Category Archives: Cardiac Tests

Should All Men Over Sixty Take a Statin Drug?

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.

Searching for Subclinical Atherosclerosis: Coronary Calcium Score-How Old Is My Heart?

Heart attacks and most sudden cases of sudden death are due to rupture of atherosclerotic plaques. Thus, it makes sense to seek out  such plaques, a process I call searching for subclinical atherosclerosis. I’ve talked about using high frequency ultrasound of the carotid arteries to the brain to look for plaque and for carotid IMT in earlier posts here and here.

There is a third method that looks directly at the coronary arteries, which supply blood to the heart.  It is variously called a heart scan, coronary calcium score, or cardioscan, and it is more widely utilized amongst physicians who are serious about preventing cardiovascular disease.

This technique utilizes the ionizing radiation inherent in X-rays to perform a CT examination of the chest. It does not require injection of any dye or the puncture of any arteries; thus, it is considered noninvasive and has no risk or pain associated with it.

When atherosclerosis first begins to form in the arteries, it generally takes the form of “soft” plaques. Soft plaques are initially full of lipids, but after a period of time, the plaques undergo change: calcium begins to deposit into this plaque.

There is a direct relationct_calciumship between coronary artery calcium (CAC) and the amount of atherosclerotic plaque in the coronary arteries.

CT scans are very accurate in identifying small amounts of calcium in the soft tissue of the body. Calcium score tests essentially look for blobs of calcium that are felt to be within the coronary arteries, count up the intensity and distribution of them, and calculate a total score that reflects the entire amount of calcium in the coronary arteries.

A large body of scientific literature has documented that higher calcium scores are associated with higher risk of significantly blocked coronary arteries and of heart attack.

You can read the NHLBI clinic’s info for patients here on the test.

How Is The Calcium Score Used To Help Patients?

The calcium score can be utilized (in a manner similar to the carotid IMT and plaque) to help determine whether a given individual has more advanced atherosclerosis than we would predict based on their risk factor profile. A score of zero is consistent with a very low risk of significantly blocked arteries and confers an excellent prognosis. On the other hand, scores of >400 indicate extensive atherosclerotic plaque burde , high risk of heart attack, and high likelihood of a significantly blocked coronary artery.

The calcium score (similar to the carotid IMT) increases with age and is higher in males versus females at any given age. We have very good data on age and gender normals. The average 50-59 year old woman has a zero score, whereas a man in that age range has a score of 30. The average man has developed some CAC by the fourth decade of life whereas the average woman doesn’t develop some until the sixth decade. More advanced CAC for age and gender is a poor prognostic sign. You can plug your own age, gender, race and CAC score into a calculator on the MESA (Multi-ethnic Study of Atherosclerosis) website here.

2013 ACC/AHA Guideline on the Assessment of Cardiovascular Risk says the following

 If, after quantitative risk assessment, a risk based treatment decision is uncertain, assessment of 1 or more of the following—family history, hs-CRP, CAC score, or ABI—may be considered to inform treatment decision making

This guideline recommended utilizing a  CAC score of >300 Agatson Units or >75th percentile for age, gender and ethnicity as a cut-off.

CAC Score Identifies Those At Very High  Risk

A forty-something year old man came to see me for palpitations. He had a stress echo which was normal except for the development of frequent PVCs and a brief run of non sustained ventricular tachycardia.  His risk factor profile was not particularly bad: no diabetes, hypertension, or cigarette smoking and an average lipid profile. When I calculated his 10 year risk of ASCVD using my iPhone app it came out at 7%: below the level at which statin treatment would be recommended.  Because his father had a coronary stent in his fifties (this does not qualify as a family history of heart disease according to the new guideline, by the way)  I recommended he get a CAC test done.

His CAC score came back markedly elevated, almost 1000.  .  A subsequent cardiac catheterization demonstrated a very high-grade coronary blockage iwhich was subsequently stented. I started him on high intensity statin therapy and he has done well.

CAC score identifies Those At Very Low Risk

Many individuals with high cholesterol values do not develop atherosclerosis.  A zero CAC score in a male over 50 or a woman over 65 (or non-zero CAC score that is <25th percentile for age, gender, ethnicity) indicates that they are not developing atherosclerosis and makes it less likely that they will benefit from statin therapy to lower cholesterol.

Some Caveats About CAC score testing

-Like carotid vascular screening, there is no reason to get a CAC test if you already have had problems related to blocked coronary arteries such as a heart attack or coronary stents or coronary bypass surgery.

-CAC score testing is not covered by insurance (except in Texas) and costs somewhere between $125 and $300 out of pocket.

-The CT scan leads to a small amount of radiation exposure-approximately 1 – 2 milliseiverts of radiation (mSv). To puts things in perspective, the annual radiation dose we receive from natural sources is around 3 mSV per year.

Some of the other approximate radiation doses for tests commonly used in medicine are:

Chest X-ray ( )            0.1 mSV
Routine CT chest:  10 mSV
CT abdomen: 10 mSV
Nuclear stress test: 10 to 20 mSV

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.

 

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 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 www.drjohnm.org, 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 www.choosingwisely.org.

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