Category Archives: Cardiac Tests

How Common Are Inaccurate Coronary Artery Calcium Scans?

One reason the  skeptical cardiologist has been so enthusiastic about coronary calcium (CAC) scans is that I have found them to be highly reproducible and highly accurate.

Unlike most  imaging tests in cardiology if we perform a CAC on the same individual in the CT scanner of hospital A and then repeat it within a few days in the CT scanner of hospital B we expect the scores to be nearly identical.

Also, unlike most other imaging tests we don’t expect false negatives or false positives. If the CAC score is zero there is no coronary calcification-high sensitivity. If the score is nonzero there is definitively calcium and therefore atherosclerotic plaque in the coronaries-high specificity.

This is  because calcium as defined in the Agatson score is literally black and white-a pixel is either above or below the cut-off. Computer software automatically identifies on the scan. A reasonably trained CT tech should be able to identify the calcium that is residing in the coronary arteries based on his or her knowledge of the coronary anatomy as registered on CT slices. Using software the total Agatson score is calculated.

A physician reader (either cardiologist or radiologist) (who should have a very good understanding of the cardiac and coronary anatomy ) should review the CT techs work and verify accuracy.

A recent case report, however, has demonstrated that the above  assumptions are not always true.

Franz Messerli, a pre-eminent researcher in hypertension and a cardiologist describes in fascinating detail a false-positive CAC scan he underwent in 2013.  He was told he had a score of 804 putting him in a high risk category consistent with extensive plaque formation.

After consulting with cardiologist friends and colleagues he decided to put himself on a statin and aspirin despite having an excellent lipid profile.

Messerli assumed that the CAC score was not a false positive (although later in his article he indicates he had questioned the reading) writing:

“although one can always quibble with ST segments or wall motion abnormalities, on the CAC the evidence is rock-hard, you actually with your own eyes can see the white calcium specks! ‘Individuals with very high Agatston scores (over 1000) have a 20% chance of suffering a myocardial infarction or cardiac death within a year’—although I did not quite classify, this patient information coming from esteemed Harvard cardiology colleagues3 was hardly reassuring.

(His reference 3 for the 20% risk of MI or cardiac death in a year for CAC score >1000 is suspect. It is a 2003 “patient page” on coronary calcium in Circulation which does not have a reference for that statistic.)

A more recent study found patients with extensive CAC (CAC≥1000) represent a unique, very high-risk phenotype with CVD mortality outcomes (0.80%/yr) commensurate with high-risk secondary prevention patients (0.77%/yr) from the FOURIER trial)

Six years after the diagnosis Messerli was at a Picasso exhibition, “leisurely ambling between his Blue and Pink Period “when he developed chest pain.

To further evaluate the chest pain he underwent a coronary CT angiogram and this demonstrated pristine and normal coronary arteries, totally devoid of calcium.

He did have a lot of mitral annular calcification (MAC). The CCTA images below show how close the MAC is to the left circumflex coronary artery (LCX).


 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

The slice above shows how the MAC would appear on the CT scan designed to assess coronary calcium.  It’s position is very close to that of the circumflex but an experienced reader/tech  should have known this was not coronary calcification.

MAC is a very common finding on echocardiograms, especially in the elderly and it is likely that this error is not an isolated one.

Dr. Messerli writes

After relating these findings to the cardiologist who did the initial CAC, he indicated that most likely someone mistook mitral annular calcification as left circumflex calcium. This was hardly reassuring, since I specifically had asked that obvious question after receiving the initial CAC

Around the time I read Messerli’s case report I encountered a similar, albeit not as drastic case. A CAC scan showed a significant area of calcification near the left circumflex coronary artery which was scored as circumflex coronary calcification.

image001

The  pattern of this calcification is not consistent with the known path of the circumflex coronary in this case. When it was eliminated from the scoring the patient had a zero score. The difference between a nonzero score and a zero score is hugely significant but for patients with scores >100 such errors are less critical.

I have also encountered cases where extracardiac calcium mimics right coronary calcification.

There are some important take-home points from my and Dr. Messerli’s experience.

  1. False positive CAC scans do occur. We don’t know the frequency. If the scans are not overread by a competent cardiologist or radiologist with extensive experience in cardiac CT these mistakes will be more common

When I asked Dr. Messerli about this problem he responded

I am afraid you are correct in that CAC scores are generated by techs and radiologists and cardiologist simply sign the report without verifying the data. Little doubt that MAC is most often missed.
     2. Like other cardiac imaging tests (such as echocardiography) having an expert/experienced/meticulous  tech and reader matters.
    3. Dr. Messerli and I agree that a research project should be done to ascertain how often this happens and to evaluate the process of reading and reporting CAC.
4. Patients should look at the breakdown of the calcium in the CAC by coronary artery. Whereas it is not uncommon to see most of the calcium in the LAD it is rare to see a huge discrepancy in which the circumflex coronary artery score is very high and the LAD score zero. Such a finding should warrant a review of the scan to see if MAC was included in error.
Skeptically Yours
-ACP
N.B. Dr. Messerli’s report can be read for free and makes for entertaining reading.
I was very intrigued by two comments he made at the end:
  1. “Had my CHD been diagnosed a decade earlier, guidelines might well have condemned me to taking beta-blockers for the reminder of my days.6 This, as Philip Roth taught us in ‘The Counterlife’, might have had rather unpleasant repercussions.7

Until recently I had never read anything by Philip Roth but when he died last year I read his Pulitzer Prize winning  1987 novel American Pastoral and liked it. Given this Roth reference involving beta-blockers I felt compelled to get my hands on “The Counterlife.” The book is a good read (much better IMHO than American Pastoral) and one of the main plot points relates to the side effects (see my post on feeling logy) a character suffers from a beta-blocker. Stimulated by a desire to be able to perform sexually if taken of the medication, the character undergoes coronary bypass surgery and dies.

2. “As stated by Mandrola and true in the present case, ‘given the (lucrative) downstream testing that often occurs when coronary calcium is found in asymptomatic people, the biggest winners from CAC screening may be the testers rather than the tested’.”

I feel the CAC in the right hands should not lead to (lucrative or inappropriate) downstream testing in the asymptomatic (see my discussion on this topic here.)

 

 

Which Ambulatory ECG Monitor For Which Patient?

The skeptical cardiologist still feels that KardiaPro has  eliminated  use of long term monitoring devices for most of his afib patients

However not all my afib patients are willing and able to self-monitor their atrial fibrillation using the Alivecor Mobile ECG device. For the Kardia unwilling and  many patients who don’t have afib we are still utilizing lots of long term monitors.

The ambulatory ECG monitoring world is very confusing and ever-changing but I recently came across a nice review of the area in the Cleveland Clinic Journal of Medicine which can be read in its entirety for free here.

This Table summarizes the various options available. I particularly like that they included relative cost. .

The traditional ambulatory ECG device is the “Holter” monitor which is named after its inventor and is relatively inexpensive and worn for 24 to 48 hours.

The variety of available devices are depicted in this nice graphic:

For the last few years we have predominantly been using the two week “patch” type devices in most of our patients who warrant a long term monitor. The Zio is the prototype for this but we are also using the BioTelemetry patch increasingly.

The more expensive mobile cardiac outpatient telemetry (MCOT) devices like the one below from BioTel look a lot like the patches now. The major difference to the patient is that the monitor has to be taken out and recharged every 5 days. In addition, as BioTel techs are reviewing the signal from the device they can notify the patient if the ECG from the patch is inadequate and have them switch to an included lanyard/electrode set-up.

The advantage of the patch monitors is that they are ultraportable, relatively unobtrusive and they monitor continuously with full disclosure.

The patch is applied to the left chest and usually stays there for two weeks (and yes, patients do get to shower during that time) at which time it is mailed back to the company for analysis.

Continuously Monitoring,

-ACP

A Patient’s Confusing Journey Into The Quagmire Of Cardiac Imaging: A Cautionary Tale

Mary-Ann, a reader from the north,  provides today’s post. Her story illustrates how easily medical care can veer off the rails while it is simultaneously railroading patients.  It is a cautionary tale with wisdom that can help most patients.

In this post I’ll just present Mary-Ann’s perspective and solicit responses.  Down the line I’ll provide some perspective on the processes, the problems and the solutions.


It started innocently enough. I showed up for a regular visit with my cardiac provider, a mid-level professional. She noted I was flushed and had a high pulse — about 100. 

Starbucks, I explained, and I flush easily — always have. She looked skeptical.

That is how I went from a half-caf Americano to a 48-hour holter monitor.

I went back for results — the usual ectopic beats but nothing scary or new. But again, she noted I had a fast heart rate and I was flushed.

And once again I explained: Starbucks — it is right down the street and okay, I might have a problem.

That is the short — but highly accurate — version of how I wound up getting a stress echo. 

I showed up for the results of the echo and that is where the runaway train started down the tracks.

“…possible inferoapical wall hypokinesis with lack of augmentation of systolic function, which are abnormal findings and may be indicative of ischemia due to underlying coronary artery disease. EF was 56% at rest and 40-50% at stress.” 

Wait — what?!

I was marched down the hall and scheduled for a cardiac angiography — and told not to run any marathons in the intervening two days. 

Marathon?! I was terrified I was going to drop dead at any moment. I contemplated just sitting the waiting room for 48 hours — just to be safe.

Then I started reading the professional literature and things were not adding up. An EF at stress of 40 – 50% is not good — in fact, it can be heading into heart failure land.

But I was active and fine — it did not make any sense.

I called the office; my provider was not available. I explained that I was worried there was a mistake. Oh no, I was assured, they are very careful to not make mistakes.

I wrote my will. I cried a lot. 

And when the person called to remind me of the procedure (like I could forget!?) I once again explained that I was worried there had been a mistake, and once again — reassurance. No mistake.

Nevertheless, she (aka me) persisted!

I sat on the hospital bed in nothing but a gown and handed the nurse my two-page letter; it started like this:

“I am reminded that what is normal and ordinary for a professional is never that for a patient. I am terrified.

First, I want to be really sure that there is not any chance of a mix-up in the stress echo test results. This is not simple denial or wishful thinking…” 

And that nurse paid attention, which is how I wound up not having a cardiac angiography. 

The cardiologist scheduled to do the procedure — we shall call him Doc #2 — wrote: 

“She has some concerns regarding the results of the stress echo study … I reviewed the most recent stress echo and it appears to me that the results for the resting versus the stress echo ejection fractions have been transposed…”

Translation: A Typo.

I was elated! Jubilant! We went to Starbucks to celebrate.

The giddy joy quickly turned to something along the lines of WTH just happened here? I read the original echo report written by Doc #1 — that lit the tinder. There were two different values for EF at stress documented in the report, and another sentence that was repeated. 

The professorial side of me was deeply affronted — in a subsequent meeting with hospital administrators I confess to saying that someone who is making hundreds of thousands of dollars a year doesn’t get to write such a sloppy ass report — and about someone’s heart, no less! 

But the best part of that meeting was learning that Doc #1 denied there was a typo — he stood by his findings. 

Oh dear.

And Doc #2 stood by his findings as well. And Doc #3 got involved somewhere along the way and he agreed with Doc #2. And the mid-level Provider also agreed with Doc #2.

The majority rule seems like an odd way to make health care decisions — wouldn’t you think all those smart people could talk among themselves and agree?

Apparently not.

That first meeting with the hospital folks included all manner of solicitous apologies and an attitude of collaboration. Of course, they said, we can send the echo to an outside cardiologist — at our expense — and get an answer.

And then I made the unthinkable mistake — and I blame the Skeptical Cardiologist for this — of asking informed questions.

“Are the cardiologists involved in reading my echo Level III echo specialists?”

“I understand that there can be variance in estimated EF between cardiologists — what level of variance is considered acceptable?”

The hospital team responded to my questions by calling a meeting — and the tone had changed considerably (Thanks a lot, Corporate Legal).

The offer to pay for an outside opinion was off the table — after all, they said, you would not have a patient-provider relationship with the cardiologist reading the echo. Ahem, I noted — I have zero relationship with the first cardiologist who read the echo and would not know him if I bumped into him at Starbucks. And you all did offer to pay for that outside opinion…

Oh never mind those minor details. No outside opinion on their dime. They would do a Lexiscan at their expense as a tie breaker. Final Offer.

Tiebreaker — really?! Is this a soccer game?

And seriously — should I have to have an invasive test to settle THEIR disagreement?! [Note: If it involves needles, it is invasive.]

Because there were not enough cardiologists involved already, I saw yet another one — from a different practice. He offered that the EF at stress looked more like 55%, placing his bet smack in the middle, and recommending a CT Angiography Coronary Arteries with Contrast as the tiebreaker.

Tiebreaker. That word implies both sides are equivalent or equal. However, my heart is not actually a game and the two teams cannot both be right — there is no equivalency in play here. What we are really trying to do involves accuracy — not breaking a tie score.

But I digress.

It doesn’t seem like you should have to make a chart to keep track of what cardiologists say about the same echo but in this case, it seemed necessary.

 And in the meantime, yet another cardiologist weighed in that the quality of the echo was poor — and no wonder they could not agree.

Deep breaths.

And so, for the past four months I have tried to navigate all this, and to understand what this actually means about cardiology and medicine and so many things. My confidence and my mind have been blown. Resources – and time – have been wasted. 

Ectopic heartbeats are typically benign in a structurally normal heart — I thought I was safe. But I have not felt safe since that day when I learned that Doc #1 and Docs #2, 3, and so on had decided to have a stand-off at the OK Corral that is my heart.

Except, I do not know if it is okay. And that is the problem. 


Unfortunately, Mary-Anne’s tale is not uncommon. It touches on many of the areas that patient’s should be aware of including

-Undergoing diagnostic imaging testing when you are free of symptoms

-Inadequate quality control in diagnostic imaging and how that leads to false positive results

-Variance in imaging performance and interpretation-how the same test can be read as normal by one doctor and markedly abnormal by another.

-The tendency of some cardiologists to recommend invasive testing when it is inappropriate and likely to cause more harm than good

-The importance of second opinions, especially if invasive testing is recommended

-The importance of patient’s doing their own research and asking good questions based on that research.

Transparently 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

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


 

A Voodoo Coronary Calcium Scan Could Save Your Life

The skeptical cardiologist received this reader comment recently:

So I went and got a Cardiac Calcium Score on my own since my cardiologist wouldn’t order one because he says they are basically voodoo.. Family History is awful for me.. I got my score of 320 and I’m 48 years old.. Doc looked at it and basically did the oh well.. so I switched docs and the other doc basically did the same thing.. I try so very hard to live a good lifestyle..I just don’t understand why docs wait so long to actually take a look at your heart.. I would have thought a score of 320 would have brought on more testing.. It did not..

I was shocked that a cardiologist practicing in 2019 would term a coronary artery calcium (CAC) scan (aka, heart scan or calcium score) “voodoo.”

I’m a strong advocate of what I wrote in a recent post with the ridiculously long title, “Prevention of Heart Attack and Stroke-Early Detection Of Risk Using Coronary Artery Calcium Scans In The Youngish“:

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 where you stand and what you can do about it.

Here’s what I told this young man:

If your cardiologist tells you coronary calcium scores are voodoo I would strongly consider changing cardiologists.

A score of 320 at age 48 puts you in a very high risk category for stroke and heart attack over the next 10 years.

You need to find a physician who understands how to incorporate coronary calcium into his practice and will help you with lifestyle changes and medications to reduce that risk


Let’s analyze my points in detail and see if these off the cuff remarks are really justified

1,  Changing cardiologists.

Recent studies and recent guideline recommendations (see here) all support utilization of CAC in this kind of patient. If you have a strong family history of premature heart disease or sudden death you want a cardiologist who is actively keeping up on the published literature in preventive cardiology,  Such cardiologists are not dismissing CAC as “voodoo” they are incorporating it into their assessment of patient’s risk on a daily basis.

2. High risk of CAC score 320  at age 48

I plugged normal numbers for cholesterol and BP into the MESA risk calculator (see my discussion on how to use this here) for a 48 year old white male.

As you can see the high CAC score puts this patient at almost triple the 10 year risk of heart attack and stroke.

Immediate action is warranted to adjust lifestyle to reduce this risk! This high score will provide great motivation to the patient to stop smoking, exercise, lose excess weight, and modify diet.

Hidden risk factors such as lipoprotein(a),  hs-CRP and LDL-P need to be assessed.

Drug treatment should be considered.

3. Find physician who will be more proactive in preventing heart disease

This may be the hardest part of all my recommendations. On your own you can get a CAC performed and advanced lipoprotein analysis.

However, finding progressive, enlightened, up-to-date preventive cardiologists can be a challenge.

We need a network of such cardiologists.

I frequently receive requests from readers or patients leaving St. Louis for recommendations on cardiologists.

If you are aware of such preventive cardiologists in your area email me or post in comments and I will keep a log and post on the website for reference.

Voodoophobically Yours,

-ACP

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

 

The MESA App-Estimating Your Risk of Cardiovascular Disease With And Without Coronary Calcium Score

Yesterday, I laid out the case for utilizing coronary artery calcium score (CACS) to further refine the assessment of youngish patients risk of developing cardiovascular disease (ASCVD). I referenced the ACC/AHA ASCVD risk estimator tool (app available here) as the starting point but if I have information on my patient’s CACS I use a new and improved tool called the MESA risk score calculator.

It is available online and through an app for Apple and Android (search in the app store on “MESA Risk Score” for the (free) download.)

The MESA tool allows you to easily calculate how the CACS effects you or your patient’s 10 year risk of ASCVD.

The Multi-Ethnic Study of Atherosclerosis (MESA) is a study of the characteristics of subclinical cardiovascular disease (disease detected non-invasively before it has produced clinical signs and symptoms) and the risk factors that predict progression to clinically overt cardiovascular disease or progression of the subclinical disease. MESA researchers study a diverse, population-based sample of 6,814 asymptomatic men and women aged 45-84. Approximately 38 percent of the recruited participants are white, 28 percent African-American, 22 percent Hispanic, and 12 percent Asian, predominantly of Chinese descent.

To use the score you will need information on the following risk factors:

age, gender, race/ethnicity, diabetes (yes/no), current smoker (yes/no), total and HDL cholesterol, use of lipid lowering medication (yes/no), systolic blood pressure (mmHg), use of anti-hypertensive medication (yes/no), any family history of heart attack in first degree relative (parent/sibling/child) (yes/no), and a coronary artery calcium score (Agatston units).

In many cases the CACS dramatically lowers or increases the risk estimate.

In this example a 64 year old man with no discernible risk factors has a CACS of 175
The 10 year risk of a CHD event almost doubles from 4.7% to 7.6% when the CACS is added to the standard risk factors and moves into a range where we need much more aggressive risk factor modification.

On the other hand if we enter in zero for this same patient the risk drops to a very low 1.9%.

It’s also instructive to adjust different variables. For example, if we change the family history of heart attack (parents, siblings, or children) from no to yes, this same patient’s risk jumps to 7.2% (2.6% with zero calcium score and to 10.4% with CACS 175.)

It can also be used to help modify risk-enhancing behaviors. For example if you click smoker instead of non-smoker the risk goes from 4.7% to 7.5%. Thus, you can tell your smoking patient that his risk is halved if he stops.

Discussions on the value of tighter BP control can also be informed by the calculator. For example, if  our 64 year old’s systolic blood pressure was 160 his risk has increased to 6.8%.

How Does Your CACS Compare To Your Peers?

A separate calculator let’s you see exactly where your score stands in comparison individuals with your same age, gender, and ethnicity

The Coronary Artery Calcium (CAC) Score Reference Values web tool will provide the estimated probability of non-zero calcium, and the 25th, 50th, 75th, and 90th percentiles of the calcium score distribution for a particular age, gender and race. Additionally, if an observed calcium score is entered the program will provide the estimated percentile for this particular score. These reference values are based on participants in the MESA study who were free of clinical cardiovascular disease and treated diabetes at baseline. These participants were between 45-84 years of age, and identified themselves as White, African-American, Hispanic, or Chinese. The current tool is thus applicable only for these four race/ethnicity categories and within this age range.

The calculator tells us that 75% of 64 year old white males have a zero CACS and that the average CACS is 61.

Unlike SAT scores or Echo Board scores you don’t want your CACS percentile status to be high. Scores >75th percentile typically move you to a higher risk category, whereas scores <25th percentile move you to a lower risk category, often with significant therapeutic implications.

Scores between the 25th and 75th percentile typically don’t significantly change the risk calculation.

Exploring Gender Differences In CACS

If we change the gender from male to female on our 64 year old the risk drops considerably from 4.7% down to 3.3%. This graph demonstrates that over 20% of women between the ages of 75 and 84 years will have zero calcium scores.

The graph for men in that same range shows that only around 10% will have a zero CACS.

I’ve been asked what the upper limit is for CACS but I don’t think there is one. I’ve seen numerous patients with scores in the high two thousands and these graphs show individuals in the lowest age decile having scores over 2981.

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.

Antiatherosclerotically Yours,

-ACP

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

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