Category Archives: Atherosclerosclerotic Cardiovascular Disease

Is Bernie Sanders Fit To Be President After His Heart Attack?

While campaigning in Las Vegas on Tuesday of last week, Vermont Senator Bernie Sanders began experiencing tightness in his chest. He was rushed to a hospital where he was diagnosed with a heart attack and had two stents implanted to open blocked arteries.

Little to nothing beyond these bare details of his health condition is known but, as Politico put it, this event has “cast a cloud over his candidacy.”

Is it appropriate for voters to lose confidence in Sanders at this point? He was already the oldest candidate in the race at age 78 years. Would he survive a 4 year term in the grueling position of head of the free world?

An American Federation of Aging white paper, Longevity and Health of U.S. Presidential Candidates for the 2020 Election, used data from national vital statistics to estimate lifespan, healthspan (years of healthy living), disabled lifespan, and four- and eight-year survival probabilities for U.S. citizens with attributes matching those of the 27 then candidates for Presidency.

Its conclusions:

Given the favorable health and longevity trajectories of almost all of the presidential candidates relative to the average member of the same age and gender group in the U.S., and the apparent current good health of all of the candidates, there is reason to question whether age should be used at all in making judgments about prospective presidential candidates

I would agree that individual health is more important than  chronological age in evaluating longevity and in Sanders’ case the heart attack may be an indicator of a poor prognosis and an inability to withstand the rigors of campaigning for and serving as president.

Unfortunately we need to know a lot more about Sanders’ heart attack and overall health to make this determination.

Big Heart Attack Or Little Heart Attack?

A heart attack or  myocardial infarction (MI) occurs when heart muscle does not get enough blood/oxygen to keep the myocardial cells alive. This typically is due to a tight blockage in one of the coronary arteries supplying blood to the heart, thus constricting the blood flow to a segment of heart muscle (myocardium).

The size of Sanders’ heart attack is an important determinant of his prognosis. The more myocardial cells that died the larger the damage. We can detect and quantify heart attacks with a blood test using a cardiac specific protein called troponin.

Some heart attacks are tiny and only detected by very slight increases in the troponin in the blood whereas larger ones result in large increases in the troponin. What kind did Sanders have?

The more damage to the main pumping chamber of the heart, the left ventricle, the weaker the pumping action as measured by the ejection fraction.  The lower the ejection fraction the more likely the development of heart failure. What is Sanders ejection fraction? Does he have any evidence of heart failure?

Stunned or Hibernating Myocardium?

With some heart attacks the heart muscle doesn’t die but becomes stunned-weakened but still living. Under other circumstances a tightly blocked coronary artery doesn’t cause a heart attack but the reduced oxygen supply causes the muscle to stop working-in effect hibernating.  Thus, 3 months from now Sanders’ heart muscle function may improve as these stunned or hibernating myocardial cells come back to full function. What will Sanders’ ejection fraction be 3 months from now.? Will he have evidence of heart failure at that time?

Troponin levels and EF are just two of many factors that will determine Sanders’ prognosis.

A recent review of such factors on the one year post MI prognosis concluded

Secular trends showed a consistent decrease in mortality and morbidity after acute MI from early to more recent study periods. The relative risk for all-cause death and cardiovascular outcomes (recurrent MI, cardiovascular death) was at least 30% higher than that in a general reference population at both 1–3 years and 3–5 years after MI. Risk factors leading to worse outcomes after MI included comorbid diabetes, hypertension and peripheral artery disease, older age, reduced renal function, and history of stroke.

Hopefully, prior to the Iowa caucases all the candidates will release their medical records for the public to review. Only by learning more details about Senator Sanders’ heart attack and his overall medical condition can we answer whether he is fit to serve as President. Similarly, heretofore unknown individual health conditions could markedly effect the prognosis of any of the other candidates and their medical records should be equally scrutinized.

Skeptically Yours,

-ACP

Graphic Cigarette Package Warnings May Soon Be Coming To Our Country

Two years ago I asked (and answered) the question Why Doesn’t The USA Have Graphic Warning Labels On Cigarette Packs Like The Netherlands?

Big tobacco had successfully blocked such labels but yesterday the FDA announced a proposed rule which would post new graphic health warnings on cigarette packages if approved:

The 13 proposed warnings, which feature text statements accompanied by photo-realistic color images depicting some of the lesser-known health risks of cigarette smoking, stand to represent the most significant change to cigarette labels in 35 years.

Here are some of the proposed graphics which aren’t quite as attention-grabbing as the ones I saw in Europe.

 

 

Cigarette smoking is by far the worse thing my patients do to compromise their health and I’m in favor of hammering home the horrible complications smokers face.

Do you want feet like this?

 

 

 

 

Or Lungs like these?

 

 

 

 

Or a scar on your chest from open heart surgery?

 

 

 

 

 

All this and more can be yours if you keep smoking!

I’ve reposted below my initial blog on the topic.


While strolling the delightful (and typically debris-free) streets of Haarlem in The Netherlands the skeptical cardiologist espied an unusual cigarette pack on the ground.

In comparison to the typical American cigarette pack I noted a very prominent and disgusting picture of a leg which had been ravaged by peripheral artery disease.

The large print translates “smoking clogs your arteries.”

This is one of many potential warnings on Dutch cigarette packs. My favorite is

Roken kan leiden tot een langzame, pijnlijke dood

(Smoking can lead to a slow, painful death)

Perhaps, if such warning had been on American cigarette packs in the 1990s my mother would have been able to walk without severe pain in her legs (claudication) from the severe blockages caused by her decades of cigarette smoking.

When cigarette smoking patients tell me that “you have to die from something” I tell them that although they are greatly increasing their chance of dying from lung and cardiac disease, the smoking may not kill them but  leave them miserable and unable to walk or breath.

Experts on tobacco control note that these large, graphic and direct warnings are much more effective than the first small boxed warnings:

After the implementation of the first warning labels in 1966, the FTC’s 1981 report concluded that the original warning labels were not novel, overexposed and too abstract to remember and be personally relevant.46 Warning labels, like advertisements, wear out over time.47 Written warning labels wear out faster than graphic ones.48,49 In response, Congress passed a law mandating four rotating warnings. Studies on them began appearing in the late 1980s, demonstrating that several years after the implementation, those written labels on cigarette packs were also not noticed and not remembered by smokers and adolescents.5053 Since then, the diffusion and evolution of tobacco warning labels have been propelled by observational and experimental studies showing the effectiveness of large graphic warning labels in informing consumers about the health harms of smoking and reducing their smoking behavior.45,54

Here’s how Australia’s warnings have evolved

autralia-cigarette.jpg

 

 

 

 

 

 

 

In 2011 the US Congress passed legislation moving America towards such effective graphic warnings:

However, the law was challenged by Big Tobacco and has never been enacted. From the FDA site:

The Family Smoking Prevention and Tobacco Control Act requires the FDA to include new warning labels on cigarette packages and in cigarette advertisements. On June 22, 2011, the FDA published a final rule requiring color graphics depicting the negative health consequences of smoking to accompany the nine new textual warning statements. However, the final rule was challenged in court by several tobacco companies, and on Aug. 24, 2012, the United States Court of Appeals for the District of Columbia Circuit vacated the rule on First Amendment grounds and remanded the matter to the agency.[1] On Dec. 5, 2012, the Court denied the government’s petition for panel rehearing and rehearing en banc. In 2013, the government decided not to seek further review of the court’s ruling.

The FDA has been undertaking research related to graphic health warnings since that time.

[1] R.J. Reynolds Tobacco Co., et al., v. Food & Drug Administration, et al., 696 F.3d 1205 (D.C. Cir. 2012)

What Other Countries Are Doing

According to a Canadian Cancer Society report from late 2016,

More than 100 countries/jurisdictions worldwide have now required pictorial warnings, with fully 105 countries/jurisdictions having done so. This represents a landmark global public health achievement.

Increasingly, the United States stands alone, because of a constitutional doctrine privileging commercial speech above public health.

Here are the countries requiring pictorial warnings courtesy of that Canadian Cancer Society report.

And some of their warning pictures:

And this a picture that FDA would have required:

 

Skeptically Yours,

-AcP

Are You Taking A Statin Drug Inappropriately Like Eric Topol Because of the MyGeneRank App?

The skeptical cardiologist was listening to a podcast discussion between Sam Harris and Eric Topol recently and became  flabbergasted.

Topol, the “world-renowned cardiologist” who is seemingly everywhere in media these days was discussing what he considers the overuse of imaging technology during the podcast which Harris’s website describes as follows:

In this episode of the Making Sense podcast, Sam Harris speaks with Eric Topol about the way artificial intelligence can improve medicine. They talk about soaring medical costs and declining health outcomes in the U.S., the problems of too little and too much medicine, the culture of medicine, the travesty of electronic health records, the current status of AI in medicine, the promise of further breakthroughs, possible downsides of relying on AI in medicine, and other topics.

Personally, I have been amazed at the hype and promotion that artificial intelligence (AI) has been getting given the near total absence in cardiology of any tangible benefits from it and I wanted to hear what the man who wrote ” Deep Medicine: How Artificial Intelligence Can Make Healthcare Human Again ” had to say about it.

About 28 minutes into the podcast, Harris, who has lately been preoccupied with promoting meditation as a cure for all ills, begins describing a procedure he underwent:

I’ve had a few adventures in cardiology. CT scan, calcium score scan.

Harris, who in neuroscience and philosophy might speak precisely, here is very vague. Did he get a coronary calcium scan (CAC) or a coronary CT angiogram? There is a huge difference and he is conflating the two imaging procedures.

Apparently he is unhappy with having undergone it but:

I might be telling a different story if my life was saved by it.

And his doctor’s rationale  for getting the scan was lacking:

The way this was dispensed to me. We now have this new tool, let’s use it.

Let me just say at this point that if your doctor’s rationale for performing a test is that he has a machine that performs the test just say no. Or demand an explanation of how the results will change your management or prognosis.

Apparently the scan that Harris had didn’t turn out either horrifically worse than expected or remarkably better and didn’t change management:

In my case at the end it didn’t make sense.

Now, I can forgive Sam Harris for being somewhat naive and misguided when it comes to coronary artery scans or coronary CT angiograms but Eric Topol , the world’s leading talking cardiology head should fully understand the value of coronary artery calcium scans.

This is where I first become flabbergasted.

Topol says in response at this point that coronary artery calcium scans are “terribly overused” and that “I’ve never ordered one.”

Eric, you cannot be serious!

Are you telling me that you wouldn’t order one on your 60 year old airline pilot friend whose father dropped dead of a massive MI at age 50 but whose lipids look fine?

Why doesn’t Eric order CACs?

Because “There are so many patients who have been disabled by the results of their calcium score even though they have no symptoms.”

This is where the degree of my flabbergastment increased by an order of magnitude.

Our job as preventive cardiologists is to identify those at high risk and lead them to lifestyle choices and medicine that dramatically lowers that risk.  We educate them that the large build up of subclinical atherosclerosis we identified does not have to result in sudden death, crippling heart attacks or strokes. We reassure them that with the right tools we can help them live a long, productive and happy life.

Eric, what do you tell these people? The calcium score is irrelevant? You’re fine. You shouldn’t have gotten it. Surely not! This would be the preventive cardiology equivalent of sticking one’s head in the sand.

This is not the first time Topol has opined on the dangers of CAC. An excerpt from his book, ‘The Patient Will See You Now: The Future of Medicine Is in Your Hands” posted on Scientific American describes the ills created in a 58 year old man who had a CAC score of 710.

My patient was told that he had a score of 710—a high calcium score—and his physician had told him that he would need to undergo a coronary angiogram, a roadmap movie of the coronary anatomy, as soon as possible. He did that and was found to have several blockages in two of the three arteries serving his heart. His cardiologists in Florida immediately put in five stents (even though no stress-test or other symptoms had suggested they were necessary), and put him on a regimen of Lipitor, a beta-blocker, aspirin and Plavix.

This case is not an example of inappropriate usage of CAC it is an example of really bad doctoring and failure to utilize the CAC information properly.

One should never order a cardiac catheterization/coronary angiogram solely on the basis of a high CAC score. Even ordering a stress test in this situation is debatable as I discuss here.

And Topol’s patients symptoms were most likely related to a beta-blocker that he didn’t need (see here).

My Gene Rank

Later in the podcast I reached maximum flabbergast  levels when Topol announced that as a result of a high score for CAD risk he received using an iPhone app called MyGeneRank he had started taking a statin drug.

He enthusiastically promoted the app which his Scripps Translational Science Institute developed and urged listeners to utilize this approach to better refine the estimate of their risk of heart attack and stroke.

Per the Scripps website:

The MyGeneRank mobile app is built using Apple’s ResearchKit, an open source framework that enables researchers and programmers to build customized mobile apps for research purposes. With user permission, the app connects with the 23andMe application program interface and automatically calculates and returns a genetic risk score for coronary artery disease.

In addition, the app calculates a 10-year absolute risk estimate for an adverse coronary event, such as heart attack, using a combination of genetic and clinical factors. Users are able to adjust behavioral risk factors to see the influence of lifestyle habits on their overall risk.

Elsewhere, Topol, has stated

“We are excited to launch a unique study that combines an iOS app and genomics to help guide important health decisions,” says Eric Topol, MD, Founder and Director of the Scripps Translational Science Institute and Professor of Molecular Medicine at The Scripps Research Institute. “Not only does participating in the study arm individuals with their own data, but it also gives them the opportunity to participate in new type of research – one that is driven by and for patients.”

Curious, I downloaded the MyGeneRank app, answered some questions and gave it permission to access my 23 and Me data. After requiring me to complete a survey on my health it then  yielded  my coronary artery disease risk score.

 

 

 

 

 

 

 

Oh, no! My genetic risk score was at the 81st percentile! In the red zone.  According to Eric Topol I should take a statin like him. Based on these results I probably should be incredibly anxious and crippled by fears of cardiac death.

Fortunately, I have superior information to allay my fears. I’ve had CAC scans in the past which are well below average for men my age. Despite my dad’s history of early CAD, a recent coronary CT angiogram showed minimal plaque. I know exactly where I stand risk-wise.

How many cardiac cripples has Topol’s MyGeneRank inappropriately created?

Is the data that MyGeneRank utilizes superior to that from CAC scans?

For coronary artery calcium scanning there is a wealth of data supporting improved risk prediction and we are looking directly at the atherosclerotic process that eventually causes the diseases we want to prevent.

It’s interesting that a recent study looking at a polygenetic risk score’s ability to predict cardiac events was comparing the risk score’s ability to predict subclinital atherosclerosis:

Each 1-SD increase in the polygenic risk score was associated with 1.32-fold (95% CI, 1.04-1.68) greater likelihood of having coronary artery calcification and 9.7% higher (95% CI, 2.2-17.8) burden of carotid plaque.

In the Scientific American article Topol quotes Mark Twain:, “To a man with a hammer, a lot of things looks like nails that need pounding.”

Topol’s hammer is artificial intelligence. We eagerly await the day he discovers a nail that he can bang on that  significantly advances medical care.

In the meantime I and the vast majority of progressive preventive cardiologists will be utilizing CAC scores intelligently to identify both those patients at high risk for cardiovascular events who need more aggressive treatment and those at low risk who can be reassured and have treatment de-escalated.

Polygenetic CAD risk scores do show promise to improve our predictive powers but more study is needed in this are before we make clinical treatment decisions based on the results.

Astoundingly Yours,

-ACP

Ilene Has High Cholesterol With A “Wonderful Ratio” And A Branch Retinal Vein Occlusion: Should She Take A Statin?

Recently the skeptical cardiologist was asked by Ilene, a reader with an HDL almost as high as her LDL and a history of branch retinal vein occlusion (BRVO) whether she should take the statin her cardiologist had prescribed.

I enjoy reading your articles and would appreciate your opinion on my situation.  I recently took a lipid panel blood test: total cholesterol: 244 HDL:112 LDL:121 VLDL:11  CRP: 1.77 Triglycerides: 57.  Also my Cardiac Agatston  score is 21.
I had a Branch Retinol Vein Occlusion a year ago in my left eye  (it’s healing beautifully) and as a precaution  am now taking Amlodipine 5mg daily (my blood pressure was never too high to begin with) along with a daily baby aspirin.
I am otherwise a healthy 72 year old woman, exercise and eat healthy.
My regular doctor (Integrative MD) says my cholesterol ratio is wonderful….my cardiologist wants me to take a statin (Atorvastatin) in a low dose.  The ONLY med I take is Amlodipine and I am not one to be taking a plethora of meds for the rest of my life (unless “absolutely” necessary.  What is your suggestion…take a statin or not.
While I can’t provide medical advice to Ilene specifically it is worthwhile  to ponder  the general aspects of her case and how I would approach it as it likely applies to thousands of other patients including many of my own.
In my mind there are two questions here: 1) Should Ilene and patients like her take a statin to prevent future heart attacks and strokes and 2) Do statins  effect the Branch Retinal Vein Occlusion (BRVO)?
Although I’m not a fan of integrative or functional medicine Ilene’s integrative MD is correct in saying that her ratio of total cholesterol to HDL cholesterol is wonderful. Perhaps that high  HDL is protecting her from a build-up of atherosclerotic plaque.
On the other hand, Ilene tells me that  “My father did have a heart attack in his 60’s”.  Perhaps she inherited something from him that puts her in a higher than average risk category.
With the information from the CAC we don’t have to guess about the influence of the high HDL and the family history of CAD. Her score is at the 48th percentile, slightly below average for white women her age, thus it would appear she is not destined for her father’s fate.
Frequent readers of skepcard (especially my posts on statin fence sitters) will know I  plug all these numbers (preferably with the calcium score available) into the MESA coronary calcium risk calculator
In this case, the CAC score does not significantly alter our risk estimate as it is so close to the average for her age
Even if we count her as having hypertension because she is on the amlodipine her 10 year risk of heart attack and stroke is low at 3.2%.
Guidelines don’t recommend statin treatment unless risk is >7.5%.
Also, note that I answered yes to “Family history heart disease” but most studies generally only consider this a risk factor if father had heart attack prior to age 55 years. If we make that a no the risk drops to <3%.
Now that we’ve answered Ilene’s real question let’s see if the BRVO warrants statin therapy.
Branch Retinal Vein Occlusion
BRVO is the blockage of a vein from the retina and the second most
common cause of vision loss from retinal vascular disease, following diabetic retinopathy. It typically  results in the painless loss of vision in one portion of one eye due to hemorrhage and edema in the retina.
A reasonable summary of BRVO provided by the American Academy of Ophthalmology can be found here.
BRVO is not clearly related to atherosclerosis or hyperlipidemia and there is no evidence that taking a statin would prevent recurrence or help the condition.

The leading theory for what causes BRVO is that the more delicate and distensible retinal veins are squished or compressed at points where the stiffer and thicker retinal arteries cross them.  Up to Date notes:

Whereas branch retinal vein occlusion (BRVO) appears to be related to compression of the branch vein by retinal arterioles at the arteriovenous crossing points, central retinal vein occlusion (CRVO) is usually associated with primary thrombus formation.

Although BRVO is more common in patients with hypertension and atherosclerosis it is not clear that one causes the other or that treatment of hypertension or atherosclerosis diminishes the risk of BRVO.  So statins are not recommended.
More Questions
Every patient case for me leads to more questions,  more investigations and more knowledge. Here are some questions that occurred to me from ilene’s case.
-Why would someone with no symptoms and no heart problems be seeing a cardiologist?
(“I started seeing a cardiologist just to make sure all systems were “go” and stayed that way!… we take care of our cars so why not my body. )
I kind of like this answer and I definitely see lots of patients with that philosophy but if we extrapolate the car analogy: going to a cardiologist would be like taking your car to a mechanic who only works on engines or perhaps one specific part of the engine (help me out here people who know about cars.)
-Why was Ilene unwilling to take a statin? (I pretty much know the answer to this (see here) for most patients.
‘m just afraid of the horrible muscle related side effects of statin drugs…and that’s why I’m taking Berberine 500mg twice a day.
Yep. I feel a post abut Berberine may be in the works!
-Finally, should a 72 year old with a CAC score of 21 and BRVO be taking a baby aspirin?
I’ve generally advocated aspirin in primary prevention for scores >100  so wouldn’t advise it for prevention of cardiovascular events in this situation.
In addition, I have seen nothing in the literature that recommends aspirin for BRVO. These two BRVO experts do not recommend either aspirin or anticoagulants.
Proretinally Yours,
-ACP
N.B. If you have a blockage of the the artery that supplies blood to the retina or a branch retinal artery occlusion ( BRAO)
you might benefit from a statin as this is often caused by a clot or plaque flying out of the heart or the carotid artery.

The Ultimate Guide To The Coronary Artery Calcium Scan (Score) Circa 2019

The skeptical cardiologist’s first post on coronary artery calcium (CAC) scan was posted in 2014 and had the wordy title “Searching for Subclinical Atherosclerosis: Coronary Calcium Score-How Old Is My Heart?”

This post still serves as a good introduction to the test (rationale, procedure, risks) but in the 5 years since it was published there has been a substantial body of data published on CAC and in 2018 it was embraced by major organizations.

Overall, I’ve written 20 posts in which CAC plays a predominant role since then and I feels it’s time to put the most important changes and concepts  in one spot.


Detection Of Subclinical Atherosclerosis: What’s Your Risk of Dropping Dead?

First, the rationale for using CAC (also known as a coronary calcium score or heart scan) is detection of “subclinical atherosclerosis”, a non-catchy but hugely important process which I describe in an early post on who should take aspirin to prevent heart attack or stroke:

We have the tools available to look for atherosclerotic plaques before they rupture and cause heart attacks or stroke. Ultrasound screening of the carotid artery, as I discussed here, is one such tool: vascular screening is an accurate, harmless and painless way to assess for subclinical atherosclerosis.

In my practice, the answer to the question of who should or should not take aspirin is based on whether my patient has or does not have significant atherosclerosis. If they have had a clinical event due to atherosclerotic cardiovascular disease (stroke, heart attack, coronary stent, coronary bypass surgery, documented blocked arteries to the legs) I recommend they take one 81 milligram (baby) uncoated aspirin daily. If they have not had a clinical event but I have documented by either

  • vascular screening (significant carotid plaque)
  • coronary calcium score (high score (cut-off is debatable, more on this in a subsequent post)
  • Incidentally discovered plaque in the aorta or peripheral arteries (found by CT or ultrasound done for other reasons)

then I recommend a daily baby aspirin (assuming no high risk of bleeding).


Help In Deciding Who Needs Aggressive Treatment

Second, CAC is an outstanding tool for further refining risk of heart attack and stroke and helping better determine who needs to take statins or undergo aggressive lifestyle reduction, something I described in detail in my post “Should All Men Over Sixty Take a Statin Drug”.

The updated AHA/ACC Cardiovascular Prevention Guidelines came out in 2013.

After working with them for 9 months and using the iPhone app to calculate my patients’ 10 year risk of atherosclerotic cardiovascular disease (ASCVD, primarily heart attacks and strokes) it has become clear to me that the new guidelines will recommend statin therapy to almost all males over the age of 60 and females over the age of 70.

As critics have pointed out, this immediately adds about 10 million individuals to the 40 million or so who are currently taking statins.

By identifying subclinical atherosclerosis, CAC scoring identifies those who do or don’t need statins.


This is particularly important for patients who have many reservations about statins or who are “on the fence” about taking them when standard risk factor calculations suggest they would benefit.


The Widowmaker

In 2015 I wrote about a documentary entitled “The Widowmaker” (see here and here) which is about the treatment and prevention  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.

Although CAC has some similarities to mammography (both utilize low dose radiation, 0.5 mSV) I concluded that CAC was not “the mammography of the heart” as the documentary proclaims.

What We Can Learn From Donald Trump’s CAC?

In 2018 I noted that “Donald Trump Has Moderate Coronary Plaque: This Is Normal For His Age And We Already Knew It.”

In October, 2016 the skeptical cardiologist predicted that Donald Trump’s coronary calcium score, if remeasured, would be >100 .  At that time I pointed out that this score is consistent with moderate coronary plaque build up and implies a moderate risk of heart attack and stroke.

Trumps’ score gave him a seven-fold increase risk of a cardiovascular event in comparison to Hilary Clinton (who had a zero coronary calcium score) .

Yesterday it was revealed by the White House doctor , Ronny Jackson, that Trump’s repeat score  was 133.

I was able to predict this score because we knew that Trump’s coronary calcium was 98 in 2013 and that on average calcium scores increase by about 10% per year.

What is most notable about the Trump CAC incident is that Trump, like all recent presidents and all astronauts underwent the screening. If the test is routine for presidents why is it not routine for Mr and Mrs Joe Q Public?

At a mininum we should consider what is recommended for aircrew to the general public:

A three-phased approach to coronary artery disease (CAD) risk assessment is recommended, beginning with initial risk-stratification using a population-appropriate risk calculator and resting ECG. For aircrew identified as being at increased risk, enhanced screening is recommended by means of Coronary Artery Calcium Score alone or combined with a CT coronary angiography investigation.

The 2018 guidelines Take A Giant Step Forward

In late 2018 I noted that CAC had been embraced by major guidelines:

I was 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.

A Few Final Points On CAC

First, it’s never too early to start thinking about your risk of cardiovascular disease. I have been using CAC more frequently in the last few years in  individuals <40 years with a strong family of early sudden death or heart attack and often we find very abnormal values (see here for my discussion on CAC in the youngish.)

coronary calcium scan with post-processing on a 45 year old white male with very strong history of premature heart attacks in mother and father. The pink indicates the bony structures of the spine (bottom) and the sternum (top). Extensive calcium in the LAD coronary artery is highlighted in yellow and in the circumflex coronary artery in ?teal. His score was 201, higher than 99% of white male his age.

 

 

 

 

 

 

 

 

 

 

 

 

 

 

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.

The Importance of Proactivity

In “The MESA App-Estimating Your Risk of Cardiovascular Disease With And Without Coronary Calcium Score” I recently wrote that:

If you want to be proactive about the cardiovascular health of yourself or a loved one, download the MESA app and evaluate your risk.  Ask your doctor if a CACS will help refine that risk further.

There are many other questions to answer with regard to CAC-should they be repeated?, how do statins influence the score?, is there information in the scan beyond just the score that is important? Is a scan helpful after a normal stress test?

I’ve touched on some of these in the past, including the really tough  question “Should All Patients With A High Coronary Calcium Score Undergo Stress Testing?

Like most things in cardiology we have a lot to learn about CAC. There are many more studies to perform. Many questions yet to be answered.

A study showing improved outcomes using CAC guided therapy versus non CAC guided therapy would be nice. However, due to the long time and thousands of patients necessary it is unlikely we will have results within a decade.

I don’t want to wait a decade to start aggressively identifying who of my patients is at high risk for sudden death. You only get one chance to stop a death.

Apothanasically Yours,

-ACP


 

Is Dean Ornish’s Lifestyle Program “Scientifically Proven To Undo (Reverse) Heart Disease?”

Supporters of vegetarian/ultra low fat diets like to claim that there is solid scientific evidence of the cardiovascular benefits of their chosen diets.

To buttress these claims they will cite the studies of Esseslystn, Pritikin and Ornish.

I’ve previously discussed the bad science underlying the programs of Esselsystn and Pritikin but have only briefly touched on the inadequacy of Dean Ornish’s studies.

The Ornish website proclaims that their program is the first program “scientifically proven to undo (reverse) heart disease.” That’s a huge claim. If it were true, wouldn’t the Dietary Guidelines for Americans, the American Heart Association, and most cardiologists and nutrition experts be recommending it?

Who Is Dean Ornish?

Dean Ornish has an MD degree from Baylor University and trained in internal medicine but has no formal cardiology or nutrition training (although many internet sites including Wikipedia describe him as a cardiologist.)

Ornish, according to the Encyclopedia of World Biographies became depressed and suicidal in college and underwent psychotherapy “but it was only when he met the man who had helped his older sister overcome her debilitating migraine headaches that his own outlook vastly improved. Under the watch of his new mentor, Swami Satchidananda, Ornish began yoga, meditation, and a vegetarian diet, and even spent time at the Swami’s Virginia center.”

Can Ornish’s Program Reverse Heart Disease?

After his medical training Ornish founded the Preventive Medicine Research Institute and has has widely promoted his Ornish Lifestyle Program.  the website of which claims:

Dr. Ornish’s Program for Reversing Heart Disease® is the first program scientifically proven to “undo” (reverse) heart disease by making comprehensive lifestyle changes.

The Ornish claims are based on a study he performed between 1986 and 1992 which originally had 28 patients with coronary artery disease in an experimental arm and 20 in a control group. You can read the details of the one year results here.and the five year results here.

There are  so many limitations to this study that the mind boggles that it was published in a reputable journal.

-Recruitment of patients. 

193 patients with significant coronary lesions from coronary angiography were “identified” but only 93 “remained eligible.” These were “randomly” assigned to the experimental or control groups. Somehow , this randomization process assigned 53 to the experimental group and 40 to the usual-care control group.

If this were truly a 1:1 randomization the numbers would be equal and the baseline characteristics equal.

Only 23 of the 53 assigned to the experimental group agreed to participate and only 20 of the control group.

The control group was older, less likely to be employed and less educated.

“The primary reason for refusal in the experimental group was not wanting to undergo intensive lifestyle changes and/or not wanting a second coronary angiogram; control patients refused primarily because they did not want to undergo a second angiogram.”

In other words, all of the slackers were weeded out of the experimental group and all of the patients who were intensely motivated to change their lifestyle were weeded out of the control group. Gee, I wonder which group will do better?

-The Intervention.

The experimental patients received “intensive lifestyle changes (<10% fat whole foods vegetarian diet, aerobic exercise, stress management training, smoking cessation, group psychosocial support).
The control group had none of the above.

Needless to say this was not blinded and the researchers definitely knew which patients were in which group.

Control-group patients were “not asked to make lifestyle changes, although they were free to do so.”

There is very little known about the 20 slackers in the control group. I can’t find basic information about them-crucial things like how many smoked or quit smoking or how many were on statin drugs.

-The Measurement

Progression or regression of coronary artery lesions was assessed in both groups by quantitative coronary angiography (QCA) at baseline and after about a year.

QCA as a test for assessing coronary artery disease has a number of limitations and as a result is no longer utilized for this purpose in clinical trials. When investigators  want to know if an intervention is improving CAD they use techniques such as intravascular ultraound or coronary CT angiography (see here) which allow measurement of total atherosclerotic plaque burden.

Rather than burden the reader  with the details at this point I’ve included a discussion of this as an addendum.

-The Outcome

Ornish has widely promoted  this heavily flawed study as showing “reversal of heart disease” because at one year the average percent coronary artery stenosis by angiogram had dropped from 40% to 37.8% in the intensive lifestyle group and increased from 42.7% to 46.1% in the control patients.

The minimal diameter (meaning the tightest stenosis) changed from 1.64 mm at baseline in the experimental to 1.65 at one year. At 5 years the minimal diameter had increased another whopping .001 mm to 1.651. 

 

 

In other words even if we overlook the huge methodologic flaws in the study the  so-called  “reversal” was minuscule.


Utlimately, dropping coronary artery blockages by <5 % doesn’t really matter unless that is also helping to prevent heart attacks or death or strokes or some outcome that really matters.

There were no significant differences between the groups at 5 years in hard events such as heart attack or death.
In fact 2 of the experimental group died versus 1 of the control group by 5 years.

There were less stents and bypasses performed in the Ornish group but the decision to proceed to stent or bypass is notoriously capricious when performed outside the setting of acute MI. The patients in the experimental group under the guidance of Ornish and their Ornish counselors would be strongly motivated to do everything possible to avoid intervention.

I’ve gotten a lot of flack for humorously suggesting that Nathan Pritikin killed himself as a result of the austere no fat diet he consumed but the bottom line on any lifestyle change is both quality and quantity of life.

If you are miserable most days due to your rigid diet you might consider that life is no longer worth living

Ornish’s Lifestyle Intervention Is Not A Trial Of Diet …And Other Points

 

Although often cited as justification of ultralow fat diet, the Ornish Lifestyle trial doesn’t test diet alone.

It is a trial of multiple different interventions with frequent counseling and meetings to reinforce and guide patients.

The interventions included things that we know are really important for long term health-regular exercise, smoking cessation, and weight management. These factors alone could account for any differences in the outcome but they are easily adopted without becoming a vegetarian.

The patients who agreed to the experimental arm were a clearly highly motivated bunch who agreed to this really strict regimen. Even in this population there was a 25% drop out rate.

Since investigators clearly knew who the “experimental patients” were and they were clearly interested in good outcomes in these patients there is a high possibility of bias in reporting outcomes and referring for interventions.

Despite all the limitations the study does raise an interesting hypothesis. Should we all be eating vegan diets?

 if Ornish really wanted to scientifically prove his approach he should have repeated it with much better methodology and much larger numbers.

Finally, this tiny study has never been reproduced at any other center.

Because of the small numbers, lack of true blinding, lack of hard outcomes and use of multiple modalities for lifestyle intervention, this study cannot be used to support the Ornish/Esselstyn/Pritikin dietary approach.

It most certainly doesn’t show that the Ornish Lifestyle Program “reverses heart disease.” Consequently, you will not find any evidence-based source of nutritional information or guideline (unless it has a vegan/vegetarian philosophy or is being funded by the Ornish/Pritikin lifestyle money-making machines) recommending these diets.

Skeptically Yours,

-ACP

N.B.1 A recent paper on noninvasive assessment of atherosclerotic plaque has a great infographic which shows how coronary artery disease progresses and how and when in the progression various imaging modalities are able to detect plaque:

I’ve inserted a vertical red arrow which shows how IVUS detects very early atheroma whereas angiography (ICA, green line) only detects later plaque when it has started protruding into the lumen of the artery.

The paper notes that “Intravascular ultrasound (IVUS)  constitutes the current gold standard for plaque quantification. Multiple studies using IVUS and other techniques have revealed a robust relation between statin therapy and plaque regression. In the ASTEROID trial coronary atheroma volume regressed by 6.8% during 24 months of high-intensity lipid therapy. A meta-analysis of IVUS trials including 7864 patients showed an association between plaque regression and decreased cardiovascular events.”

While I believe Ornish started off as a legitimate scientist several authors have pointed out that he has joined the ranks of pseudoscientific practiioners.

Here’s one analysis from Science Blogs :

In the end, the problem is that Dr. Ornish has yoked his science to advocates of pseudoscience, such as Deepak Chopra and Rustum Roy. Why he’s done this, I don’t know. The reason could be common philosophy. It could be expedience. It could be any number of things. By doing so, however, Dr. Ornish has made a Faustian deal with the devil that may give him short-term notoriety now but virtually guarantees serious problems with his ultimately being taken seriously scientifically, as he is tainted by this association. Let me yet again reemphasize that this relabeling of diet, exercise, and lifestyle as somehow being “alternative” is nothing more than a Trojan Horse. Inside the horse is a whole lot of woo, pseudoscience and quackery such as homepathy, reiki, Hoxsey therapy, acid-base pseudoscience, Hulda Clark’s “zapper,” and many others,

Is An Unneeded Beta-Blocker Making You Feel Logy?

The skeptical cardiologist saw a patient recently who  had undergone stenting of a 95% blocked right coronary artery. Mr Jones had presented  a year ago to our ER 2 days after he first began experiencing a light pressure-type discomfort in his left shoulder and scapular region. This pain persisted, waxing and waning, without a clear relationship to exertion or position or movement of his shoulder.

Upon arrival in the ER, his ECG was normal but his cardiac enzymes were slightly elevated (troponin peaking 0.92), thus he was diagnosed with a non-ST elevation myocardial infarction (MI).

He’s done great since the stent procedure fixed the coronary blockage that caused his infarct and chest pain, but during our office visit he related that since his hospitalization he had been feeling “logy.” 

Being a lover of words, my ears perked up at this new-to-me adjective, and I asked him to describe what he meant by logy. For him, loginess was a feeling of fatigue or lacking energy.

Indeed, the online Merriam-Webster dictionary defines logy as sluggish or groggy. It is pronounced usually with a long o and a hard g.

The origin is unclear but has nothing to do with rum:

Based on surface resemblance, you might guess that “logy” (also sometimes spelled “loggy”) is related to “groggy,” but that’s not the case. “Groggy” ultimately comes from “Old Grog,” the nickname of an English admiral who was notorious for his cloak made of a fabric called grogram – and for adding water to his crew’s rum. The sailors called the rum mixture “grog” after the admiral. Because of the effect of grog, “groggy” came to mean “weak and unsteady on the feet or in action.” No one is really sure about the origin of “logy,” but experts speculate that it comes from the Dutch word log, meaning “heavy.” Its first recorded use in English, from an 1847 London newspaper, refers to a “loggy stroke” in rowing.

Fatigue is a common, nonspecific symptom that we all feel at times. It is more common as we age and it can be challenging for both patients and physicians to sort out when it needs to be further evaluated.

Occasionally, fatigue is the only symptom of a significant cardiac condition, but more frequently in the patient population I see it is either noncardiac (low thyroid, anemia, etc.) or iatrogenic

When a patient tells me they are feeling fatigued I immediately scan their med list for potential logigenic drugs.

In this case, my patient had been started on a low dosage of the beta-blocker carvedilol (brand name Coreg) after his stent, and I suspected this was why he had felt logy for the past year.

In cardiology, we utilize beta-blockers in many situations-arrhythmias, heart failure, and heart attacks to name a few, and they are well-known to have fatigue as a common side effect. There was a really good chance that Mr. Jones’s loginess was due to the carvedilol.

It’s important to review all medications at each patient visit to check for side effects, interactions and benefits, and in the case of Mr. Jones’ carvedilol, loginess.

Do All Patients Post-Revascularization or Post-MI Need To Take Beta-Blockers

Beta-blockers (BBs) are frequently started in patients after a stenting procedure or coronary bypass surgery, and continued indefinitely. However, the evidence for their benefit in such  patients with normal LV function long term is lacking.

If any post-revascularization population benefits from BBs, it is those, like Mr. Jones who have had a myocardial infarction (MI, heart attack) prior to the procedure, however the smaller the infarct, the less the benefits.

And with the widespread use of early stenting to treat MI, infarcts are much smaller and dysfunction of the left ventricle (LV) less likely.

In those patients with minimal damage and normal LV function, the benefits appear minimal. For this reason in the last 5 to 10 years I’ve been stopping BBs in this population if there are any significant side effects.

An “Expert Analysis” published in JACC in 2017 noted that:

A 2015 meta-analysis of 10 observational acute MI studies including more than 40,000 patients showed that beta-blockers reduced the risk of all-cause death  However, the benefit of these agents was not found in all subgroups and seemed confined to the patients with reduced LVEF, with low use of other secondary prevention drugs, or NSTEMI.

In a study of almost 180,000 patients post MI with normal LV systolic function in the UK between 2007 and 2013 there was no difference in mortality at one year in patients discharged with or without beta-blockers.

The only way to answer this question definitely would be with a randomized controlled trial and, to my surprise and delight, such a study (CAPITAL-RCT (Carvedilol Post-Intervention Long-Term Administration in Large-scale Randomized Controlled Trial) was published in PLOS One in August of 2018.

I’ll save readers the details, but the bottom line is that patients treated with optimal contemporary therapy for acute MI, whose LV function was not significantly impaired, did not benefit in any way from treatment with carvedilol, the beta-blocker my patient was taking.

It’s rare that we get such definitive evidence for a change in treatment that reverses what is in current guidelines. This has the potential to affect tens of thousands of patients and improve their quality of life. It should be trumpeted far and wide. The cynic in me suspects that if it were a study demonstrating the benefits of a new drug, physicians would be bombarded with the new information.

Helping Patients Feel Less Logy

We will be ordering an echocardiogram on Mr. Jones, and if his LV function is normal we will stop his carvedilol and see if he feels significantly better.  

I feel like stopping a drug that is not beneficial and that is causing a lifetime of loginess is an incredibly important intervention a cardiologist can make. It’s not as life-saving as stenting for acute MI, but saving quality of life is something this non-invasive cardiologist can do every day for every patient.

Skeptically Yours,

-ACP

N.B. The summary of the recent CAPITAL-RCT:

STEMI patients with successful primary PCI within 24 hours from the onset and with left ventricular ejection fraction (LVEF) ≥40% were randomly assigned in a 1-to-1 fashion either to the carvedilol group or to the no beta-blocker group within 7 days after primary PCI. The primary endpoint is a composite of all-cause death, myocardial infarction, hospitalization for heart failure, and hospitalization for acute coronary syndrome. Between August 2010 and May 2014, 801 patients were randomly assigned to the carvedilol group (N = 399) or the no beta-blocker group (N = 402) at 67 centers in Japan. The carvedilol dose was up-titrated from 3.4±2.1 mg at baseline to 6.3±4.3 mg at 1-year. During median follow-up of 3.9 years with 96.4% follow-up, the cumulative 3-year incidences of both the primary endpoint and any coronary revascularization were not significantly different between the carvedilol and no beta-blocker groups (6.8% and 7.9%, P = 0.20, and 20.3% and 17.7%, P = 0.65, respectively). There also was no significant difference in LVEF at 1-year between the 2 groups (60.9±8.4% and 59.6±8.8%, P = 0.06).

 

 

 

 

Can The Apple Watch Or Kardia ECG Monitor Detect Heart Attacks?

The skeptical cardiologist recently received this email from a reader:

With the new Apple Watch that’s out now, people have suggested my husband (who had a heart attack at 36) should get it since it could detect a heart attack. But I keep remembering what you said – that these devices can’t detect heart attacks and that Afib isn’t related to a heart attack most of the time – is that still the case? I don’t really know how to explain to people that it can’t do this, since absolutely everyone believes it does.

The answer is a resounding and unequivocal NO!

If we are using the term heart attack to mean what doctors call a myocardial infarction (MI) there should be no expectation that any wearable or consumer ECG product can reliably diagnose a heart attack.

The Apple Watch even in its latest incarnation and with the ECG feature and with rhythm monitoring activated is incapable of detecting a myocardial infarction.

Similarly, although the AliveCor Kardia ECG monitor is superb at diagnosing rhythm abnormalities it is not capable of detecting an MI

To make this even clearer note that when you record an ECG on the Apple Watch it intermittently flashes the following warning:

 

Note: “Apple Watch never checks for heart attacks”

How did such this idea take root in the consciousness of so many Americans?

Perhaps this article in 9-5 Mac had something to do with it

The article begins
Scott Killian never imagined his Apple Watch might save his life, but that’s exactly what happened a few weeks ago when he had a heart attack in the middle of the night. Killian recently shared his personal experience with 9to5Mac, and the details of his story are absolutely amazing.
In reality,  the man received an alarm that his resting heart rate was high at night. Apparently he also was experiencing chest pain and went to an ER where a cardiac enzyme was elevated.  Subsequently he underwent testing that revealed advanced coronary artery disease and he had a bypass operation. 
Even if we assume all the details of this story are accurate it is absolutely not a case of Apple Watch diagnosing an MI.
 
A high resting heart rate is not neccessarily an indicator of an MI and most MIs are not characterized by high heart rates.  We have had the technology with wearables to monitor resting heart rate for some time and no one has ever suggested this can be used to detect MI.
 
The rate of false alarms is so high and the rate of failure to diagnose MI so low that this is a useless measure and should not provide any patient reassurance.
 
The writer of this story and the editors at 9-5 Mac should be ashamed of this misinformation.
 
Several other news sources have needlessly muddied the water on this question including Healthline and Fox News:
 
 
 
 
 
 
 
The Fox News article entitled “Could The Apple Watch Series 4 save you from a heart attack” quotes a non-physician who suggests that AW can detect early signs of a heart attack:
 

In clear cut cases the Apple Watch could make the difference between life and death,” says Roger Kay, president of Endpoint Technologies Associates. Because you wear the Apple Watch at all times, it can detect an early sign of a stroke or a heart attack, and that early indication is critical, he says.

And the Healthline article on the new Apple Watch also incorrectly implies it can diagnose MI:

The device, which was unveiled last week, has an electrocardiogram (ECG) app that can detect often overlooked heart abnormalities that could lead to a heart attack.

And if you are felled by a heart problem, the fall detector built into the Apple Watch Series 4 could alert medical professionals that you need help

Fox News and Healthline should modify their published articles to correct the misinformation they have previously provided.

And it is still true that  although both Apple Watch and Kardia can diagnose atrial fibrillation the vast majority of the time acute heart attacks are not associated with atrial fibrillation.

Readers, please spread the word far and wide to friends and family-Apple Watch cannot detect heart attacks!

Skeptically Yours,

-ACP

Are You Doing Enough Push Ups To Save Your Life?

The skeptical cardiologist has always had a fondness for push-ups. Therefore I read with interest a recent study published in JAMAOpen which looked at how many push-ups a group of 30 and 40-something male firefighters from Indiana could do and how that related to cardiovascular outcomes over the next ten years.

The article was published in the peer-reviewed journal JAMA Network Open, and is freely available to access online.

The British National Health Service pointed out that “The UK media has rather over exaggerated these findings:”

Both the Metro and the Daily Mirror highlighted the result of 40 push-ups being “the magic number” for preventing heart disease, but in fact being able to do 10 or more push-ups was also associated with lower heart disease risk.

What Was Studied?

The study involved 1,104 male firefighters (average age 39.6) from 10 fire departments in Indiana who underwent regular medical checks between 2000 and 2010. 

At baseline the participants underwent a physical fitness assessment which included push-up capacity (hereafter referred to as the push-up number (PUN))and treadmill exercise tolerance tests conducted per standardized protocols.

For push-ups, the firefighter was instructed to begin push-ups in time with a metronome set at 80 beats per minute. Clinic staff counted the number of push-ups completed until the participant reached 80, missed 3 or more beats of the metronome, or stopped owing to exhaustion or other symptoms (dizziness, lightheadedness, chest pain, or shortness of breath). Numbers of push-ups were arbitrarily divided into 5 categories in increments of 10 push-ups for each category. Exercise tolerance tests were performed on a treadmill using a modified Bruce protocol until participants reached at least 85% of their maximal predicted heart rates, requested early termination, or experienced a clinical indication for early termination according to the American College of Sports Medicine Guidelines (maximum oxygen consumption [V̇ O2max]).

The main outcomes assessed were new diagnoses of heart disease from enrollment up to 2010. 

Cardiovascular events were verified by periodic examinations at the same clinic or by clinically verified return-to-work forms. Cardiovascular disease–related events (CVD) were defined as incident diagnosis of coronary artery disease or other major CVD event (eg, heart failure, sudden cardiac death)

Here’s the graph of the probability of being free of a CVD event on the y-axis with time on x-axis.

The black line represents those 75 firefighters who couldn’t make it into double digits, the green those 155 who did more than 40 pushups.

Participants able to complete more than 40 push-ups had a significant 96% lower rate of CVD events compared with those completing fewer than 10 push-ups.

It is surprising that the push up number seemed a better predictor of outcomes than the exercise test, This should be taken with a grain of salt because although the investigators report out “VO2 max” the stress tests were not maximal tests.

The firefighters with lower push up numbers were fatter, more likely to smoke and had higher blood pressure, glucose and cholesterol levels.

What useful information can one take from this study?

You definitely cannot say that being able to do more than 40 pushups will somehow prevent heart disease. The PUN is neither causing nor preventing anything.

The PUN is a marker for the overall physical shape of these firefighters. It’s a marker for how these men were taking care of themselves. If you are a 39 year old fireman from Indiana and can’t do 11 push-ups you are in very sorry condition and it is likely evident in numerous other ways.

The <11 PUN crew were a bunch of fat, diabetic, insulin resistant, hyperlipidemic, out-of-shape hypertensives who were heart attacks in the waiting.

Push-ups Are A Great Exercise

Despite the meaningless of this study you should consider adding push-ups to your exercise routine. Doing them won’t save your life but it will contribute to mitigating the weakness and frailty of aging. Don’t obsess about your PUN.

I’ve always liked push-ups and highly recommend them. They require no special equipment or preparation. It’s a quick exercise that builds upper body muscle strength, adds to my core strength and gets my heart rate up a bit. For some reason my office in O’Fallon is always cold so several times during the day when I’m there I’ll do 100 jumping jacks and drop on the carpet and do some push-ups in an effort to get warm.

I don’t do them every day but the last time I tried I could do 50 in less than a minute and that has me convinced I will live forever!

Calisthenically Yours,

-ACP

N.B. In my post on mitigating sarcopenia in the elderly I talked about the importance of resistance exercise:

Americans spend billions on useless supplements and vitamins in their search for better health but exercise is a superior drug, being free  and without drug-related side effects

I’ve spent a lot of time on this blog emphasizing the importance of aerobic exercise for cardiovascular health but I also am a believer in strength and flexibility training for overall health and longevity.

As we age we suffer more and more from sarcopenia-a gradual decrease in muscle mass.

Scientific reviews note that loss of muscle mass and muscle strengh is quite common in individuals over age 65 and is associated with increased dependence, frailty and mortality

Push-ups are a great resistance exercise. For a description of the perfect form for a push up see here.

Should All Patients With A High Coronary Calcium Score Undergo Stress Testing?

Coronary artery calcium (CAC) scans are an excellent tool for better defining coronary heart disease risk in many individuals. In light of the recent ACC/AHA guidelines endorsement of CAC, the skeptical cardiologist anticipates that primary care physicians will be ordering more and will often be faced with the question of what to do with abnormally high results.

There are two, diametrically opposed viewpoints which have been taken on this issue.

The Argument For Stress Testing

The majority of cardiologists are likely to fall into the camp of “more testing is good” which was summarized in a  State of The Art article that Dr. Harvey Hecht wrote in JACC recently.

The argument appears logical and is as follows:

  1. There is a high yield of abnormal results from stress testing when done on patients with high CAC.

The appropriateness of stress testing after CAC scanning in asymptomatic patients is directly related to the CAC score. The incidence of abnormal nuclear stress testing is 1.3%, 11.3%, and 35.2% for CAC scores 400, respectively .

2. The higher yield for ischemia/abnormal tests in patients with >400 CAC implies the ability to further risk stratify patients thus leading to guideline recommendations:

It is only in the >400 group that the pretest likelihood is sufficiently high to warrant further evaluation with myocardial perfusion imaging, for which there is a IIb recommendation

Hecht references a 2010 guideline issued by ACC/AHA (2010 ACCF/AHA Guideline for Assessment of Cardiovascular Risk in Asymptomatic Adults) which states

1. Stress myocardial perfusion imaging (MPI) may be considered for advanced cardiovascular risk assessment in asymptomatic adults with diabetes or asymptomatic adults with a strong family history of CHD or when previous risk assessment testing suggests a high risk of CHD, such as a coronary artery calcium (CAC) score of 400 or greater. (Level of Evidence: C)

Stress MPI testing is more sensitive than stress ECG testing alone but in clinical practice I see a very high rate of false positive stress MPI results. Stress MPI is also much more expensive than stress ECG testing and delivers significant radiation exposure to patients.

Thus if stress MPI is performed on all individuals with CAC>400 we are likely to generate lots of abnormal tests followed by lots of unnecessary down-stream testing.

Further support for the stress test approach comes from a 2013 report on appropriate use issued by an alphabet soup of cardiovascular professional organizations

Below is the incredibly complicated chart summarizing what tests can follow another abnormal test. Interestingly, in this chart the report consider it appropriate (A) to perform stress tests on individuals with calcium scores >100

Stress Testing-Costs and Downsides

The cynic in me has to point out that the average CAC score  for white males of 67 years is 98 and that of 68 years is 115. Thus, this algorithm has the potential to recommend stress testing be performed on half of all white males with no symptoms over the age of 67.

The costs of this approach would be astronomical.

This guideline supports stress ECG, stress MPI and stress echo as appropriate.  Stress MPI is considerably more expensive than stress ECG and carries substantial radiation burden. Stress echo in my experience,  if performed and read properly has the lowest incidence of false positives and is more appropriate therefore for screening asymptomatic individuals.

All this stress testing stands to benefit the various members of the alphabet soup above, especially those who read nuclear stress tests or stress echo or who do catheterizations with stents. (Full disclosure I am board certified in nuclear cardiology and echocardiography and read both stress MPI and stress echos. I don’t do catheterizations.)

It’s also important to point out that these appropriate usage criteria, with rare exceptions are based primarily on the expert opinion of the stakeholders who stand to benefit from the additional testing.

The unspoken third leg of the argument for stress testing is that once an abnormal stress test is found and the patient is noted to be in a higher risk category for events, therapy will be changed and this therapeutic intervention will improve outcomes.

This therapeutic intervention could be more intense management of risk factors for CAD but in most cardiologist’s and patient’s minds the next step is coronary angiography with the potential to stent blocked coronaries or to perform coronary bypass surgery.

Diabetic Patients With High CAC

Asymptomatic individuals with diabetes are recognized as intrinsically higher risk for cardiac events and commonly do not experience symptoms even with advanced CAD.

Thus, they are often the focus of more intense screening recommendations.

In 2017, The Imaging Council of the American College of Cardiology published their review of evidence regarding the use of noninvasive testing to stratify asymptomatic patients with diabetes with regard to to coronary heart disease, ultimately coming up with the algorithm below.

Their arguments were similar to Hecht’s for the general population:

Asymptomatic patients with diabetes who have high CAC scores have a high prevalence of inducible ischemia on stress imaging. In a prospective study, 48% of patients with diabetes with a CAC score of 400 had silent ischemia on SPECT imaging, and in those with a score of 1000, 71.4% had inducible ischemia . The majority of the defects were moderate to severe. Patients with diabetes with inducible ischemia have a higher annual death

Despite higher rates of ischemic stress test results in diabetics they did not recommend stress testing for all:

the data in DM suggest that routine screening with MPI of all asymptomatic patients is likely to have a low yield and have a limited effect on patient outcome. The yield of MPI can be improved by selecting a higher-risk group of patients with symptoms, peripheral vascular disease, CKD, an abnormal ECG, or a high CAC score (e.g., >400) (83,84). In such patients, intense medical therapy appears to retard progression of asymptomatic and symptomatic CAD (72).

Importantly, they noted the absence of evidence for revascularization in this population:

Whether coronary revascularization offers additive prognostic benefit to medical therapy when the ischemic burden exceeds any particular threshold is still unclear for the asymptomatic diabetic population.

The Argument Against Stress Testing

The argument for stress testing for high CAC rests on the assumption that identifying those individuals with significant ischemia due to tightly blocked coronary arteries can improve outcomes. This hypothesis has never been tested, let alone proven.

It may seem logical that those asymptomatic individuals with high risk CAC scores >400 and ischemia would benefit from an invasive strategy with coronary angiography followed by either stenting or bypass surgery but it is entirely possible that such an invasive strategy could cause more harm than good.

Harm comes from subjecting those individuals with abnormal stress tests to a potentially lethal procedure-cardiac catheterization.

David Schade, an endocrinologist, has opined persuasively on the inadvisability of either stress testing or cardiology referral in those with high CACS.

He correctly points out the limitations of coronary angiography which some cardiologists are very eager to perform

In many locations, stress testing is performed after referring the asymptomatic patient to a cardiologist. After a positive stress test, the next step is usually coronary angiography to identify obstructive lesions. A recent review of coronary angiography recommends caution in the use of this test because (1) the resolution of coronary angiography is low; (2) the obtained images are two dimensional, making it difficult to define the shape of the vessel; and (3) the assessment of obstruction does not include the presence of previously developed collateral vessels, which may provide adequate blood flow past the obstruction 

He quotes the USPSTF on the possible harm of this approach:

And he correctly points out that since the 2007 publication of the COURAGE trial we have known that catheterization followed by stenting does not improve outcomes in patients with stable CAD

Accord to the US Preventive Services Task Force: “The primary tangible harm of screening exercise tolerance testing is the potential for medical complications related to cardiac catheterization done to further evaluate a positive result. Coronary angiography is generally considered a safe procedure. Of all persons undergoing outpatient coronary angiography, however, an estimated 0.08% will die as a result of the procedure and 1.8% will experience a complication. Complications of coronary angiography include myocardial infarction, stroke, arrhythmia, dissection of the aorta and coronary artery, retroperitoneal bleeding, femoral artery aneurysm, renal dysfunction, and systemic infection”

In many locations, stress testing is performed after referring the asymptomatic patient to a cardiologist. After a positive stress test, the next step is usually coronary angiography to identify obstructive lesions. A recent review of coronary angiography recommends caution in the use of this test because (1) the resolution of coronary angiography is low; (2) the obtained images are two dimensional, making it difficult to define the shape of the vessel; and (3) the assessment of obstruction does not include the presence of previously developed collateral vessels, which may provide adequate blood flow past the obstruction 

Schade’s algorithm for management of a high CAC specifically recommends against referral to a cardiologist or performance of a stress test.

It emphasizes very intense management of risk factors with lifestyle changes and medical therapy with LDL goal <70.

As a cardiologist with a strong interest in prevention of atherosclerosis I agree with many of Schade’s points. I do, however, believe that high risk patients can benefit from seeing a cardiologist who is very focused on prevention of atherosclotic complications rather than performing procedures.

I don’t routinely recommend stress testing for my patients with high CAC but I have a low threshold for recommending stress testing in them based on worrisome symptoms, especially in those who are more sedentary or are diabetic.

A randomized trial comparing the outcomes of stress testing versus aggressive optimal medical therapy for the asymptomatic individual with high CAC is sorely needed. Until then, I remain

Skeptically Yours,

-ACP