the left atrium. I sent him to a cardiac surgeon who repaired the ruptured leaflet. Although he has a form of “heart disease,” this is a form that has nothing to do with cholesterol, hypertension or diabetes and is not associated with ASCVD.
However, it is my job to assess in him, like all individuals, the risk of developing coronary heart disease or ASCVD.
He has no family history of ASCVD and he feels great since the surgery, exercising aerobically 4-5 times per week.
His BMI is 23.87 which is in the normal range. His BP runs 116/80.
His total cholesterol is 210 and LDL or bad cholesterol is 142. Good or HDL cholesterol is 56 and triglycerides 59. The total and LDL cholesterol levels are considered “high,” but they could be perfectly acceptable for this man.
When I ran his 10 year ASCVD risk (risk of developing a heart attack or stroke over the next 10 years), it came back as 14%. The new guidelines would suggest having a conversation with him about starting a statin if his risk is over 7.5%. His risk is double this and statins are definitely recommended in this intermediate risk range. Interestingly, I cannot enter a cholesterol level or blood pressure for a man of this age that yields a risk less than 7.5%.
When I had my discussion with him about his risk for ASCVD, I plugged his numbers into my iPhone and showed him the results and gave him the guideline recommendation.
Lifestyle Changes to Lower Cholesterol
The new Cardiovascular Prevention Guidelines have a section devoted to Lifestyle Management to Reduce Cardiovascular Risk. Unfortunately, none of the lifestyle changes they recommend have been shown to reduce ASCVD risk in an individual like Robert. He already exercises the recommended amount, is at his ideal body weight and eats a healthy diet. If we were to tighten up on his diet by, say reducing red meat, eggs and high fat dairy, all we would accomplish would be to lower his LDL and HDL cholesterol levels and make his life and meals less satisfying. The lower total cholesterol and LDL cholesterol would not lower his risk of ASCVD and the calculated 10 year ASCVD risk would still be in the range where statins are recommended.
Therefore, I am not going to tell Robert that he should reduce his saturated fat consumption (he already has incorporated that into his diet since he’s been bombarded with the low fat mantra for 30 years).
Searching for Subclinical Atherosclerosis
I’m going to tell Robert that we need to know if he has atherosclerosis, the disease that we are attempting to modify.
We started with an ultrasound to look at the lining of the large arteries in his neck that supply blood to the brain, the carotid arteries (a process I describe in more detail here). Although severe atherosclerotic blockages in these arteries put one at risk of a stroke, I was much more interested in the subtle changes in the arteries that precede symptoms and are an early harbinger of atherosclerosis.
Careful ultrasound recording and measurement of the main common carotid arteries from both the left and right side showed that the IMT or thickness was lower than average for his age, gender and ethnicity. His carotid IMT was at the average for a 60 year old, therefore, his so-called vascular age was 60 years, younger than his chronological age. If I plug that age into the ASCVD risk estimator, I get an 8.2% 10 year risk, just barely above the statin treatment cut-off.
Careful scrutiny with ultrasound of the entire visible carotid system in the neck on both sides did not reveal any early fatty plaques or calcium in the lining of the carotid arteries. He had no evidence for atherosclerosis, even very subtle early forms, in this large artery, a finding which is usually predictive of what is going on in the other large arteries in the body, including the coronary arteries, which supply blood to the heart.
At this point, I think, we could have stopped the search for subclinical atherosclerosis and agreed that no statin therapy was warranted. However, Robert wanted further reassurance that his coronary arteries were OK, therefore we set him up with a coronary calcium study (see my full description of this test here).
Searching for Subclinical Atherosclerosis: The Calcium Score
Robert’s coronary calcium score came back at 21 (all in the LAD coronary artery) , which put him at the 26th percentile compared to normal men of his age and gender. A score of 21 is average for a 59 year old man and 82% of men aged 69 have a score greater than zero. Robert had much less calcium in his coronaries than men his age, another factor putting him in a low risk category.
Given the low risk findings from both the vascular screening and the coronary calcium, I felt comfortable recommending no statin therapy and going against the guidelines.
Statins: Better Targets for The Two-edged Sword
This is not an unusual scenario; many of my older patients without heart attacks, strokes or diabetes fall into the risk category that would warrant statin therapy and if they have no clinical or subclinical evidence of atherosclerosis, I don’t advise statin therapy. My patients are free to follow the guidelines and take statin drugs after this advice, but most are very grateful that another pill (which they likely have heard bad things about on the internet or from friends with adverse experiences) can be avoided.
Statins are wonderful drugs when utilized in the right population, but they also carry a 9% increased risk of diabetes and about a 10% real world risk of developing muscle aches and weakness (myalgia).
I think it is essential to aim these two-edged swords at the right targets if we are to maximize the overall health benefits.