Donald Trump recently appeared on the Dr. Oz show and handed a letter to the celebrity medical charlatan and TV host, Mehmet Oz.
The letter was written by his personal physician , Dr. Harold Bornstein,
and summarized various laboratory and test results which led Bornstein to conclude that Mr. Trump is in excellent health (Bornstein did not repeat his earlier, bizarre statement that “If elected, Mr. Trump, I can state unequivocally, will be the healthiest individual ever elected to the presidency.”)
From a cardiovascular standpoint the following sentence stood out:
“His calcium score in 2013 was 98.”
Regular readers of the skeptical cardiologist should be familiar with the coronary calcium scan or score (CAC) by now. I’ve written about it a lot (here, here, and here) and use it frequently in my patients, advocating its use to help better assess certain patient’s risk of sudden death and heart attacks.
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.
Calcium only develops in the coronary arteries when there is atherosclerotic plaque. The more plaque in the arteries, the more calcium. Thus, the more calcium, the more plaque and the greater the risk of heart attack and death from heart attack.
What Does Donald’s Trump’s Calcium Score Tell Us About His Risk Of A Major Cardiac Event?
We know that, on average, even if you take a statin drug (Trump is taking rosuvastatin or Crestor), the calcium score goes up at least 10% per year which means that 3 years after that 98 score we would predict Trump’s calcium score to be around 120.
Based on large, observational studies of asymptomatic patients, Calcium scores of 101 to 400 put a patient in the moderately high risk category for cardiovascular events.
When I read a calcium score of 101-400, I make the following statements (based on the most widely utilized reference from Rumberger
This patient has:
-Definite, at least moderate atherosclerotic plaque burden
-Non-obstructive CAD (coronary artery disease) highly likely, although obstructive disease possible
-Implications for cardiovascular risk: Moderately High
Since we know that Hillary Clinton recently had a calcium scan with a score of zero, we can estimate that Trump’s risk of having a heart attack or dying from a cardiac event is markedly higher than Clinton’s.
Clinton, born October 26, 1947 is 68 years old and we can enter her calcium score into the MESA calcium calculator to see how she compares to other women her age. A coronary calcium score of 6 is at the 50th percentile for this group.
Interestingly, Trump’s score of 98 at age 67 years was exactly at the 50th percentile. In other words half of all white men age 67 years are below 98 and half are above 98, creeping into the moderately high risk category.
So, based on his coronary calcium score from 2013, Donald Trump has a moderate build up of atherosclerotic plaque in his coronary arteries and is at a seven-fold higher risk of a cardiac event compared to Hilary Clinton.
It is a reasonable question. If statins are a treatment for abnormally high cholesterol levels why would we start them on a patient with normal or low levels.
The answer is that we are not concerned with cholesterol levels. What we are concerned with is atherosclerotic cardiovascular disease (ASCVD) and its downstream consequences including heart attack and stroke.
Thus, the new guidelines recommend calculating a patient’s 10 year risk of heart attack and stroke due to ASCVD ( see here for my discussion of smart phone app that makes this calculation) and if it is over 7.5% to consider starting a statin drug to reduce ASCVD risk.
Cholesterol is just one of many factors that effect the risk but we know that irrespective of cholesterol level, starting a statin will substantially lower the risk.
A patient who has smoked cigarettes lifelong asked me this question recently.
When I plugged the patient’s excellent cholesterol values into the ASCVD app, the 10 year risk of heart attack or stroke was quite high, 14.9%. Bad cholesterol (LDL) was 90, well below what is considered optimal. Good cholesterol (HDL) was 60, well above what is considered optimal.
Studies have demonstrated that even patients with cholesterol numbers this good benefit from statin therapy. Their risk of heart attack and stroke will be substantially reduced over time.
My patient has not yet had a heart attack or stroke and it is likely that despite engaging in the extremely damaging behavior of cigarette smoking , the genetically programmed excellent cholesterol values have somewhat protected from ASCVD.
However, a vascular screening study has demonstrated that early atherosclerotic plaque in both the patients carotids. The patient has ASCVD and it is only a matter of time if the patient keeps smoking before the patient has a clinical event related to it.
I told my patient that if he/she stopped smoking cigarettes his/her estimated 10 year risk would drop to 9.7% and I would not recommend statin therapy.
We discussed methods to help quit and the patient indicated that the patient would start using a nicotine patch and try to quit in the next few months.
Unfortunately, at follow up smoking was ongoing.
Thus, my recommendation to start statin therapy despite her excellent cholesterol values.
Other groups of patients besides cigarette smokers can have advanced or premature ASCVD with excellent or “normal” cholesterol values. Diabetics often have low bad cholesterol values associated with low good cholesterol and high triglycerides.
Sometimes, ASCVD develops prematurely even in patients who have a low 10 year risk based on standard risk factors. This is usually in patients with a strong family history of ASCVD who have an inherited atherogenic abnormality of lipid metabolism that is not manifested in the standard cholesterol parameters (see Dealing With the Cardiovascular Cards You’ve Been Dealt).
To identify these patients a search for subclinical atherosclerosis by vascular screening or coronary calcium scan is necessary. When advanced plaque is identified statin therapy is often warranted even with a low estimated 10 year risk and normal cholesterol values.
So some patients can have very high cholesterol values and I don’t recommend any therapy, some have low and I do. I’m much more focused on the presence or absence of ASCVD in my treatment decisions.
Ultimately we are not treating “high cholesterol” when we start cholesterol lowering therapy we are working to prevent or slow the progression of ASCVD,
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.
For most of the last 25 years I have told patients when I recommend a statin drug to them that they should take it in order to lower their bad cholesterol (and raise the good cholesterol) thereby lowering their risk of future heart attacks.
I based this statement on my understanding of large statin trials which demonstrated reduction in heart attacks seemingly closely tied to drops in the bad cholesterol level.
Although I was aware of the so-called “pleiotropic” (meaning effecting multiple pathways leading to atherosclerosis) of statins it was easier to point to the cholesterol lowering effects and unify that message with the recommendation to reduce fat and cholesterol in the diet , thereby lowering cholesterol in the blood and arteries and cut heart attack risks.
Thus emerged a very simple (and likely false) paradigm: Fat in the diet causes fat in the blood which causes fat in the arteries which causes fatty plaques in the coronary arteries which causes heart attacks when they get too big and block off the blood flow.
I, like most cardiologists and lay people mistakenly assumed that since lower bad cholesterol levels associated with taking a statin drug were associated with lower heart attack risks then dietary changes aimed at lowering bad cholesterol levels would also lower heart attack risk.
It turns out that we don’t really know how the statins reduce heart attacks . As a recent review points out:
some of the cholesterol-independent or “pleiotropic” effects of statins involve improving endothelial function, enhancing the stability of atherosclerotic plaques, decreasing oxidative stress and inflammation, and inhibiting the thrombogenic response. Furthermore, statins have beneficial extrahepatic effects on the immune system, CNS, and bone. Many of these pleiotropic effects are mediated by inhibition of isoprenoids, which serve as lipid attachments for intracellular signaling molecules. In particular, inhibition of small GTP-binding proteins, Rho, Ras, and Rac, whose proper membrane localization and function are dependent on isoprenylation, may play an important role in mediating the pleiotropic effects of statins.
Supporting the non cholesterol lowering effects of statins on reducing CVD are the following observations
-Most heart attack victims don’t have elevated bad cholesterol levels and dietary reduction of bad cholesterol doesn’t seem very effective at preventing heart attacks.
-Drugs, like Zetia or ezetimibe which lower cholesterol level by other mechanisms don’t seem to prevent atherosclerosis even though they substantially lower bad cholesterol levels.
-Statin drugs reduce heart attacks in patients who have normal or low bad cholesterol levels
What Causes Atherosclerosis?
An article (Innate and adaptive inflammation as a Therapeutic Target in Vascular Disease) published in JACC recently by Tousoulis,et al. summarizes the current understanding of how atherosclerosis develops and the multiple ways that statins may affect that process. They write
Atherosclerosis, once thought to be a lipid storage disease, is now considered a chronic low-grade inflammatory condition that affects the vascular wall. It is characterized by the deposition of cholesterol and lipids followed by infiltration of T cells and macrophages, all as a result of an endothelial injury response.
I’m including this figure from the article to give you some idea of how incredibly complicated the process is.
Can you imagine trying to explain this to the average patient?
My eyes glazed over once I reached MCP-1.
Thus, doctors end up giving the simple, accepted conventional wisdom that we are “treating” high cholesterol by giving statin drugs. What we are really treating is atherosclerosis. And statins are the only effective drug treatment we have identified for this ubiqitous and complex process.
It is entirely possible that the lower LDL cholesterol caused by statin drugs is totally unrelated to their ability to forestall atherosclerosis. The new cholesterol guidelines reflect this concept as they don’t recommend treating to an LDL target level.
I end with the closing comments from the article by Tousoulis, et al.
Given the fact that atherosclerosis is a multivariable disease, with several molecules involved in each stage, it is vey difficult to find an effective treatment. However, statins prove to be the most effective treatment so far because they interfere with most of the critical components of the atherosclerotic process and have been proven to have beneficial effects. Further to their well-established impact on nonspecific low-grade inflammation, statins also appear to have significant effects on innate and adaptive immunity that have been underestimated so far.
The skeptical cardiologist just returned from Washington, DC where he attended the American College of Cardiology (ACC) annual conference and visited Ford’s Theatre. I was hoping to gather more information on diet and cardiovascular disease but most of the discussions on prevention of heart disease centered around the new ACC/AHA guidelines for treating cholesterol.
A recently published analysis of the impact of these guidelines found that
As compared with the ATP-III guidelines, the new guidelines would increase the number of U.S. adults receiving or eligible for statin therapy from 43.2 million (37.5%) to 56.0 million (48.6%). Most of this increase in numbers (10.4 million of 12.8 million) would occur among adults without cardiovascular disease.
If you are a man over the age of 59 (which I just became), even without any cardiovascular disease or diabetes, there is an 87% chance the guidelines would suggest you take a statin drug.
This is a startling increase and consequently there has been a lot of criticism and questioning of the validity of these recommendations.
More importantly, for an individual patient, should you take a statin drug if your doctor recommends it? This is an especially good question if you have no evidence of any atherosclerotic cardiovascular disease (so-called primary prevention). At a minimum, you should have a very detailed discussion with your doctor about the risk and benefits of taking the medication in your particular situation.
What are statin drugs?
Statins are the most powerful, safe and effective drugs available for lowering LDL or bad cholesterol levels. They inhibit 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase, involved in cholesterol biosynthesis. Low density lipoprotein (LDL) cholesterol concentration is lowered by reducing its production in the liver and increasing removal from the circulation. Statins also have anti-inflammatory effects, improve endothelial function, and reduce thrombus formation.
Common examples of statin drugs are Lipitor which is now available as a generic called Atorvastatin , Pravastatin, and Crestor (Rosuvastatin), which is only available in brand name form.
What are the risks of statin drugs?
When large scale randomized trials of statin drug therapy are analyzed, rates of adverse events (17%) or stopping treatment due to adverse events (12%) are similar in the statin compared to placebo/control groups.
The incidence of cancers, liver enzyme elevations, kidney dysfunction or arthritis was the same in the two groups.
There are only two side effects from taking statins I consider significant and mention to my patients:
1. There does appear to be a 9% increase in the risk of developing diabetes. Most of the patients who develop diabetes on statins were at high risk for this to begin with and the overall benefits of lowering CV disease outweighs the development of diabetes in patients who take statins.
2. Statins definitely can cause muscle aches (myalgias) and this seems to happen in about 10% of patients over time. If these develop, we stop the statin and the myalgias go away if they are due to the drug. There are no reliable studies showing any long term residual muscle weakness or ache. A very, very small number of patients develop rhabdomyolysis, in which there is severe muscle damage. These patients are almost always taking multiple medications which interact with the statins and often have kidney failure to begin with.
Some things you don’t need to be concerned with while on statins:
1. That the drug will give you Alzheimer’s or make you stupid. There is much anecdotal misinformation on the web about this, but no solid evidence of any adverse effect on cognition.
2. That the drug will destroy your liver. A small percentage of patients will develop elevations of their liver enzymes (AST or ALT) but this does not lead to liver damage and is considered so insignificant now that the FDA now longer advises checking liver enzymes in patients on statin drugs.
What are the benefits of statins in people without known heart disease?
They lower all-cause mortality by 14%, combined fatal and nonfatal cardiovascular disease by 25%, and stroke by 22%. They lower the chances that you would need a stent or bypass surgery by 38%.
Another way of looking at the benefits of a treatment is the number needed to treat (NNT).
To save one life, you would need to treat 138 patients for 5 years with statin drugs. This means that 137 patients would have done fine without taking the drug.
The higher your risk of developing atherosclerotic cardiovascular disease (ASCVD (all the disease that occurs as a result of fatty plaque build up in the body, including heart attack and stroke)), the more likely you will benefit from taking a statin drug.
Thus, the new guidelines utilize a risk estimator that takes into account your total and good cholesterol values, your systolic blood pressure, age and whether you smoke, have diabetes or treated hypertension to calculate your risk of developing clinical ASCVD over the next ten years.
If this ten year risk is over 7.5%, statin therapy should be considered.
I’ve looked over the guidelines carefully, read a lot of the original studies and listened to the discussion and I think this is a reasonable approach. I try to present each patient with the risks and benefits and let them make the decision as to whether they want to take the drug.
Each individual has a different perspective, perhaps heavily influenced by their father having died of a heart attack in his fifties or by a close friend who feels that statins ruined his life.
Two important new concepts from the new guidelines
The new guidelines no longer look at the LDL or bad cholesterol level as a goal or as a level for initiating treatment (unless it is super high, above 190). Thus, the only reason to be checking follow up cholesterol panels on patients who are taking good levels of statin drugs is to verify compliance and an effective reduction in LDL from baseline. I will not try to get your LDL below 100 or 70 and you will not have to worry that it is not at that level.
The new guidelines rightly emphasize statin drugs as the only drug therapy that has good outcomes data (meaning they have been show to reduce heart attacks and strokes) supporting their use in primary prevention.
Ezitimibe (Zetia) is a commonly prescribed drug which lowers LDL cholesterol but is expensive and has never been shown to lower heart attack or stroke risk and, in my opinion, should not be prescribed.
Our goal should be prevention of heart disease, not lowering LDL levels or triglyceride levels.
I believe that we can fine tune which patients will and will not benefit from statin therapy by looking for evidence of what is called “subclinical atherosclerosis.” I plan to review this in a future post.
For now, I leave you with the humorous line from the play “Our American Cousin” that caused the distracting laughter during which John Wilkes Booth shot Lincoln in Ford’s Theatre (which is not far from the Washington Convention Center and well worth visiting!)
“Don’t know the manners of good society, eh? Well, I guess I know enough to turn you inside out, old gal — you sockdologizing old man-trap.”
Tell your cardiologist you will sockdologize him if he doesn’t give you a good discussion of the risks and benefits of the statin drug he is recommending.