Tag Archives: sudden cardiac death

What Can You Really Learn From Celebrity Bob Harper’s Heart Attack And Near Sudden Death?

Until recently I had never heard of Bob Harper (The Biggest Loser) but apparently he is a celebrity personal trainer and had a heart attack and nearly died.  He  is known “for his contagious energy, ruthless training tactics, and ability to transform contestants’ bodies on The Biggest Loser” (a show I’ve never seen.)

When celebrities die suddenly (see Garry Sanders, Carrie Fischer) or have a heart attack at a youngish age despite an apparent healthy lifestyle this get’s people’s attention.

The media typically pounce on the story which combines the seductive allure of both health and celebrity reporting.

It turns out Harper inherited a high Lipoprotein (a) (see here) which put him at high risk for coronary atherosclerosis (CAD) which ultimately caused the heart attack (MI)  that caused his cardiac arrest.

To his credit, Harper has talked about Lipoprotein (a) and made the public and physicians more aware of this risk factor which does not show up in standard cholesterol testing.

Since his heart attack, Mr. Harper of “The Biggest Loser” has embarked on a newfound mission to raise awareness about heart disease and to urge people to get tested for lp(a).

Harper As Brilinta Shill

Unfortunately , he has also become a shill for Brilinta, an expensive brand name anti platelet drug often prescribed in patients after heart attacks or stents.

At the end of the TV commercial he says “If you’ve had a heart attack ask your doctor if Brilinta is right for you. My heart is worth Brilinta.”

At least this video is clearly an advertisement but patients and physicians are inundated  by infomercials for expensive, profit-driving drugs like Brilinta.

This Healthline article pretends to be a legitimate piece of journalism but is a stealth ad for Brilinta combined with lots of real ads for Brilinta.

Harper As Lifestyle Coach.

Harper also changed his fitness and diet regimens after his MI reasoning that something must have been wrong with his lifestyle and it needed modification.  For the most part he talks about more “balance” in his life which is good advice for everyone. His fitness regimens pre-MI were incredibly intense and have been toned down subsequently.

After his heart attack, Bob abandoned the Paleo lifestyle for the Mediterranean diet, as it’s been proven to improve heart health and reduce the risk of a heart attack, stroke, and heart-disease-related death by about 30 percent. But recently, he’s moved closer to a vegetarian regimen.

Of course, vegans and vegetarians have seized on this change in his diet as somehow proving the superiority of their chosen diets as in this vegan propaganda video:

Unfortunately there is no evidence that changing to a vegan or vegetarian diet will lower his risk of repeat MI.  Those who promote the Esselstyn, Pritikin or Ornish type diets claim to “reverse heart disease” and to be science-based but, as I’ve pointed  out (see here) the science behind these studies is really bad.

In fact, we know that neither diet nor exercise influence lipoprotein(a) levels which Bob inherited.  Some individuals just inherit the risk and must learn to deal with the cardiovascular cards they’ve been dealt.

What Can We Really Learn From Bob Harper’s Experience?

  1. Lipoprotein (a) is a significant risk marker for early CAD/MI/sudden cardiac death. Consider having it measured if you have a a) strong family history of premature deaths/heart attack (b) if you have developed premature subclinical atherosclerosis (see here) or clinical atherosclerosis (heart attack, stroke, peripheral vascular disease) or (c) a family member has been diagnosed with it.
  2. Everyone should learn how to do CPR and how to utilize an AED. (see here for my rant on these two incredibly important 3-letter words). Harper was working out in the gym when he collapsed. Fortunately a nearby medical student had the wherewithal to do CPR on him until he could be defibrillated back to a normal rhythm and transported to a hospital to stop his MI.
  3. Dropping dead suddenly is often the first indicator that you have advanced CAD. If you have a strong family history of sudden death or early CAD consider getting a coronary artery calcium scan to better assess your risk.

Focus on celebrities with heart disease helps bring awareness to the public about important issues but we can only learn so much about best lifestyle or medications from the experience of one individual, no matter how famous.

Brilliantly Yours,

-ACP

Do You Know What’s On Garry Shandling’s And Your Parent’s Death Certificate?

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Better Call Saul’s Bob Odenkirk and Kathy Griffin “hanging” with an apparently healthy Larry Sanders on March 20. These two appeared on Shandling’s brilliant Larry Sanders TV show.

When someone who had appeared to be healthy dies suddenly, it is often assumed that he/she died of “a massive heart attack.” Certainly, this was the case in the recent unexpected sudden death of Garry Shandling, the actor and comedian.  Shandling, aged 66, died March 24 of this year.

ET online reported:

“His publicist Alan Nierob told the ET that Shandling had no history of heart problems, but that doctors believe he died as the result of a heart attack.”

Although a heart attack resulting in ventricular fibrillation is the most common cause of a sudden, unexpected death in individuals over the age of 40, it is not the only one.

In fact, People  magazine reported that Sanders experienced shortness of breath and pain in his legs just a day before his death, and that he spoke to a doctor friend about his symptoms, who stopped by that night to check on him,

Shortness of breath and pain in the legs raise the possibility of a clot or DVT in the leg, which can break loose and embolize into the pulmonary arteries. Such a pulmonary embolism, if massive, can result in swift and sudden death.

The LA Coroner’s office could not get Sanders’ physician to sign his death certificate and the cause of death has still apparently not been determined, pending toxicology testing which typically takes 6 weeks.

What’s On Your Parent’s Death Certificate

More important than what is on Garry Shandling’s death certificate is what is on your parent’s death certificate, and whether it is accurate. If one of your parents died prematurely and suddenly, it is  important to know with precision what caused it. If the cause was an heritable cardiovascular condition, hopefully, appropriate testing can determine if you have that condition, and steps can be taken to prevent your premature demise.

Examples of inherited cardiovascular conditions (in addition to heart attack (myocardial infarction) or pulmonary embolism) that can cause sudden and unexpected death include aortic aneurysm dissection, hypertrophic cardiomyopathy, arrhythmogenic right ventricular dysplasis, and long QT syndrome.

Unfortunately I find that, at least in my patients, uncertainty about the cause of death of one’s parents is the norm.

Many of my patients, for example, tell me one of their parents died of a “massive heart attack” and they assume that they are at increased risk of the same fate. When I press for details, typically no autopsy was performed.  Mom or dad may have been found dead at home, or they may have suddenly keeled over but not survived to make it to the hospital for a definitive diagnosis.

Without an autopsy in such circumstances, it is not possible to be sure of the cause of death.

Even if you have a cause of death listed on your parent’s death certificate, there is no guarantee that it is accurate.  The doctor that filled it out, without an autopsy in many circumstances, is just speculating on the cause based on what he/she knew about prior medical conditions and the circumstances surrounding the death.

I was recently asked to fill out the death certificate of an elderly patient of mine who had atrial fibrillation and congestive heart failure and was living in a nursing home.

One night she was noted by the staff to be very short of breath and was taken to a local  emergency room where she was pronounced dead.

Based on the information available to me, I had no idea what caused her death. Although she had quite signifiant cardiac problems, when I last saw her she was stable and I have numerous patients with the same conditions who live for decades.

I filled out the death certificate, listing all of her conditions, and entered in that the cause of death was unknown.

Although the CDC guide for physicians filling out death certificates clearly states that this is acceptable, I was subsequently informed that the funeral home did not accept unknown cause of death and that they had found another doctor to fill in a cause  of death.

I guarantee you, whatever he put on as the cause of death was total speculation.

Jerry Seinfeld was good friends with Garry Shandling and, oddly enough, not too long ago, featured him in an episode of his internet series “Comedians in Cars Getting Coffee” entitled “It’s Great That Garry Shandling Is Still Alive.

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Shandling mentions “I had hyperparathyroidism,” making a joke that “the symptoms are so much like being an older Jewish man, no one noticed!”

James Fallows, the excellent The Atlantic writer, highlights his own experience with hyperparathyroidism (a disease that leads to high calcium levels and is easily treated with surgery), in a recent Atlantic article. The subtitle of this article, “a rare and under-publicized condition that can sometimes be fatal,” suggests that hyperhyperparathyroidism might have led to Shandling’s death.

I don’t think this is likely because Shandling suggests that the disease is in the past tense (i.e. he has already had the surgery), and sudden death from hyperparathyroidism would be extremely unlikely.

Fortunately, Shandling is getting a full examination and autopsy to fully determine the cause of his death. If he has offspring, this will be extremely helpful to them in understanding what medical conditions they can expect later in life.

If he was not a celebrity, his death, like many of your parents’, most likely would have been ascribed to a “massive heart attack.”

 

 

Is Coronary Calcium Scanning the Mammography of the Heart?

If you have watched The Widowmaker as suggested by the skeptical cardiologist you have likely been convinced that the developers and promoters of coronary artery calcium (CAC) scans, for the early detection of heart disease, are true heroes in the cardiology world.

These members of the “calcium club” are portrayed as unbiased self-less promoters of the prevention of heart attacks and sudden death, fighting an uphill battle against the evil procedure and money-driven forces who push coronary stents-greedy interventional cardiologists and the device, hospital and insurance industries.

A constant theme in the documentary is that CAC scanning should be to the heart what mammography is to the breast. It should be done on all patients over a certain age and should be covered by insurance.

As a non-invasive cardiologist with a strong interest in prevention, I am definitely a strong proponent of CAC scans in the right population. As the skeptical cardiologist, however, I find flaws with the mammography comparison.

Let’s review some of the established science regarding CAC scans.

What Is A CAC Scan?

coronary calcium
Coronary calcium scan from a 52 year old man I was seeing for palpitations. He had had an equivocal stress test but had a strong family history of CAD. Standard risk factors were unremarkable. As shown here, he has very extensive calcium in his coronary arteries. The left anterior descending (LAD) has lots of calcium (CA, indicated by arrows). His total score was 1798 which is at the 99th percentile for caucasian men his age. This means that his score is higher than 99% of caucasian men. Such a high score for age puts him in an extremely high risk category of heart attack and death.

The CAC scan utilizes computed tomography (CT)  X-rays, without the need for intravenous contrast, to generate a three-dimensional picture of the heart. Because calcium is very apparent on CT scans, and because we can visualize the arteries on the surface of the heart that supply blood to the heart (the coronary arteries), the CAC scan can detect and quantify calcium in the coronary arteries with great accuracy and reproducibility.

A preventive cardiologist, Dr. Arthur Agatson, who is interviewed in the film (and who is also the creator of the South Beach Diet, a low carbohydrate, high fat diet), developed a method for counting up the amount of calcium in the coronary arteries (the Agatson or calcium score).

Calcium only develops in the coronary arteries when there is atherosclerotic plaque. The more plaque in the arteries, the more calcium.

What Is The Risk Of  A High CAC Score

Multiple observational studies have shown that a high versus low calcium score is indicative of high risk for heart attack and death.

For example, a large study published in 2008 (the MESA study), followed 6,814 individuals for 3.8 years. Compared with patients with a CAC score of 0, patients with a CAC score of 101-300 had a 7.7 fold increase risk of a coronary event (heart attack). CAC score of >300 conferred almost a tenfold increase risk.

Screen Shot 2015-09-06 at 8.32.02 AMBased on data from 5 large studies and almost 15,000 patients, we can put patients with CAC score in very low to high risk categories for cardiac events over the next 10 years.

What Is The Value Of A Zero Calcium Score?

Just as important as identifying patients with advanced or premature atherosclerosis who should be getting intensive therapy  for prevention of cardiac events, is identifying those patients who may not warrant therapy.

A CAC score of zero puts a patient in an extremely low risk category.  A recent study, with the provocative title of:

A 15-Year Warranty Period for Asymptomatic Individuals Without Coronary Artery Calcium

…demonstrated that a zero calcium score confers this low risk of cardiac events for up to 15 years.

Thus, many patients, who are considered intermediate risk based on standard risk factors, do not have significant plaque by CAC score and may not need otherwise indicated statin therapy.

Mammography

The comparison of mammography to CAC scanning is appropriate in that both have created considerable controversy and are at the epicenter of discussions on the value of mass screenings in the prevention of life-threatening disease.

In contrast to CAC, mammography has been widely accepted and promoted by most professional organizations. In recent years, however, the value of mammography for all women over the age of 40 has been questioned.

In 1980, a randomized controlled trial of screening mammography and physical examination of breasts in 89, 835 women, aged 40 to 59, was initiated in Canada. It was called the Canadian National Breast Screening Study.

The findings published last year were:

Annual mammography in women aged 40-59 does not reduce mortality from breast cancer beyond that of physical examination or usual care when adjuvant therapy for breast cancer is freely available. Overall, 22% (106/484) of screen detected invasive breast cancers were over-diagnosed, representing one over-diagnosed breast cancer for every 424 women who received mammography screening in the trial.

Recently, the Swedish Medical Board recommended that all mammography screening be phased out in that country.

The US preventive services task force draft guidelines, updated earlier this year, will recommend screening for women aged 50-74 but not in those aged 40-49 years.

Downsides of breast cancer mammography screening include:

-Over-diagnosis: finding and treating breast cancer that would not have been a threat to the patient.

-False positives: the test identifies a possible cancer which is not subsequently confirmed. False positives lead to breast biopsies, which are not needed and often cause needless anxiety and stress.

-Radiation exposure.

Is CAC Screening The Cardiac Equivalent Of Mammography?

CAC scans differ fundamentally from mammography because atherosclerosis is a continuous and diffuse arterial process, whereas breast cancer is (most often) localized, and either present or not.

The development of atherosclerosis starts with fatty streaks in multiple arterial beds fairly early in life, followed by progressive plaque development with progressive build up of calcium in the plaques.

Thus, the CAC score ranges continuously from zero up to several thousand.

The calcium score is not subject to false positives-if calcium is detected, atherosclerotic plaque is present.

A mammogram is either abnormal, suggesting cancer and requiring a biopsy, or it is normal. There is no continuous grading of risk.

The second fundamental difference in the two disease processes is that atherosclerosis can kill suddenly without warning.

As pointed out in numerous examples in The Widowmaker, an individual can seem fit and hearty one minute, and be dead the next, from a heart attack caused by a lethal abnormal rhythm.

Breast cancer deaths on the other hand, occur slowly after diagnosis, and are generally predictable.

Nuclear Stress Tests are the Mammography of the Heart

If we are looking for a cardiac test that has characteristics similar to mammography, the nuclear stress test is much closer than CAC.

With a nuclear stress test we are using a radio tracer injected intravenously, which subsequently traverses the coronary arteries into the heart muscle. Subsequent imaging of the photons emitted by the radio tracer allows assessment of the status of blood flow down the coronary arteries.

The test is designed to identify coronary arteries with flow limiting blockages (usually >70% blocked), caused by atherosclerotic plaques. Such blockages are more likely to be causing symptoms and therefore more likely to require treatment with coronary stents or bypass surgery.

Like mammography, then, nuclear stress tests are either abnormal or normal, and when abnormal they can be falsely abnormal.

Nuclear stress tests have a very high incidence of false positives. These false positives result in invasive catheterization procedures to more directly image the arteries, and may result in inappropriate coronary stenting or bypass procedures with associated risks.

It is because of the high risk of false positives and attendant harm that in the last decade, all cardiac societies recommend against the routine use of stress testing in asymptomatic patients.

As pointed out in the Widowmaker, there is no data which suggest that stress testing improves outcomes for cardiac patients.

Stress tests by design tell us nothing about the noncritical build up of atherosclerotic plaque. You can have a normal stress test and have a huge burden of plaque in your arteries.

It is this silent build up of atherosclerosis, with sudden rupture of plaque, which results in sudden death in most cardiac patients.

What Is The Breast Cancer Equivalent Of CAC?

A CAC of the breast would identify abnormal cells as soon as they began on the presumably multi-year road to becoming a full flown cancer.

To be fully equivalent to the CAC, the breast CAC would have to have a proven treatment that could be instituted once a certain stage of cell transformation had been reached.

For atherosclerosis, that treatment is statin drugs, which are recommended for those with high risk CAC scores.

For breast cancer, the treatment of choice is mastectomy.

 Would Widespread Institution of CAC Screening Save Millions of Lives?

For mammograms based on a review of all the evidence, the US PTF concluded:

Over a 10-year period, screening 10,000 women ages 50 to 59 years will result in 8 (95% confidence interval [CI], 2 to 17) fewer breast cancer deaths, and screening 10,000 women ages 60 to 69 years will result in 21 (95% CI, 11 to 32) fewer deaths.

To scientifically determine how many lives are saved by CAC screening, we would need an extremely large randomized controlled trial lasting for at least 6 years.

Individuals with low or intermediate risk from standard risk factors for atherosclerosis would receive a standard approach to management or would undergo CAC screening with treatment determined by calcium score.

Such trials have been proposed but to date have not been funded by the NIH thus we may not have a definite answer for a long time.

Should CAC Scans Be Covered Like Mammography?

I am very conflicted on this question.

On one hand I do believe that appropriate use of CAC scans prevents heart attacks and sudden death. How many, remains to be seen. As we saw for mammography, only large scale randomized trials will tell us for sure who will benefit and how much.

On the other hand, I can see potential for abuse, and in the wrong hands, excessive downstream invasive testing, which will minimize the benefits of early detection.

If CAC scans are covered by insurance and used widely, they could become a method for unscrupulous cardiology centers and doctors to proceed to unnecessary testing that would ultimately increase the amount of inappropriate coronary stenting.

Indeed, it is quite ironic that the major theme of The Widowmaker, that of the medical-industrial stent complex suppressing CAC scan usage, is quite illogical, for widespread, injudicious use of CAC scanning would be a boon for stent inserters and makers.

The inappropriate use of CAC scan information is limited currently because most of the doctors ordering them are primarily interested in prevention, not in generating more testing and procedures.

The other limit on its use is cost. For 99% of my patients the $125 for a CAC scan at my hospital is not a limiting factor.

On the other hand, in a less affluent population, this would be a large and limiting expense; the poor would be getting a lesser standard of care.

The cases of patients in The Widowmaker who feel like a CAC scan saved their lives are very similar to those of breast cancer patients who feel mammography saved theirs.

These patients often become passionate advocates for a specific test based on their own experience. The Widowmaker, in fact, was funded by David Bobbett, an Irish millionaire who discovered that he had an extremely high calcium score and now feels like everyone should get the test.

Bobbett is convinced that the test saved his life, but all anecdotal patient stories about CAC scans “saving their life” have to be taken with a grain of salt.

After this (far too long) discussion I have to conclude that although they share many features, CAC scans are not the mammography of the heart.

uncharacteristically verbosely yours,

-ACP

The Widowmaker: Stents versus Calcium Scans

I’ve just finished watching a documentary on Netflix called The Widowmaker which alternately had me fascinated, disgusted, bored, excited, and angry.

This movie is about the treatment of coronary artery disease and what we can do about the large number of people who drop dead from heart attacks, some 4 million in the last 30 years.

The documentary, as all medical documentaries tend to do, simplifies, dumbs down and hyperbolizes a very important medical condition. Despite that it makes some really important points and I’m going to recommend it to all my patients.

At the very least it gets people thinking about their risk of dying from heart disease which remains the #1 killer of men and women in the United States.

Perhaps it will have more patients question the value of stents outside the setting of an acute heart attack. This is a good thing.

Perhaps it will stimulate individuals to be more proactive about their risk of heart attack. This is a good thing.

Take a look. Think about it. If you decide you might benefit from a coronary calcium scan of your heart let me know.

I’ll dissect this movie in detail in subsequent posts. There are a lot of inaccuracies  but some fundamental and important points are made that patients need to now.

Stents do not prevent heart attacks.

Standard risk factors do not do well at predicting who will have a heart attack.

-ACP

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 Age

I’ve discussed in a previous post the importance of detecting subclinical atherosclerosis.

The process of atherosclerosis (the build up of fatty plaques in all arteries) occurs silently and often the first symptom is sudden death due to a heart attack.

Examining the large arteries in the neck (the carotids) with ultrasound for early fatty  plaques helps establish whether atherosclerosis is present or not.

If there is plaque in the carotids this is a strong indicator that atherosclerosis is present throughout the large arteries of the body including the coronary arteries supplying blood to the heart.

Ruptured plaques in the coronary arteries are what cause heart attacks and most cases of sudden cardiac death are due to heart attacks.

If we can identify those who have subclinical (i.e. before significant blockages and symptoms develop) atherosclerosis, we can better target aggressive therapy to those at the highest risk.

Carotid IMT: The window to your vascular age

There is a second technique which uses carotid ultrasound  available to evaluate an individual’s longer term risk of heart disease even before plaque develops.

This technique is termed carotid IMT. IMT (intimal-medial thickness ) refers to the thickness of the wall of the artery which includes the thin layer of cells lining the inside of arteries or intima and the smooth muscle in the wall of the artery (media).

The Carotid IMT has been shown to be related to all of the risk factors that medical science knows for atherosclerosis. It progressively increases with normal aging and we have data on what the normal value is for white and black  men and women between the ages of 40 and 70.

By making multiple precise and careful measurements of an individual’s CIMT we can determine where that individual stands in comparison to normal individuals of the same age, gender and race.

Individuals whose CIMT is great than that of 75% of individuals of the same age and gender are at significantly higher risk of heart attack and stroke even if no carotid plaque is discovered.

Thus, the CIMT serves somewhat as an early warning signal for unhealthy arteries.

We can also determine a so-called vascular age from this technique.

 

Carotid IMT is the distance between the lines the two arrows point at
Carotid IMT is the distance between the lines the two arrows point at

An example of this is shown to the left. . The individual was an asymptomatic young man. He had no plaque but his CIMT measured 0.770, which is significantly higher than the normal CIMT for a similarly aged white male of 0.598.  This is thicker than 80% of normal individuals of the same age and gender. It is normal for an individual who is 65 years old. Thus, this individual’s vascular age is 65 years, 20 years greater than his chronological age.

In my office I usually recommend a combination of CIMT and carotid plaque be performed in individuals in whom I am trying to assess risk of cardiovascular disease between the ages of 40 and 70.

There is no reason to do CIMT in patients who have documented coronary heart disease (heart attack/stroke/stent/bypass surgery), carotid disease (stroke/carotid surgery), or peripheral arterial disease. These patients have already passed the early warning phase of atherosclerosis.

This technique should only be done by physicians/technicians who have been adequately trained and have dedicated themselves to performing the meticulous tiny measurements required in an accurate manner.

Major cardiovascular organizations differ on recommending  CIMT for screening purposes.  Well-respected scientific papers have clearly established CIMT as reproducible and highly predictive of vascular events but there is no randomized , controlled trial which establishes that utilizing it in conjunction with treatment decisions based on the results will improve cardiovascular outcomes.

For this reason, even though it is cheap, painless, harmless and quick insurance companies do not reimburse for the costs.

Some caveats:

*We don’t have good data sets on individuals under the age of 40 years. I offer CIMT to this group and extrapolate the good data  but more studies are needed in this age range.

*We don’t have good data sets on ethnicities other than the African-americans and European and American whites.

*Multiple methods of CIMT recording and measurement  have been published.

*I don’t find CIMT useful in individuals over the age of 70. Carotid plaque is much more helpful. Most men have carotid plaque by this age. If you don’t have any carotid plaque over the age of 70 years then you are in a very low risk category and are unlikely to benefit from statin or aspirin therapy.

Next post we’ll discuss the third noninvasive tool at cardiologists disposal to assess individuals for subclinical atherosclerosis: a direct look at calcium in the coronary arteries

N.B. As noted here.

The full process underlying intimal thickening is not fully understood but is thought to be similar, though not identical, to that underlying atherosclerosis. The hypothesis that IMT represents subclinical vascular disease may be supported by the finding of graded associations between IMT and concurrent atherosclerotic change visualized in the coronary arteries during angiography. It is important to note, however, that whilst in many cases thickening of the intima–media does represent atherosclerotic change, in other cases it may represent non-atherosclerotic lesions such as hypertrophy in response to shear stress on the artery wall.

 

 

 

 

 

 

 

 

Moogfest, the Z-pak, the QT interval and Sudden Cardiac Death


kraftwerk
The skeptical cardiologist was planning on attending Moogfest 2014 in Asheville, North Carolina last weekend. I was going with the old friend and life coach of the skeptical cardiologist (OFLCSC) and planned on taking in electronic and synthesizer legends like Kraftwerk and Keith Emerson, riding bikes and drinking lots of craft beer. Unfortunately, a very bad upper respiratory infection took hold of me, progressing to what felt like a pneumonia (shaking chills, fever, coughing up dark, thick sputum, rattling emerging from the depths of my lungs) and I had to cancel the trip.

After processing multiple factors of risk versus benefit (not to mention the contribution to resistant bacteria), I decided to start myself on a Z-pak which is commonly utilized for community acquired pneumonia (does this mean I have a fool for a doctor?)

Azithromycin (the macrolide antibiotic in the Z-pak) , due to its broad antibiotic spectrum and perceived favorable safety profile, became one of the top 15 most prescribed drugs and the best-selling antibiotic in the United States, accounting for 55.4 million prescriptions in 2012.

The time between onset of electrical activation of the ventricles (Q) and the depolarization or reset of the ventricles (T) is called the QT interval. You can be born with a prolonged QT interval or it can become prolonged due to certain conditions. Prolonged QT intervals increase risk of sudden death
The time between onset of electrical activation of the ventricles (Q) and the depolarization or reset of the ventricles (T) is called the QT interval. You can be born with a prolonged QT interval or it can become prolonged due to certain conditions. Prolonged QT intervals increase risk of sudden death from abnormal rhythms like torsades de pointes type of ventricular tachycardia

Between 2004 to 2011, the FDA received 203 reports of azithromycin-associated QT prolongation (see graphic to the left) Torsades de Pointes (graphic) ventricular arrhythmia, or, in 65 cases, sudden cardiac death.

This prompted a review of Tennessee medicaid data which was published in 2012.

tdp
Torsades Des Pointes (fancy French word  for twisting of the points: note how the deflections seem to be oscillating slowly (somewhat like a sine wave I would have heard at Moogfest) . This is felt to be the way QT prolongation from medications like the Z-pak cause sudden death.

This study found that people taking azithromycin over the typical 5 days of therapy, had a rate of cardiovascular death 2.88 times higher than in people taking no antibiotic, and 2.49 times higher than in people taking amoxicillin. Most of the risk appeared to be those patients who had a baseline high risk of cardiovascular disease and the excess risk of death resolved after the 5 days of therapy.

As a result, the FDA added a warning to the azithromycin package insert and urged health care professionals to use caution  when prescribing it to patients known to have risk factors for drug-related arrhythmias, including those with long QT intervals, either congenitally or induced by drugs, low potassium or magnesium levels, slow heart rates or on other medications drugs used to control abnormal heart rhythms (amiodarone, sotalol and dofetilde). 

I survived my 5 day brush with a three-fold increased risk of sudden death and I really think the Z-pak substantially helped me get over the bacterial lung infection I felt I had. I knew my risk factors in detail and they were low. I was totally aware of any interacting drugs that could prolong my QT interval.

You can survive too. Make sure you definitely need the drug (i.e. you have a bacterial infection not just the common cold) and be cautious if you have any of the following

  • Family history of sudden death
  • Personal history of unexplained passing out or dizziness
  • Use of other medications that prolong QT interval (PDF)
  • Low potassium or magnesium levels (not uncommon in heart failure patients who are on water pills)
  • Severe heart disease of any kind

A complete listing is available here.

Meanwhile, Enjoy a sample of whatl I missed at Moogfest: Dorit Chrysler playing the theremin

 

 

 

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.