How Coronary Calcium Informed a Sexagenerian Flaneur’s Decision on Statin Therapy

As I strolled into my PCP’s office this past September for my annual checkup & flu shots, I had no idea that I was about to become a “case study” for the renowned Skeptical Cardiologist.  Had I known, I would have faced the annual ritual with considerably more trepidation!

Brief bio: 66 y/o male, never smoker, no medications, family history of congestive heart failure.  Brooklyn resident, reasonably active flaneur, vegetarian for 20 years (a favorite New Yorker cartoon reads: “At first I was a vegetarian for diet reasons; then later for political reasons; but now just to annoy people”).

Luckily for me, as it turned out, I am also a son of Oklahoma, where I had the good fortune long ago to become friends with the Skeptical Cardiologist.  (My late father-in-law, a native New Yorker, was fond of saying to me: “You can take the boy out of Oklahoma, but you can’t take Oklahoma out of the boy.”  I’m still unsure whether that was a compliment, or an insult!)

The checkup was routine until my labs, excerpted below, arrived via email:

Cholesterol 224 H

HDL Cholesterol 95

LDL Cholesterol 114 H

Total Cholesterol / HDL Ratio 2.4 L

At the top of the report my PCP had written these words:

I have reviewed your recent results. Overall your labs look very good. My only concern is your cholesterol. You have a high good HDL cholesterol, but you are getting to the point where a statin medication may be helpful.

None of this meant anything to me; I didn’t know which kind was the “good” cholesterol; I didn’t know the difference between a statin and a stent!  But the prospect of starting a medication prompted me to attempt to educate myself.

I had never been more than a very casual reader of the Skeptical Cardiologist’s blog, but I knew it contained a great deal of valuable information.  When I told the Skeptical Cardiologist, via text message, what my PCP had said, he observed that like many PCPs, mine had done a rather poor job at communicating why a statin drug might be necessary.

On the recommendation of the Skeptical Cardiologist, I read every article on his statins page.  I further learned about a test called the Coronary Artery Calcium (CAC) scan, and read many articles about that as well.  I decided that the scan might help determine not only whether I should take a statin, but also whether I am at risk of dropping dead at any minute, which seems like a good thing to keep in the back of one’s mind.

I chose a diagnostic center on E. 84th Street in Manhattan, mostly because of its proximity to Central Park and to the Metropolitan Museum of Art — both are prime locations for flaneuring* after the test!

The test itself took 15 minutes.  Outside, the day was fine, and Central Park’s fall foliage was glorious, so after a socially-distanced repast al fresco on the Upper East Side, I spent the rest of the day wandering all over the park’s spectacular woods:


Later, my neighbor Peter, with whom I share an occasional socially-distanced martini in my rear garden, advocated on behalf of statins.  My same age, he’s been taking them for 15 years, and says they’re great; he says “they knock the cholesterol right down.”  Everyone seems to be taking them!  Even the diagnostician who did my CAC scan said she takes one!  Should all men over 60 take a statin?  Was I getting statin FOMO?

A few days later, the Skeptical Cardiologist texted my CAC results:


No need for a statin!?  This seems like good news indeed!!  At the least, it will inform my discussions with my PCP.  I am very glad I invested in the CAC scan, and that I took the time to educate myself via the Skeptical Cardiologist’s blog.  I wish to extend my great thanks to the Skeptical Cardiologist for his generosity in sharing his blog with the public.

*Postscript: For those who may be unfamiliar with the term flaneur: it is said to refer to the act of doing nothing, raised to an art form.  More information may be found here.


My friend David’s story (absent my input) is likely being repeated daily in doctor’s offices nationwide. Doctors typically start with the guideline-recommended risk estimator available as a smartphone app.

When you enter in David’s numbers the app estimates his 10 year risk of heart attack or stroke at 9.1%. As I’ve pointed out pretty much any male in his sixties will get a 10 year risk estimate >7.5% from this calculator which per the guidelines should trigger discussion of drug treatment with a statin to lower both the LDL cholesterol and the long term risk of heart attack/stroke.

The MESA risk calculator helps refine David’s risk by incorporating additional conventional risk factors (like family history) and most importantly the CAC score which measures subclinical atherosclerosis.

As you can see after incorporating the zero CAC score, the more precise estimate of David’s 10 year risk is 1.5%. This is extremely low and adding a statin therefore makes little sense.

It also makes no sense to take aspirin at this low risk level.

Proflaneuringly Yours,



26 thoughts on “How Coronary Calcium Informed a Sexagenerian Flaneur’s Decision on Statin Therapy”

  1. Can you explain the DEVO reference? I love reading your missives and have told lots of folks about your blog. I am a bike rider too!

  2. Age 60 female here. I had a full work up last year after my husband had a fully occlusive LAD heart attack, the Widowmaker. He survived coding 6 times with no damage to his heart. His EF went back up to 65 in 3 days! Yes, he’s a miracle and we know it! But I had a lot of anxiety after seeing him code on our dining room floor and needed to get checked out for my own peace of mind. I insisted on a CAC score and went thru a stress echo, a CT angiogram, chest x-ray, blood work, etc. I’ve eaten low carb/keto most of the time for many years and I knew my cholesterol was over 200, but the ratio is excellent. My CAC came back as zero and arteries “widely patent”. I was very relieved.

  3. Its awesome to see how individualized medicine is starting to play out with diagnostic tools like CAC for better risk stratification. Preventative cardiology is so important in situations like this because PCP’s and HCP’s are still lacking in differentiating which patients are the best candidates for statin use. Its also reflective of how multi variable atherosclerosis development is, high cholesterol unto itself, often does not manifest itself in pathological sense but many other variables in the presence of high cholesterol that make it deleterious. I thought it was especially telling when your friend’s PCP mentioned his “good” cholesterol being high. The CETP drug class failures showed that artificially manipulating “good cholesterol” (APOA) is not beneficial and in fact may be harmful. APOA might be just an indicator of metabolic health or maybe something else, but its quantification appears to be ambiguous in providing criteria for interventions.

    I liked your answer to Nancy F. I too was surprised that APO-B seems to be a better tracker of particle count than LDL-P. From my understanding APO-B is universally measured by the same immunoassay and you can better track how interventions impact baseline due to homogeneity of results . NMR has much more variability in technology and instrumentation sensitivity, this consequently provides different results and making it much more difficult to track interventions in the long run.

  4. My husband, who is 52, and has genetically high cholesterol and had been trying to delay starting statins and aspirin, was pleased to get a coronary calcium score of zero (he was 49 at the time) But, a subsequent carotid ultrasound showed subclinical atherosclerosis, which was disappointing. So which test to defer to? Which has more importance in guiding decisions on treatment?

    • Excellent question and something I’ve been meaning to write about.
      In the youngish (let’s say men 50, women <60) a zero coronary calcium scan is the norm and therefore in this group I have utilized carotid IMT and carotid plaque screening (see here)
      to better risk stratify the zero CAC score individuals who have a strong family history of heart attack or have very worrisome lipid values or lp(a).
      I have numerous examples of abnormal Carotid IMT or carotid plaque preceding the development of nonzero CAC in this age group.

      • Well I’m a female age 57 with a CAC of 82 and I feel like I’ve been handed a death sentence. I have family history of heart disease (father) but I’m slim, athletic, vegetarian, but pretty low carb. Any tips?

        • Well, first and foremost that CAC score is not a death sentence! You can live a healthy, normal life. I recommend you read my post on “dealing with the cardiovascular cards you’ve been dealt.” given that your lifestyle is outstanding you will need most likely drug therapy to lower your risk but fortunately modern medicine has the tools to dramatically lower your risk in the long term.

    • Nancy,
      Most lipidologists and cutting edge preventive cardiologists are moving aaway from LDL particle size or number, an expensive test measured by NMR and more toward apolipoprotein B (which I need to write about) which is sometimes discordant with LDL C but tracks the overall numbers of apo B, the lipoprotein that is felt to be responsible for entering the arterial lining.
      That being said the bottom line on cholesterol, no matter how we are measuring its atherosclerotic potential is how the lipoprotein particles are contributing to plaque build up.
      If they aren’t causing plaque buildup we don’t worry about them. W
      What we measure with our tests is the concentration of lipoproteins but we don’t have ways to measure their function which is equally i mportant in the development of atherosclerosis.

  5. Are there not exceptions, as with every rule?
    It’s my understanding that calcification is often the final step of healing chronic injuries such as in plantar fasciitis, tennis elbow, or lesions in the coronary arteries. But that’s variable, person-to-person, is it not?
    I submit that the Agatston score is not the perfect indicator as characterized.
    Are there not plaques out there in the populace without protective dense calcification waiting to rupture?
    Are there not extensive dense calcifications from healed lesions that are not a cause for concern about ischemia or blockage?

    If so, it would be gratifying to be able to discern these exceptions, their causes, and their rate of occurrence.

    • Are we not men? We are Devo.
      David’s risk is not zero so we are not talking in absolutes. It’s just a lot lower than the average 66 year old man.
      As far as soft plaque he could have some but his overall plaque burden is really low. Soft plaque starts forming depending on the milieu in men in their thirties and fourties. If by age 66 no soft plaque has progressed to even small areas of calcification you are well ahead of the game.
      A coronary CT angiogram would likely show small areas of noncalcificied, soft plaque in David but his estimated risk would not be altered by that finding.

    • I don’t recommend PLAC testing in my patients. If I’m concerned about measuring inflammation I utilize hs-CRP. However, CAC is a much more powerful risk stratifier than CRP, the biomarker with the most evidence. So, an elevated PLAC or CRP would not change my recommendations for a 66-year-old with a zero CAC.

      • So if someone had zero CAC, low CRP but also had a PLAC test that put them in the top 2% (eg 630) for risk what would you tell them? CAC is not repeatable on a regular basis whereas PLAC could be taken every 3 months for example. See: (I haven’t got full access

          • Christopher,
            The paper you referenced on PLAC concludes
            “The PLAC test for Lp-PLA 2 activity provides little additional value beyond standard cardiovascular risk assessment, and any potential benefits are likely outweighed by harms. Current guidelines do not include the PLAC test nor other tests for Lp-PLA 2 activity in risk assessment. 1617 Other tests with greater utility that are supported by the American College of Cardiology/American Heart Association guidelines for primary prevention include high-sensitivity C-reaction protein, lipoprotein(a), apolipoprotein B, ankle-brachial index, and the coronary artery calcium score. 16”
            I’ll email you a PDF .
            Dr P

      • Thank you very much Dr P for responding and also for emailing the study. I do have one question though. I had a CAC, PLAC and CRP test all over three weeks. Te CAC was zero. The PLAC was 735 (very high) and CRP was 0.7 (very good.) Also my weight was 87 kgs but I am 6ft 2″ so not too bad. Very low stress. BP: 125/80

        And I got a stroke.

        Coincidental? Not measured/indicated by CAC scores? Strongly indicated by PLAC….

        • You are welcome. It’s crazy that the scientific publishing puts papers behind paywalls. Another good reference for PLAC is here ( They delve into the issues with using PLAC concentration-the assay can be unreliable depending on handling of the samples.
          Bottom line on PLAC is that very few reliable doctors use it due to multiple problems. I did notice that if you Google PLAC and stroke one of the first article comes from Dr. Stephen Sinatra who belongs in the cardiology quack hall of fame.

          With respect to your stroke. Unexplained stroke or cryptogenic stroke is common. The fact that you had a high PLAC doesn’t tell us anything about what caused your stroke. There are two studies that look at potential cardiac causes of stroke that I recommend to most patients with cryptogenic stroke 1) a transesophageal echocardiogram to look for clots, masses, holes etc. that could have caused a clot to come from the heart and go to the brain and 2) a 30 day monitor to look for atrial fibrillation. If those are negative (and presumably) the arteries to your brain have been imaged and are OK) then treatment would be aspirin and aggressive control of standard cardiac risk factors.

          • Thank you again. I had (2) but not (1). The irony of your suggestion re treatment/preventive action…the PLAC study you sent me stresses that a harm of PLAC is a high PLAC can lead to an unnecessary statin prescription which is probably (after lifestyle) the main treatment of standard cardiac risk factors. I guess you’re not a fan of VAP/NMR tests?

          • The Mayo document states: “Lp-PLA2 is an enzyme involved with atherosclerotic plaque formation. Elevations in plasma Lp-PLA2 concentration and activity are associated with increased risk of cardiovascular disease”


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