Searching for Subclinical Atherosclerosis: Vascular Screening

I reviewed in a previous post  the importance of detecting sublinical atherosclerosis when trying to assess someone’s risk of heart attack and of dying suddenly.  Subclinical atherosclerosis refers to the build-up of plaque in the lining of our arteries which occurs long before any symptoms of atherosclerosis occur.

Since the process tends to be diffuse, occurring in all the large arteries of the body, it makes sense that if we can easily visualize one artery this will give us a window into what is happening in other arteries (including the coronary arteries supplying blood to the heart muscle).

Vascular Screening

The vascular screening I offer in my office uses high frequency ultrasound to image the large artery, the carotid artery, that supplies blood to the brain.

normalimtNormally the lining of that artery is smooth and thin as in the example to the left. As the process of atherosclerosis works its damage on the artery lining it becomes thicker and plaque begins to develop. High frequency ultrasound is an excellent tool for identifying these early, subclinical stages of atherosclerosis because it is painless, harmless, inexpensive, and quick. 

Identifying Higher Risk Patients

Mr. M is  a 60 year old man who I was seeing for an abnormal heart rhythm. Using the ACC risk estimator I calculated his 10 year risk of atherosclerotic cardiovascular disease (ASCVD) as <7.5%. However, he had a brother who had cardiac stents placed in his coronary arteries (indicating coronary artery disease (CAD)). His carotid artery screening (shown below) shows a large, soft plaque

Large, relatively echo lucent (soft) plaque found in the internal carotid artery of Mr. M.

This indicates that although his known risk factors for atherosclerosis were not tremendously high, the combination of known and unknown factors (likely genetic, given his brother’s premature CAD) were damaging the lining of his arteries leaving him at a  high risk for stroke and heart attack.


A patient like Mr. M I consider to have documented atherosclerotic cardiovascular disease (ASCVD)and I  will strongly recommend statin therapy along with a baby aspirin

Several studies have shown in those patients who are reluctant to start statin therapy, documenting subclinical atherosclerosis serves as a strong motivational factor for lifestyle change or compliance with medications.

Identifying Lower Risk Patients

Equally important as identifying advanced subclinical atherosclerosis, imaging the carotid artery can identify those patients who are at lower risk and save them from a lifetime of unnecessary treatment.

Ms N is 64 years old whom I see h for high blood pressure and supra ventricular tachycardia (an abnormal heart rhythm). She has a total cholesterol of 219, HDL(or good) cholesterol of 74, systolic blood pressure of 130 and the ACC risk estimator gives her an 8.4% risk of ASCVD over the next 10 years. She greatly dislikes taking medications, but her mother died in her early fifties from  a “massive heart attack” .

huelsingHer carotid exam shows the carotid thickness as less than average for her age and gender, equivalent to that of a 58 year old. There is no plaque anywhere in her carotid system. I feel comfortable not recommending statins to this type of patient. In many cases, I often  stop cholesterol treatment in patients with no evidence for subclinical atherosclerosis who have marginal cholesterol levels and intermediate risk.

What vascular screening allows me is the ability to see if my patients do or do not have the disease that we are trying to prevent or mitigate: atherosclerosis.

As the skeptical cardiologist I must point out that national guidelines do not endorse vascular screening primarily because there are no randomized controlled trials showing that it influences outcomes. I’ll talk more about potential pitfalls of vascular screening when done by for profit ventures in a subsequent post  and we’ll discuss the other good way of assessing for subclinical atherosclerosis: coronary calcium.


Is A Snickers Bar Healthier Than Yoplait Yogurt?

This container of Yoplait comes from the refrigerator in the Doctor’s Lounge at my hospital. It is often the go-to snack for busy doctors and health conscious consumers.
I used to consider Yoplait about as healthy a snack as I could get. After all, it was low in fat, owned by French farmers and it had pictures of fruit on it. How could I go wrong?yoplait

In addition, Yoplait is focused on making “so good yogurt” as the company (now owned by General Mills) explains

“Ultimately, we’re focused on making so good yogurt, and here’s how we see it: you can eat something that tastes amazing but isn’t that good for you. You can eat stuff that’s really good for you, but doesn’t always leave you yummed up. So good yogurt does both. All of you is happy, not just your tongue. And while so goodness will never be perfect, we’ll keep working on ways to make our yogurt more so good than it is today.”

The significant other of the skeptical cardiologist (SOSC) made the claim recently that women who felt they were having a healthy lunch by consuming fat free yogurt and salad with sugary, fat-free salad dressing might as well be eating a candy bar. At least they would enjoy it more! Could this be true?

Yoplait made the bold step in 2012 of taking out the high fructose corn syrup they had been adding to their yogurt (or yoghurt as they like to spell it), but it’s still chock full of added sugar (which is probably why it leaves you “yummed up”)

What is now in “original” Yoplait?

Original Yoplait has 12 ingredients. They are Cultured pasteurized Grade A Low Fat Milk, Sugar, Blueberries, Modified Corn Starch, nonfat milk, kosher gelatin, citric acid, tricalcium phosphate, pectin, natural flavor colored with beet juice concentrate, Vitamin A and Vitamin D3.Yoplait_Original_Mountain-Blueberry

Indeed, the fat has been taken out but in its place – added sugar, 26 grams of sugar to be precise.

Of the 170 calories you are consuming, 104 of them are coming from sugar.

How healthy is a Snickers Bar?

snickers.jpgA regular-sized Snickers candy bar has a total of 280 calories with 13.6 grams of fat (5 grams saturated fat), 35 grams of carbohydrates (29 grams of sugar) and 4.3 grams of protein. It is made with peanuts, milk chocolate, egg whites and hydrogenated soybean oil. If we ate 2/3 of the bar to make the calories the same as the Yoplait, there would be 19 grams of sugar (compared to 26 for Yoplait) and 8 grams of fat.

A recent review of the cardiovascular effects of tree nuts and peanuts concluded:

there is impressive evidence from epidemiological and clinical trials and in vitro studies of beneficial effects of nut consumption and their constituents on the risk of CVD (cardiovascular disease), including sudden death, as well as on major and emerging CVD risk factors.

This is because in addition to a favorable fatty acid profile, nuts and peanuts contain other bioactive compounds that provide cardiovascular benefits. Other macronutrients include plant protein and fiber; micronutrients including potassium, calcium, magnesium, and tocopherols; and phytochemicals such as phytosterols, phenolic compounds, resveratrol, and arginine.


Curb your hunger.jpgSo, consuming 2/3 of a Snickers bar is arguably healthier than Yoplait. It contains peanuts, which have demonstrable benefits in lowering cardiovascular disease despite a high fat content. Yoplait has had the heart healthy dairy fat removed and replaced with added sugars. As I mentioned in a previous post, added sugar is clearly related to increased cardiovascular risk. The higher fat and fibre content of the peanuts in the Snickers bar will increase satiety and arguably be less likely to cause obesity due to rebound overeating later in the day.

A much healthier choice than low fat, added sugar products like Yoplait (and candy bars) is full fat, plain yogurt (preferably from grass-fed cows) as I’ve discussed in previous posts. It can be combined with real fruit or even with nuts. Full fat yogurt is surprisingly hard to find on a grocery shelf. Even at Whole Foods, the vast majority of yogurt and dairy products are low fat. I’ve only been able to find two brands, Supernatural and Trader’s Point Creamery, which consistently offer full fat yogurt.

Disclaimer and clarifications

godzilla.jpgI do not receive any payments from Snickers nor from Mars, Inc., one of the most known and beloved brands of chocolate.  I do not plan on seeing Godzilla, May 16. Although Snickers loves you, you do not need to like Snickers.snickersloves you.jpg






Searching for Subclinical Atherosclerosis: Am I about to drop dead?

Nearly every day I see a patient in the office who has just experienced a friend or relative suddenly “dropping dead.”  Understandably, they are very concerned about this and want to know “Is this going to happen to me?”

There is very good reason to be concerned. Cardiac disease is the leading cause of death in America. Despite considerable progress, regrettably 50% of deaths occur suddenly, without any previous symptoms which would have suggested a cardiac problem. It doesn’t just hit the overweight or the smoker. It not uncommonly strikes the very fit and seemingly healthy, as in the case of the St. Louis Cardinal pitcher, Daryl Kile, who was found dead in his hotel room at the age of 34. This question of who is going to suddenly drop dead (sudden cardiac death or SCD) is one of the fundamental unsolved mysteries in current cardiology.

Atherosclerosis and Dropping Dead

Most SCD in individuals over the age of 35 is related  to the development of fatty plaques (atherosclerosis) in the arteries that supply blood to the heart (coronary arteries) and the subsequent sudden rupture of these plaques (thrombosis).hrtatk-07 The result of this rupture is the complete blockage of the artery and the total cessation of blood flow to a portion of the heart muscle. When that heart muscle portion becomes starved for oxygen, the muscle cells start dying and a myocardial infarction (MI) or heart attack occurs. You can view an animation of this process here With any MI, the dying muscle cells can become electrically irritable and initiate an abnormal heart rhythm called ventricular tachycardia (VT) or ventricular fibrillation (VF). This abnormal rhythm is what causes people to “drop dead” suddenly. Basically, the heart cannot pump blood efficiently in VT or VF; thus, there is no blood flowing to the brain and other vital organs. This is a long, complicated chain of events, but basically it begins with the development of fatty plaques or atherosclerosis. It makes sense that we can stop people dropping dead from MI by stopping the development and progression of atherosclerosis. Atherosclerosis develops long before any clinical signs or symptoms of disease. You can feel totally fine and have a huge build up of plaque in all of the arteries of your body. This is termed subclinical atherosclerosis. It makes sense, and it has been scientifically proven, that those with a huge buildup of plaque (high plaque burden) are at higher risk for MI and death than those with low or no plaque burden. It also makes sense that treating those patients with high plaque burden will be most beneficial.

How Do you know if you have atherosclerosis

I discussed the standard recommended method for determining risk of MI/SCD in my last post on statins. Basically, this is simply adding up the factors we know contribute to atherosclerosis: diabetes, cigarette smoking, hypertension, age, gender and cholesterol levels. However, most heart attacks and strokes occur in people who are classified by traditional risk factor scoring as low or intermediate risk. Conversely, others are misclassified as high risk and mistakenly advised to take drugs to reduce their risk factors for the rest of their lives.

How Can We Detect Subclinical Atherosclerosis?

In my office practice I offer patients two tests which directly detect and quantify subclinical atherosclerosis. One looks for plaque  and thickening in the larger arteries of the neck, the carotid arteries, and one looks for calcium in the coronary arteries. I’ll go into detail about both of these in subsequent posts. For now, I will just say that the carotid screening technique uses harmless ultrasound while the coronary calcium technique uses ionizing radiation from a CT scan. Neither test is covered by insurance or Medicare. Both tests have been shown to improve our ability to identify those at risk for MI and stroke.

These tests are helpful in two general areas:

*The first scenario is the patient who appears to be at low or intermediate risk for atherosclerosis based on the risk estimator, but who has a strong family history of MI, sudden death or stroke. If we identify significant subclinical atherosclerosis in this patient, statin therapy is more likely to be beneficial.

*The second scenario is the patient who has been put on statins for primary prevention based on standard risk estimator but has no family history of ASCVD and is questioning the need for treatment. In this patient if we find no subclinical atherosclerosis, a strong argument can be made to stop the statin drug.

SHAPE Guidelines II Slide_Page_38
Proposed method for utilizing carotid vascular and coronary calcium tests for better identification of subclinical atherosclerosis and more appropriate utilization of treatment in order to prevent heart attacks and sudden cardiac death

There is an organization dedicated to promoting the detection of SA by these tests and an algorithm for treatment called SHAPE  (Society for Heart Attack Prevention and Education). Interestingly, after a female Texas state representative suffered an MI, in 2009, Texas Governor Ricky Perry signed off on the Texas Heart Attack Prevention Bill mandating health-benefit plans to cover screening tests for SA. No other state to my knowledge has such a law.

How to Stop Sudden Cardiac Death

The two tests I mentioned are a good second step towards identifying the individual at risk for MI and SCD but we still don’t know who among those with advanced subclinical atherosclerosis is going to experience a sudden rupture of plaque, have an MI and drop dead.

We need a way to identify those patients with vulnerable plaque (one that is about to rupture) and aggressively treat those patients. This is an area of intense research focus. You can view a fascinating video (accompanied by weirdly cool music) created by SHAPE here and another (featuring a gun shooting a heart) here emphasizing the importance of the vulnerable plaque.

Should I Take A Statin Drug? Risks, Benefits and the New Guidelines

StatinsThe 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.

Why I Recommend the Mediterranean Diet

I recommend the Mediterranean diet (MED) to my patients. Every unbiased, systematic review of the research on diet and heart disease in the last 8 years has concluded that it is the most likely dietary model to provide protection against coronary heart disease. One review concludes

Among the dietary exposures with strong evidence of causation from cohort studies, only a Mediterranean dietary pattern is related to CHD (coronary heart disease) in randomized trials.

The MED is the only comprehensive dietary approach that has been proven to reduce total death  and heart attacks in comparison to standard diets. There are two major randomized controlled trials (the only kind of study that proves the value of a dietary intervention) with this diet.

From Eric Roehm at

  The first, called the Lyon heart Study,  was in patients who had had heart attacks (secondary prevention) . As this graph demonstrates, those patients randomized to receive instruction on following the Mediterranean diet had a 60% lower death rate and a 70% lower heart attack rate. The second was published last year in the New England Journal of Medicine and was a primary prevention study: that is, participants had not had heart attacks. Participants were randomized to one of three diets: a MED supplemented with extra-virgin olive oil,  MED supplemented with mixed nuts or a control diet (advice to reduce dietary fat). Participants received quarterly individual and group educational sessions and either free provision of olive oil, mixed nuts or small nonfood gifts. The high extra virgin olive oil group ingested an average of 3.6 tablespoons/day (51 grams/day equal to 459 calories/day) of olive oil with 98% of it being extra virgin olive oil. The high nut group ate 8.2% of their total daily calories in the form of nuts, including an additional approximately one ounce packet of nuts (15g of walnuts, 7.5 g of almonds, and 7.5g of hazelnuts) provided by the study coordinators. 7447 persons were enrolled (ages 55 to 80 years) for an average 4.8 years. Those persons following the MED diet (either supplemented with olive oil or nuts) were 30% less likely to have  a major cardiovascular event (heart attack, stroke or death from cardiovascular causes.) There was a statistically significant reduction in stroke rate (≈39%) when considered as an isolated endpoint. We don’t know exactly what components of the MED are the most beneficial.  This trial suggests that olive oil and nuts are at least two of the key ingredient so it makes sense to increase your consumption of these foods. Other studies strongly support fish consumption and alcohol consumption as key components. As I’ve discussed (?ad nauseam) in other posts, full fat dairy and eggs, although banned by most “heart healthy diets”, have not been shown to increase heart disease risk.  Fermented dairy consumption, in particular, in the form of plain full-fat yogurt (not adulterated with sugar) and full-fat cheese is consistently associated with a lower risk of coronary heart disease. Plain full-fat yogurt and full-fat cheese (from goat milk) were consumed by the inhabitants of Crete, the Greek Island on which the original MED was based.

It has to be emphasized that within this pattern of eating you want to be consuming real foods, not processed products of the industrial food industry which have been manipulated to appear healthy due to being “low-fat” or “low cholesterol.”

This is a pattern of eating which is varied, interesting and sustainable.

It’s one that can last a lifetime. ,

Full Fat Dairy Lowers Your Risk of Obesity

ButterWhen i tell my patients that I am fine with them consuming full fat dairy products including butter I see  a mixture of responses. For many, there is a great relief that the butter they have been avoiding for the last 20 years (or consuming guiltily) can now be used. For others, the prospect of consuming full fat milk, cheese or yogurt still seems risky. After all, they have been hearing from the American Heart Association, the USDA nutritional guidelines and pretty much every nutritional advice column for the last 30 years that these products increase their risk of heart disease and contribute to obesity. Why should they believe their local cardiologist, a lone voice promoting full fat dairy against a chorus of naysayers?
Hopefully, by continuing to present scientific research on the topic I can make this concept more acceptable and counter the misinformation that is so prevalent

Researchers in Sweden have followed a cohort of rural men for over 12 years. In a previous study they found that daily intake of fruit and vegetables in combination with a high dairy fat intake was associated with a lower risk of coronary heart disease. Recently they examined their data to answer the question : how does dairy fat intake impact on the risk of developing central obesity in this middle-aged male cohort?

What is central obesity?

Central obesity refers to fat that builds up inside the abdomen. It is often measured by measuring the waist circumference: > 102 cm for males and 88 cm for females is a  marker of central obesity. Central or abdominal obesity indicates insulin resistance and is part of the metabolic syndrome and well known to increase the risk of diabetes.  It is also associated with heart disease, various cancers, and dementia. In this Swedish study, central obesity was defined as waist hip ratio ≥ 1.
The study found that 197 men (15%) developed central obesity during follow-up. A low intake of dairy fat at baseline (no butter and low fat milk and seldom/never whipping cream) was associated with a higher risk of developing central obesity (OR 1.53, 95% CI 1.05-2.24) and a high intake of dairy fat (butter as spread and high fat milk and whipping cream) was associated with a lower risk of central obesity (OR 0.52, 95% CI 0.33-0.83) as compared with medium intake (all other combinations of spread, milk, and cream) after adjustment for intake of fruit and vegetables, smoking, alcohol consumption, physical activity, age, education, and profession

Yes, these data show that participants were three times more likely to develop central obesity if they consumed skim milk and no butter compared to those who drank high fat milk and butter.

This is not an isolated finding. There is a wealth of data supporting the concept that full fat diary is less associated with obesity and markers of the metabolic syndrome, diabetes and insulin resistance.

120px-CheeseAnother recent study in a Basque population in Spain found that  participants with low or moderate consumption of cheese (high fat) compared to high consumption of cheese (high fat) had a higher prevalence of excess weight

Why do people falsely believe that fat in general and high fat dairy in particular promotes obesity?

In the past, supporters of this concept (and there are less and less in the scientific world)  would point to the energy density of fat which contains 9 calories per gram compared to 4 calories per gram for carbohydrates or protein. Obviously, if obesity is determined by calories in versus calories out then the food with more % fat compared to carbs or protein is providing more calories. All things being equal, one could expect to grow fatter on the higher % fat diet. All things are not equal, however, because one doesn’t determine how much one consumes based on the volume or weight of the food entering the mouth.

There are far more complex factors at work. How does the mixture of food components effect satiety? What is the insulin response to the food? What are the other components of the food such as vitamins, fiber, calcium and how do they interact with food absorption and metabolism?

So, even though this contradicts what has been drummed into your head for 30 years: eat full fat yogurt , cheese and milk , not fat-free, if you want to avoid getting fat

Should You Get a Routine Annual Electrocardiogram (ECG)?

Recently, the skeptical cardiologist  was asked by his  old friend and life coach (OFALCSC) whether he was correct to refuse the annual electrocardiogram (ECG) which his primary care doctor had recommended during an annual physical.

ECG showing atrial fibrillation
ECG showing atrial fibrillation

Most of my patients feel that the ECG has the ability to tell me  quite a bit about their heart. The technique utilizes electrodes on the arms, legs and chest region which  record with precision, the depolarization and repolarization of the upper chambers (atria) and lower chamber (ventricles) of the heart.

The ECG is THE tool for assessing the rhythm of the heart.  If performed and interpreted properly (not always a given) it tells us very precisely whether we are in normal (sinus) rhythm, wherein the atria contract synchronously before the ventricles contract, or in an abnormal rhythm. It is also very good at telling us whether you are having a heart attack.

If you are, however, like the OFALSC, and feel fine (meaning without symptoms or asymptomatic), exercise regularly, have never had heart problems,  and have a pulse between 60 and 90, the value of the routine annual ECG is very questionable. In fact, the United States Preventive Services Task Force (USPFTF)

“recommends against screening with resting or exercise electrocardiography (ECG) for the prediction of coronary heart disease (CHD) events in asymptomatic adults at low risk for CHD events”

(for asymptomatic adults at intermediate or high risk for CHD they deem the evidence insufficient). The USPSTF feels that that the evidence only supports an annual BP screen along with measurement of weight and a PAP smear.

To many, this seems counter-intuitive: how can a totally benign test that has the potential to detect early heart disease or abnormal rhythms not be beneficial?

There is a growing movement calling for restraint and careful analysis of the value of all testing that is done in medicine. Screening tests, in particular are coming under scrutiny.
Even the annual mammogram, considered by most to be an essential tool in the fight against breast cancer, is now being questioned.

My former cardiology partner, Dr. John Mandrola, who writes the excellent blog at, has started an excellent discussion of a recent paper that shows no reduction of mortality with the annual mammogram. He looks at the topic in the context of patient/doctor perception that “doing something” is always better than doing nothing, and the problem of “over-testing.”

In my field of cardiology there is much testing done. It ranges from the (seemingly) benign and (relatively) inexpensive electrocardiogram to the invasive and potentially deadly cardiac catheterization. For the most part, if patients don’t have to pay too much, they won’t question the indication for the tests we cardiologists order. After all, they want to do as much as possible to prevent themselves  from dropping dead from a heart attack and they reason that the more testing that is done, the better, in that regard.

The Problem of False Positives and False Negatives

But all testing has the potential for negative consequences because of the problem of false positives and negatives. To give just one example: ECGs in people with totally normal hearts are regularly interpreted as showing a prior heart attack. This is a false positive. The test is positive (abnormal) but the person does not have the disease. At this point, more testing is likely to be ordered; specifically, a stress test. Stress tests in low risk, asymptomatic individuals often result in false positive results. After a false positive stress test, it is highly likely that a catheterization will be ordered. This test carries potential risks of kidney failure, heart attack, stroke and death. It is bad enough that the cascade of testing initiated by an abnormal, false positive,  screening test results in unnecessary radiation, expense and bother but  in some cases it end up killing patients rather than saving lives.

On the other end of the spectrum is the false negative ECG. Most of my patients believe that if their ECG is normal then their heart is OK. Unfortunately the ECG is very insensitive to cardiac problems that are not related to the rhythm of the heart or an acute heart attack.

Patients who have 90% blockage of all 3 of their major coronary arteries and are at high risk for heart attack often have a totally normal ECG. This is a false negative. The patient has the disease (coronary artery disease), but the test is normal. In this situation the patient may be falsely reassured that everything is fine with their heart. The next day when they start experiencing chest pain from an acute heart attack, they may dismiss it as heart burn instead of going to the ER.

More and more, screening tests like the ECG and the mammogram  are rightfully being questioned by patients and payers. For a more extensive discussion about which tests in medicine are appropriate check out the American Board of Internal Medicine’s

Keep in mind: not uncommonly,  doing more testing can result in worse outcomes than doing less.

Estimating Your Risk of Heart Attack and Stroke: There’s an App For That

I’ve been meaning to blog on the new ACC/AHA (ACC=American College of Cardiology, AHA=American Heart Association) guidelines for treatment of high cholesterol but have been waiting for the initial controversy to die down and to get more experience with using them.  One of the areas of controversy has been the ASCVD (atherosclerotic cardiovascular disease) risk estimator. These guidelines attempt to look at risk of both stroke and heart attack (the components of atherosclerotic cardiovascular disease) and what published scientific research tells us works to reduce that risk.

They differ substantially from previous guidelines recommendations and suggest treatment with statin drugs(no other cholesterol lowering agents) for the following groups

1. Diabetics

2. Patients with known clinical ASCVD  (this includes stroke/TIA, heart attack, and peripheral arterial disease)

3. LDL or bad cholesterol over 190

4. Individuals without ASCVD whose 10 year risk of developing ASCVD (heart attack or stroke) is > 7.5%

It is the last category that has garnered the most controversy as it appears this will substantially increase the number of patients in whom statin therapy is recommended. In addition, the accuracy of the risk estimator has been questioned. When the guidelines were released the risk estimator was available as a downloadable Excel spreadsheet which was very cumbersome to use (and did not work on my Mac).

Today, the ACC announced that  an iphone/ipad app version of the risk estimator was available on itunes . You can download it for free here. It’s pretty well done. You enter your age, race, gender, HDL (“good” cholesterol) and total cholesterol along with yes/no answers to whether you have diabetes, treatment for hypertension or are a smoker.IMG_0847

Your 10 year risk of ASCVD appears as a percentage.

In the example to the left, the individual (whose numbers are eerily similar to those of the skeptical cardiologist) has a 10 year risk of 6.2% compared to 5.2% for an individual with “ideal” risk factors. In this case, the 6.2% 10 year risk is below the proposed 7.5% cut point for treatment. (As a side note, this individual’s HDL rose from 53 to 80 when he switched from skim milk , egg-whites and low-fat processed food to full fat dairy, eggs and grass-fed beef. An HDL of 53 would raise the risk to 8.5% which would trigger a recommendation for statin therapy!)

A lifetime risk is also given for those aged 20 to 59 years but the app seems flawed because in every case I entered the lifetime risk was 50% for the individual and 5% for the ideal risk factor individual

I’ll be utilizing this on every patient I see that does not have clinical ASCVD. I would encourage everybody to download this app and find out what your risk is. The higher your risk, the more likely your are to benefit from taking a statin drug, the lower it is, the less likely the benefits of lifelong drug treatment will outweigh the risks.

Understanding your risk of ASCVD is the crucial first step to having an informed discussion with your physician about atherosclerosis and the risks and benefits of drug therapy to prevent strokes and heart attacks.

More Evidence That Sugar is the Major Toxin in our Diets

A can of Coke (12 fl ounces/355 ml) has 39 grams of carbohydrates (all from sugar, approximately 10 teaspoons),[47] 50 mg of sodium, 0 grams fat, 0 grams potassium, and 140 calories. Image courtesy of Gwyneth Pearson who likely consumed it
A can of Coke (12 fl ounces/355 ml) has 39 grams of carbohydrates (all from high fructose corn syrup, equivalent to approximately 10 teaspoons of sugar), 50 mg of sodium, 0 grams fat, 0 grams potassium, and 140 calories. Image courtesy of Gwyneth P, who likely consumed it (the beverage in the can, that is, not the image)
The skeptical cardiologist had to temporarily interrupt his scintillating research into Canola Oil and the Mediterranean diet in order to highlight a study published yesterday in the Journal of the American Medical Society that adds further evidence to the paradigm that sugar is not just causing obesity but is actually killing us.

In a previous post on low-fat yogurt I emphasized that a great pseudo-scientific scam had been foisted on Americans, the promotion of low fat substitutes for real food. The low-fat substitutes masquerade as more heart healthy because saturated fat has been removed but they are actually less healthy because sugar or high fructose corn syrup has been added. Substantial evidence indicates that consumption of sugar and refined carbohydrates are contributing to obesity and cardiovascular disease (CVD), not the unjustly demonized  saturated fats. Now there is evidence to suggest sugar is actually directly promoting heart disease.

In the article, the authors analyzed data from subjects who participated in the National Health and Nutrition Examination Survey (NHANES). They estimated the “usual percentage of calories from added sugar” for individuals.

Added sugar “includes all sugars used in processed or prepared foods, such as sugar-sweetened beverages, grain-based desserts, fruit drinks, dairy desserts, candy, ready-to-eat cereals and yeast breads, but not naturally occurring sugar, such as in fruits and fruit juices.”
Among the 11733 participants there were 831 CVD deaths with a median follow up of 14.6 years.

Those who consumed 25% or more of calories from added sugar were 2.75 times more likely to die than those who consumed less than 10% of calories from added sugar. The risk of CVD mortality increased exponentially with increased  percentage of calories from added sugar.

Major sources of added sugar in American adults diet included sugar-sweetened beverages (37%), grain-based desserts (14%), dairy desserts (6%) and candy (6%). One 360-ml can of regular soda contains about 35 g of sugar (140 calories) or 7% of total calories.

The authors discussed emerging evidence suggesting multiple pathways by which sugar might play a role, including promoting hypertension, increased de novo lipogenesis in the liver (resulting in high triglycerides) and promoting inflammation.

My first dietary recommendation to my patients is to cut out the added sugar. This is both for weight management and lower heart attack risk. The low-fat,  processed “food-like substances” you have been choosing are far worse for you than the unprocessed high fat food they replaces.

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