Category Archives: Sudden Cardiac Death

Prevention of Heart Attack and Stroke-Early Detection Of Risk Using Coronary Artery Calcium Scans In The Youngish

Since 1/3 of Americans die from atherosclerotic cardiovascular disease (ASCVD, mostly heart attacks and strokes) and dropping dead is often the first symptom of ASCVD it’s incredibly important to identify early, “subclinical” ASCVD and begin measures to reduce risk.

How early to begin that process is open to debate. The recent sudden death of the 41-year old son of a patient of mine, however, has reinforced to me how crucial it is to begin risk assessment and potential treatments as early as possible, especially in individuals with a strong family history of premature ASCVD.

We use standard risk factors like lipids, smoking, age, gender and diabetes to stratify individuals according to their 10 year risk of ASCVD (using this online risk calculator) but many apparent low risk individuals (often due to inherited familial risk) drop dead from ASCVD and many apparent high risk individuals have no subclinical ASCVD and don’t need preventive therapy.

Recent studies provide compelling support for the early utilization of cardiac imaging in to identify high risk individuals.

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. There are a number of ways to search for sublinical plaques but the two most widely studied are carotid ultrasound screening and coronary artery calcification (CAC) measurement.

I’ve been utilizing CAC (also termed  heart scan, coronary calcium score, or cardioscan) to help assess my patient’s risk of ASCVD for years although the procedure is not covered by insurance and until recently was not strongly endorsed by major guidelines. (For a complete description of the test and the risks/benefits see here). As I pointed out here, in November the new ACC/AHA guidelines finally embraced CAC for

adults 40 to 75 years of age without diabetes mellitus and with LDL-C levels ≥70 mg/dL- 189 mg/dL (≥1.8-4.9 mmol/L), at a 10-year ASCVD risk of ≥7.5% to 19.9%, if a decision about statin therapy is uncertain

Typically, if we have calculated (using the ASCVD risk estimator) a 10 year risk >7.5% we have a discussion with the patient about beginning drug treatment to reduce risk.

To inform the decision and help us “get off the fence” I usually recommend a CAC. To see how this works in a typical sixty something see my posts here and here.

Significant Of CAC Score

As the new ACC/AHA guidelines state:

If CAC is zero, treatment with statin therapy may be withheld or delayed, except in cigarette smokers, those with diabetes mellitus, and those with a strong family history of premature ASCVD.

A duo of studies from Walter Reed Army Hospital have provided more support for the value of the zero CAC for risk prediction and identifying who should get treatment for prevention of both heart attacks and strokes.

Over 10,00 subjects underwent CAC and were assessed for the primary outcomes of all-cause mortality, incident MI, stroke, and the combination of major adverse cardiovascular events (MACE), defined as stroke, MI, or cardiovascular death over an average 11.4 years

Patients were classified on the basis of the presence or absence of calcium and further subdivided into CAC score groups of 0, 1 to 100, 101 to 400, and >400

Patients without a zero CAC had a very low number of events , with a 1.0% rate of mortality and 2.7% rate of MACE over a 10-year period.

On the other hand subjects without any traditional risk factors (n = 6,208; mean age 43.8 years), the presence of any CAC (>0) was associated with a 1.7 fold increased risk of MACE after adjustment for traditional risk factors.

f2.large-3
Patients with CAC who were prescribed a statin had a significantly reduced risk of MACE (aSHR: 0.76; 95% CI: 0.60 to 0.95; p = 0.015), whereas patients without CAC had no associated MACE reduction (aSHR: 1.00; 95% CI: 0.79 to 1.27; p = 0.99). p = 0.097 for interaction between statin treatment and CAC presence. aSHR = adjusted subhazard ratio; CAC = coronary artery calcium; CI = confidence interval; MACE = major adverse cardiovascular event(s)

The red line of the >400 score individuals has a much higher risk of death, stroke and heart attack (myocardial infarction) than the blue (CAC 1-100) or the gray line of the zero CAC scorers.

Furthermore, when these investigators looked at outcomes in those individuals who received statins versus those who didn’t, the zeros didn’t benefit from statin therapy over the 10 year follow-up.

f3.large
Benefit of statin therapy was significantly related to CAC group with benefit in patients with CAC score >100 but not in patients with CAC <100. aSHR = adjusted subhazard ratio; CAC = coronary artery calcium; CI = confidence interval; MACE = major adverse cardiovascular event(s).

But there was a tremendous reduction in bad CV events in those with scores >100 who received statin (red line) versus those who did not (blue line).

Here’s the figure which encapsulates both the risk prediction power of the CAC (and the benefits of statin treatment restricted to those with >0 (blue lines)

f2.large-4

 

Benefits of CAC Testing In The Young

So these new studies provide powerful data supporting the use of CAC in younger individuals to help us refine risk estimates and target the individual at high risk of MI and sudden death. It seems highly appropriate to consider CAC testing beginning at age 40 years as the AHA/ACC guidelines suggest.

But what about the individual who has a strong family history of premature CAD and is age say 35 or 39 years of age. Do we ignore advanced risk assessment? Very few individuals die in their 30s from ASCVD but I have a number of patients who suffered heart attacks in their forties. In addition, the earlier we can start risk modification the better as the process begins very early in life and accumulates over time.

The Coronary Artery Risk Development in Young Adults (CARDIA) Study published in 2017 has demonstrated the early development of nonzero CAC score in the youngish and the predictive value of the high CAC score for mid life ASCVD events.  It was  a prospective community-based study that recruited 5115 black and white participants aged 18 to 30 years from March 25, 1985, to June 7, 1986. The cohort has been under surveillance for 30 years, with CAC measured 15 (n = 3043), 20 (n = 3141), and 25 (n = 3189) years after recruitment. The mean follow-up period for incident events was 12.5 years, from the year 15 computed tomographic scan through August 31, 2014.

The conclusions:

Any CAC in early adult life, even in those with very low scores, indicates significant risk of having and possibly dying of a myocardial infarction during the next decade beyond standard risk factors and identifies an individual at particularly elevated risk for coronary heart disease for whom aggressive prevention is likely warranted.

screen shot 2019-01-19 at 12.36.44 pmI read CAC scans every day and it is not uncommon to see a non-zero scores in individuals in their late 30s or early 40s.

The two sons of another one of my patients both in their late 50s with unremarkable risk factor profiles and both developing anginal type symptoms limiting their activities each underwent multi vessel stent procedures in the last month. If I had seen them  10 to 20 years ago we would have identified the subclinical atherosclerosis building up in their coronaries, started treatment and avoided the need for invasive, expensive procedures.

Other Risk-Enhancing Factors To Consider In The Young

The ACC/AHA guidelines list some “risk-enhancing factors” some of which I find useful.

screen shot 2019-01-19 at 7.33.39 am

Clearly family history of premature ASCVD is important but the devil is in the details. What relatives count? What was the event in the family member? If it was sudden death was an autopsy done?

What about nontraditional lipid/biomarkers?  I consider an assessment of Lp(a) and some more sophisticated measurement of atherogenic dyslipidemia (apoB, LDL-P) and inflammation (CRP) essential.

Interestingly the guidelines include ABI (which I do not find helpful) but not carotid vascular screening which has frequently guided me to earlier therapy in youngish individuals with abnormal biomarkers or strong family history.

Vascular screening in young subjects may detect subclinical atherosclerosis as measured by thickening of the carotid wall (IMT) or early carotid plaque prior to the formation of calcium in the coronary arteries. Advanced IMT precedes the formation of soft plaque in arteries and only later is calcium deposited in the plaque.

It’s never too early to start thinking about your risk of cardiovascular disease. If heart disease runs in your family or you have any of the “risk-enhancing” factors listed above, consider a CAC, nontraditional lipid/biomarkers, or vascular screening to better determine were you stand and what you can do about it.

Included in my discussions with my patients with premature ASCVD is a strong recommendation to encourage their brothers, sisters and children to undergo a thoughtful assessment for ASCVD risk. With these new studies and the new ACC/AHA guideline recommendations if they are age 40-75 years there is ample support for making CAC a part of such assessment.

Hopefully very soon, CMS and the health insurance companies will begin reimbursement for CAC. As it currently stands, however, the 125$ you will spend for the test at my hospital is money well spent.

Skeptically Yours,

-ACP

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

Coronary Artery Calcium Scan Embraced By New AHA/ACC Cholesterol Guidelines: Will Insurance Coverage Follow?

The skeptical cardiologist has been utilizing coronary artery calcium (CAC) scans to help decide which patients are at high risk for heart attacks, and sudden cardiac death for the last decade. As I first described in 2014, (see here) those with higher than expected calcium scores warrant more aggressive treatment and those with lower scores less aggrressive treatment.

Although , as I have discussed previously, CAC is not the “mammography of the heart” it is incredibly helpful in sorting out personalized cardiovascular risk. We use standard risk factors like lipids, smoking, age, gender and diabetes to stratify individuals according to their 10 year risk of atherosclerotic cardiovascular disease (ASCVD) but many apparent low risk individuals (often due to inherited familial risk) drop dead from ASCVD and many apparent high risk individuals don’t need statin therapy.

Previously, major guidelines from organizations like the AHA and the ACC did not recommend CAC testing to guide decision-making in this area. Consequently, CMS and major insurers have not covered CAC testing. When my patients get a CAC scan they pay 125$ out of their pocket.. For the affluent and pro-active this is not an obstacle, however those struggling financially often balk at the cost.

I was, therefore, very pleased to read that the newly updated AHA/ACC lipid guidelines (full PDF available here) emphasize the use of CAC for decision-making in intermediate risk patients.

 

 

 

 

 

 

 

 

For those patients aged 40-75 without known ASCVD whose 10 year risk of stroke and heart attack is between 7.5% and 20% (intermediate, see here on using risk estimator) the guidelines recommend “consider measuring CAC”.

If the score is zero, for most consider no statin. If score >100 and/or >75th percentile, statin therapy should be started.

I don’t agree totally with this use of CAC but it is a step forward. For example, how I approach a patient with CAC of 1-99 depends very much on what percentile the patient is at. A score of 10 in a 40 year old indicates marked premature build up of atherosclerotic plaque but in a 70 year old man it indicates they are at much lower risk than predicted by standard risk factors. The first individual we would likely recommend statin therapy and very aggressive lifestyle changes whereas the second man we could discuss  taking off statins.

Neil Stone, MD, one of the authors of the guidelines was quoted  as saying that the imaging technique is “the best tiebreaker we have now” when the risk-benefit balance is uncertain.

“Most should get a statin, but there are people who say, ‘I’ve got to know more, I want to personalize this decision to the point of knowing whether I really, really need it.’ … There are a number of people who want to be certain about where they stand on the risk continuum and that’s how we want to use it,”

Indeed, I’ve written quite a bit about my approach to helping patients “get off the fence” on whether or not to take a statin drug.

I recommend reading “Are you on the fence about taking a statin drug” to understand the details of using CAC in decision-making and the follow up post on a compromise approach to reducing ASCVD risk.

Deriskingly Yours,

-ACP

Full title of these new guidelines includes an alphabet soup of organization acronyms

2018 AHA/ACC/AACVPR/AAPA/ABC/ACPM/ADA/AGS/APhA/ASPC/NLA/PCNA Guideline on the Management of Blood Cholesterol

N.B. For your reading pleasure I’ve copied the section in the new guidelines that discusses in detail coronary artery calcium.

Two interesting sentences which I’ll need to discuss some other time

-When the CAC score is zero, some investigators favor remeasurement of CAC after 5 to 10 years

CAC scans should be ordered by a clinician who is fully versed in the pros and cons of diagnostic radiology.

In MESA (Multi-Ethnic Study of Atherosclerosis), CAC scanning delivered 0.74 to l.27 mSv of radiation, which is similar to the dose of a clinical mammogram 

-4.4.1.4. Coronary Artery Calcium

Substantial advances in estimation of risk with CAC scoring have been made in the past 5 years. One purpose of CAC scoring is to reclassify risk identification of patients who will potentially benefit from statin therapy. This is especially useful when the clinician and patient are uncertain whether to start a statin. Indeed, the most important recent observation has been the finding that a CAC score of zero indicates a low ASCVD risk for the subsequent 10 years (S4.4.1.4-1–S4.4.1.4-8). Thus, measurement of CAC potentially allows a clinician to withhold statin therapy in patients showing zero CAC. There are exceptions. For example, CAC scores of zero in persistent cigarette smokers, patients with diabetes mellitus, those with a strong family history of ASCVD, and possibly chronic inflammatory conditions such as HIV, may still be associated with substantial 10-year risk (S4.4.1.4-9–S4.4.1.4-12). Nevertheless, a sizable portion of middle-aged and older patients have zero CAC, which may allow withholding of statin therapy in those intermediate risk patients who would otherwise have a high enough risk according to the PCE to receive statin therapy (Figure 2). Most patients with CAC scores ≥100 Agatston units have a 10-year risk of ASCVD≥7.5%, a widely accepted threshold for initiation of statin therapy (S4.4.1.4-13). With increasing age, 10- year risk accompanying CAC scores of 1 to 99 rises, usually crossing the 7.5% threshold in later middle age (S4.4.1.4-13). When the CAC score is zero, some investigators favor remeasurement of CAC after 5 to 10 years (S4.4.1.4-14–S4.4.1.4-16). CAC measurement has no utility in patients already treated with statins. Statins are associated with slower progression of overall coronary atherosclerosis volume and reduction of high-risk plaque features, yet statins increase the CAC score (S4.4.1.4-17). A prospective randomized study of CAC scoring showed improved risk factor modification without an increase in downstream medical testing or cost (S4.4.1.4-18). In MESA (Multi-Ethnic Study of Atherosclerosis), CAC scanning delivered 0.74 to l.27 mSv of radiation, which is similar to the dose of a clinical mammogram (S4.4.1.4- 19). CAC scans should be ordered by a clinician who is fully versed in the pros and cons of diagnostic radiology.

Downloaded from http://ahajournals.org by on November 11, 2018

from Grundy SM, et al.
2018 Cholesterol Clinical Practice Guidelines

Do The Zen Diaries of Garry Shandling Yield Insight Into The Cause of His Death?

The skeptical cardiologist watched a little bit of the Judd Apatow HBO Documentary on Garry Shandling last night. For fans of the comedian like me, it is fascinating. As I watched I was reminded of two posts I had written about the cause of his death and the physician detective in me searched for clues to his ultimate demise.

Right after his sudden death at the age of 66, media sources reported that he had died of a massive heart attack “according to insiders.”

At the time, TMZ reported that  “Sources familiar with the situation tell TMZ Shandling died from a massive heart attack, with no prior warning whatsoever”

In a post I wrote entitled “Do You Know What is on Garry Shandling’s and Your Parent’s Death certificate?” I pointed out that his cause of death was unknown and that:

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.

I wrote another post on this after his autopsy was released.

His autopsy revealed that he  died from a pulmonary embolism, the disease I had raised as a likely  alternative cause of his sudden death in my post in April, 2016. The actual death certificate can be viewed here.

The medical report on his death reveals that Shandling had a prior
history of clots in the leg (s) (DVT) and that previously he had had an IVC filter implanted.

An IVC filter is an umbrella shaped device that is inserted into the major vein draining blood from the the lower half of the body (the inferior vena cava) to physically obstruct the vein and thereby prevent clots from reaching the pulmonary artery. These are used in cases where the normal medical treatment for blood clots (anticoagulants or blood thinners) can’t be utilized due to bleeding risk or have proven ineffective.

Although effective 95% of the time in preventing legs clots from migrating to the pulmonary artery there are reported failures and Shandling was clearly one.

Risk factors for DVT and PE include cancer, surgery and immobility. Shandling, it appears, was recently in Hawaii and long plane flights like the one he must have taken back to LA are notorious causes of immobility that can lead to DVT.

What Can We Learn From Shandling’s Death

Some take home points

-When some one dies suddenly and unexpectedly  it is not automatically due to a massive heart attack. Do not assume your family member or spouse who  was found dead in bed suffered a myocardial infarction.

-Unless the victim was quite old or had advanced cancer consider asking for an autopsy to find out the true cause of death. Whatever disease caused the death could be  inherited by the victim’s offspring.

-Pulmonary embolism can be a rapidly lethal disease. Consider a medical evaluation for it if you are experiencing leg pain/swelling, sudden, unexplained shortness of breath or chest pain which worsens upon taking a breath. If you have risk factors for leg clots or prior leg clots be even more vigilant.

 

Watching the Zen Diaries of Garry Shandling gave me no further insights into his death. Sudden death typically happens without warning to the victim and even those who are closest to him/her.

Antithrombotically Yours

-ACP

 

N.B. In the second post I talked about Carrie Fisher’s death (also widely reported falsely as due to a “massive heart attack”) and speculated that we might never know the cause of her death because I anticipated that her autopsy (with toxicology) would not be released.

I was right about her not dying of a “massive heart attack” .

Her cause of death was listed as sleep apnea with other factors.

The other factors appear to be LOTS of drugs:

“Fisher’s toxicology review found evidence of cocaine, methadone, MDMA (better known as ecstasy), alcohol and opiates when she was rushed to Ronald Reagan UCLA Hospital on Dec. 23, a toxicology report showed.”

No autopsy was done per family request but CT scanning was performed.

What Really Caused Garry Shandling’s Death: The Exploding Heart That Wasn’t

In March , 2016, Garry Shandling died suddenly and unexpectedly. At the time, TMZ reported that  “Sources familiar with the situation tell TMZ Shandling died from a massive heart attack, with no prior warning whatsoever”

This alleged cause of death  was reported widely.

 Radar Online (a site I strongly recommend avoiding) wrote

“According to an insider close to the comedian, “We are hearing that Garry had a massive and sudden heart attack.” and

“The word is that his heart basically exploded.”

LAPD, LAFD, Shandling’s rep, and LA coroner Ed Winter all declined to comment on the specifics of Shandling’s passing.

 

 

 

 

Beware The Insider’s Information

In a post I wrote entitled “Do You Know What is on Garry Shandling’s and Your Parent’s Death certificate?” I pointed out that his cause of death was unknown and that:

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.

What Did Shandling Die Of?

In a post dated 12/27/2016 (which I was unaware of until last week) TMZ reported the details of Shandling’s medical examination .

It turns out that Shandling did not die of a massive heart attack or an explosion of his heart.

His autopsy revealed that he  died from a pulmonary embolism, the disease I had raised as a likely  alternative cause of his sudden death in my post in April, 2016. The actual death certificate can be viewed here.

The medical report on his death reveals that Shandling had a prior
history of clots in the leg (s) (DVT) and that previously he had had an IVC filter implanted.

An IVC filter is an umbrella shaped device that is inserted into the major vein draining blood from the the lower half of the body (the inferior vena cava) to physically obstruct the vein and thereby prevent clots from reaching the pulmonary artery. These are used in cases where the normal medical treatment for blood clots (anticoagulants or blood thinners) can’t be utilized due to bleeding risk or have proven ineffective.

Although effective 95% of the time in preventing legs clots from migrating to the pulmonary artery there are reported failures and Shandling was clearly one.

Risk factors for DVT and PE include cancer, surgery and immobility. Shandling, it appears, was recently in Hawaii and long plane flights like the one he must have taken back to LA are notorious causes of immobility that can lead to DVT.

What Can We Learn From Shandling’s Death

Some take home points

-When some one dies suddenly and unexpectedly  it is not automatically due to a massive heart attack. Do not assume your family member or spouse who  was found dead in bed suffered a myocardial infarction.

-Unless the victim was quite old or had advanced cancer consider asking for an autopsy to find out the true cause of death. Whatever disease caused the death could be  inherited by the victim’s offspring.

-Pulmonary embolism can be a rapidly lethal disease. Consider a medical evaluation for it if you are experiencing leg pain/swelling, sudden, unexplained shortness of breath or chest pain which worsens upon taking a breath. If you have risk factors for leg clots or prior leg clots be even more vigilant.

Antithrombotically Yours

-ACP

N.B. Carrie Fisher was also reported to have suffered a “massive heart attack” by Radar Online (a most despicable website) and multiple other media outlets:

The Star Wars star, 60, suffered a massive heart attack on a United Airlines Flight from London on December 2, 2016, and was rushed to the hospital in LA upon landing, where she died four days later. Her death certificate was released by the Los Angeles County Department of Health and her cause of death was listed as “cardiac arrest/deferred,” which means it was likely a heart attack, but the final result is pending investigation.

No Radar Online! Cardiac arrest is the final mechanism of almost all deaths no matter what the cause. It does not mean she had a heart attack.

The CDC does not want cardiac arrest listed as a cause on death certificates:

In Part I, the immediate cause of death is reported on line (a). This is the final disease, injury, or complication directly causing the death. An imme­ diate cause of death must always be reported on line (a). It can be the sole entry in the cause-of-death section if that condition is the only condition causing the death.

The immediate cause does not mean the mechanism of death or terminal event (for example, cardiac arrest or respiratory arrest). The mechanism of death (for example, cardiac or respiratory arrest) should not be reported as the immediate cause of death as it is a statement not specifically related to the disease process, and it merely attests to the fact of death. Therefore, the mechanism of death provides no additional information on the cause of death.

We may never know the cause of carrie Fisher’s death because the autopsy (with accompanying toxicology) may never be released.

Has The Digoxin Death Knell Sounded: Farewell To Foxglove?

The lovely but deadly foxglove plant encountered randomly on a hike through glorious Wales on a dreary, rainy day.

The skeptical cardiologist is fascinated by the cardiac drug digoxin and the plant from which it is derived, the foxglove.

I wrote about “foxglove equipoise” in a previous post, touching on the contributions of William Withering in the 1700s, to understanding the toxicity and therapeutic benefits of the foxglove, and more recent concerns that digoxin increases mortality in patients with heart failure.

At the American College of Cardiology Scientific Sessions in Washington, D.C. yesterday, a paper showing higher mortality for patients on digoxin may be the final nail in the foxglove coffin.

Despite lack of evidence for its safety in the treatment of atrial fibrillation from randomized trials, digoxin is used in 30% of patients with atrial fibrillation (AF) worldwide, and current AF guidelines recommend it for rate control in patients with AF (with and without heart failure).

The investigators used data from the ARISTOTLE study of apixiban versus warfarin for their analysis.

They looked at mortality in patients taking or not taking digoxin at baseline, using a Cox model with propensity weighting, which included demographic features as well as biomarkers and digoxin levels at baseline. Major findings:

-In patients already taking digoxin, mortality was not higher in digoxin users, however, the risk of death was related to dig levels: for every 0.5 ng/ml increase in dig level, the risk of death rose by 19 percent and if dig level was >1.2 ng/ml the death rate increased by 56 percent. 

Patients not taking digoxin before the trial who began taking it over the course of the study had a 78 percent increase in the risk of death from any cause and a four-fold increased risk of sudden death after starting digoxin use.  Most sudden deaths occurred within six months after digoxin was started.

Risk of death with initiation of digoxin was increased in patients with and without heart failure.

The use of foxglove to treat dropsy is a fascinating and instructive chapter in the history of medicine.

This study added to prior systematic reviews suggests that it is time to end the use of digitalis and close the chapter.

William Withering might turn over in his grave but at least we won’t be sending afib patients to join him prematurely!

Dropsily Yours,

-ACP

 

Two Three Letter Words For Saving Lives: CPR and AED

Every two years the skeptical cardiologist has to get recertified in Basic Life Support for medical personnel. This involves a review of what, the American Heart Association has decided, are important changes in guidelines for Emergency Cardiac Care and cardiopulmonary resuscitation (CPR).

I highly recommend all of you undergo such training. Although the survival rate of patients with “out of hospital cardiac arrests” is very low, your appropriate actions could be crucial in saving the life of a stranger or a loved one.

About a year ago one of my patients suddenly, and without any warning symptoms, collapsed at work. Fortunately for him, a co-worker had undergone CPR training and initiated chest compressions right away. When paramedics arrived 15 minutes later he was defibrillated from ventricular fibrillation and taken to a nearby hospital.

Our best information on cardiac arrest suggests that without CPR, irreversible brain damage (due to lack of oxygen) develops in about four minutes after the heart stops beating. Even with good CPR, the longer the time interval from arrest to defibrillation, the less likely the patient is to survive with good brain function.

Thus, the two keys to helping someone who drops dead next to you are beginning effective CPR (and compression only is OK) and defibrillating a fibrillating heart as soon as possible.

My patient was comatose on arrival to the hospital and was put into a hypothermic state, a process which has been shown to improve neurological outcome in cardiac arrest victims. Doctors informed his wife that they thought his prognosis was bad-less than 5% chance of surviving with intact brain function.  After three days he awoke from his coma and was transferred to my hospital.

I visited him in the ICU and other than a sore chest and an inability to remember the events surrounding his cardiac arrest, he was mentally normal and felt great. He continues to do very well to this day, but without the bystander CPR that he received (followed by the defibrillation) he would be one of the 350,000 who die of cardiac arrest in the US each year.

If the co-worker had not initiated CPR for the many minutes it took for EMRs to arrive, my patient’s brain would have been dying from lack of oxygen and it is most likely he would have suffered severe encephalopathy or brain death.

Recognizing Cardiac Arrest

Recognizing when someone needs CPR is a critical first step in the chain of events that can improve survival in cardiac arrest.

You are looking for two things before starting CPR:

  1. Unresponsiveness. The victim  does not move and does not respond at all to either verbal or physical stimulation.
  2. Breathing is absent or atonal (meaning ineffective , intermittent gasps).

Agonal respirations have also been described as “snoring, snorting, gurgling, or moaning or as barely, labored, noisy, or heavy breathing.”  Studies have shown that agonal respirations are common in the early minutes after cardiac arrest and are associated with good outcomes.

Two Steps To Save A Life

The two key components of resuscitation are CPR and defibrillation.

Performing these steps is simple and straightforward.

The earlier they are started, the more likely the victim is to survive.

If someone collapses near you and they are unresponsive and not breathing, they need CPR and an AED. Call for help as you are starting CPR.

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Cardiopulmonary Resuscitation (CPR)

CPR consists of repeated compressions of a victim’s chest.

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I came across this machine recently. You can learn and practice hands-only CPR using it.

Everyone has seen dramatizations of CPR and it is quite simple to do even without training. Basically, you want to “push hard and fast in the center of the chest.”

CPR training undergoes some tweaking over time as more scientific data is obtained but the fundamentals remain the same. The changes that the AHA is emphasizing in their current CPR courses are:

-depress the chest at least 2 inches

-depress the chest 100-120 times per minuCPR-Certificationte (as opposed to just >100 time per minute).

Of note, the recommended sequence has changed from A, B, C, to C, A, B. Compressions right away followed by assessment of airway and then mouth-to-mouth breathing.  In fact, because compressions without breaths have been shown to be as effective as with breaths, if you are uncomfortable giving breaths, recommendations now are to just do CPR.

 

Initiating CPR and calling 911 are the greatest initial things you can do for the person who collapses next to you.

However, the earlier you can defibrillate that person from ventricular fibrillation, the better their chance of survival.

Ambulatory electronic defibrillators or AEDS , if available, are very easy to use devices that can shorten the time to defibrillation and are the second key to successful resuscitation of cardiac arrest victims in the community.

I’ll talk about using them in a subsequent post.

antimortatorially yours

-ACP

 

Donald Trump Has Moderate Plaque Buildup In His Coronary Arteries and his Risk For A Cardiac Event Is Seven Times Hilary Clinton’s Risk

Donald Trump recently appeared on the Dr. Oz show and handed a letter to the celebrity medical charlatan and TV host, Mehmet Oz.

The letter was written by his personal physician , Dr. Harold Bornstein,  screen-shot-2016-10-04-at-3-21-11-pm
and summarized various  laboratory and test  results which led Bornstein to conclude  that Mr. Trump is in excellent health (Bornstein did not repeat his earlier, bizarre statement that “If elected, Mr. Trump, I can state unequivocally, will be the healthiest individual ever elected to the presidency.”)

From a cardiovascular standpoint the following sentence stood out:

“His calcium score in 2013 was 98.”

Regular readers of the skeptical cardiologist should be familiar with the coronary calcium scan or score (CAC) by now.  I’ve written about it a lot (here, here, and here) and use it frequently in my patients, advocating its use to help better assess certain  patient’s risk of sudden death and heart attacks.

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Image from a patient with a large amount of calcium in the widowmaker or LAD coronary artery (LAD CA).

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

Calcium only develops in the coronary arteries when there is atherosclerotic plaque. The more plaque in the arteries, the more calcium. Thus, the more calcium, the more plaque and the greater the risk of heart attack and death from heart attack.

What Does Donald’s Trump’s Calcium Score Tell Us About His Risk Of A Major Cardiac Event?

We know that, on average, even if you take a statin drug (Trump is taking rosuvastatin or Crestor), the calcium score goes up at least 10% per year which means that 3 years after that 98 score we would predict Trump’s calcium score to be around 120.

Based on large, observational studies of asymptomatic patients, Calcium scores of 101 to 400 put a patient in the moderately high risk category for cardiovascular events.

When I read a calcium score of 101-400, I make the following statements (based on the most widely utilized reference from Rumberger

This patient has:

-Definite, at least moderate atherosclerotic plaque burden

-Non-obstructive CAD (coronary artery disease) highly likely, although obstructive disease possible

-Implications for cardiovascular risk: Moderately High

Patients in this category have a 7-fold risk of major  cardiac events (heart attack or death from coronary heart disease) compared to an individual with a zero calcium scorescreen-shot-2016-10-04-at-3-16-25-pm

 

 

Clinton versus Trump: Zero is Better

Since we know that Hillary Clinton recently had a calcium scan with a score of zero, we can estimate that Trump’s risk of having a heart attack or dying from a cardiac event is markedly  higher than Clinton’s.

Clinton, born October 26, 1947 is 68 years old and we can enter her calcium score into the MESA calcium calculator to see how she compares to other women her age. A  coronary calcium score of 6 is at the 50th percentile for this group.

Interestingly, Trump’s score of 98 at age 67 years was exactly at the 50th percentile. In other words half of all white men age 67 years are below 98 and half are above 98, creeping into the moderately high risk  category.

(This should not be surprising, I touched on the high estimated cardiovascular risk of all aging men in my post entitled “Should all men over age sixty take a statin drug?”)

So, based on his coronary calcium score from 2013, Donald Trump has a  moderate build up of atherosclerotic plaque in his coronary arteries and is at a seven-fold higher risk of a cardiac event compared to Hilary Clinton.

Let the law suits and tweets begin!

Electorally 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