Great approach. I’ll do it shortly. Thx.
One complicating factor is my wife - who puts A LOT of thought into diet and such - has been on a long process to avoid/get off HTN meds and statins. She had very bad pain from the statins. And had a grandmother die of cirrhosis - expected reaction to longterm rx drugs. It isn’t her decision, but we generally discuss our healthcare choices with each other.
Sage Rat - I figure it is all risk. The statins will make me immortal! 
“Risk” is short for “risk of death by heart attack”, “risk of heart attack”, “risk of varying things that you’d prefer to not have”, or just “risk of getting numbers in later tests that will make your doctor frown”?
Time to try to reduce my ignorance yet again!
I’m guessing that a calcium score of zero is fairly uncommon in a 60 plus individual with high LDL. My guess though is based on nothing. Any sense of how improbable that actually is?
The guidance specifies family history of premature coronary disease not atherosclerotic disease elsewhere inclusive of strokes. Intuitively I’d include the bigger group. Any idea of the support behind restricting it to coronary only?
Thanks.
I don’t know, I can only provide the evidence that UpToDate used to support their recommendations in the topic of Coronary artery calcium scoring: Image acquisition and clinical utilization:
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PubMed
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2019 ACC/AHA Guideline on the Primary Prevention of Cardiovascular Disease: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines.
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Arnett DK, Blumenthal RS, Albert MA, Buroker AB, Goldberger ZD, Hahn EJ, Himmelfarb CD, Khera A, Lloyd-Jones D, McEvoy JW, Michos ED, Miedema MD, Muñoz D, Smith SC Jr, Virani SS, Williams KA Sr, Yeboah J, Ziaeian B
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Circulation. 2019;140(11):e596. Epub 2019 Mar 17.
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PMID
30879355
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Impact of Statins on Cardiovascular Outcomes Following Coronary Artery Calcium Scoring.
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Mitchell JD, Fergestrom N, Gage BF, Paisley R, Moon P, Novak E, Cheezum M, Shaw LJ, Villines TC
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J Am Coll Cardiol. 2018;72(25):3233.
BACKGROUNDCompared with traditional risk factors, coronary artery calcium (CAC) scores improve prognostic accuracy for atherosclerotic cardiovascular disease (ASCVD) outcomes. However, the relative impact of statins on ASCVD outcomes stratified by CAC scores is unknown.
OBJECTIVESThe authors sought to determine whether CAC can identify patients most likely to benefit from statin treatment.
METHODSThe authors identified consecutive subjects without pre-existing ASCVD or malignancy who underwent CAC scoring from 2002 to 2009 at Walter Reed Army Medical Center. The primary outcome was first major adverse cardiovascular event (MACE), a composite of acute myocardial infarction, stroke, and cardiovascular death. The effect of statin therapy on outcomes was analyzed stratified by CAC presence and severity, after adjusting for baseline comorbidities with inverse probability of treatment weights based on propensity scores.
RESULTSA total of 13,644 patients (mean age 50 years; 71% men) were followed for a median of 9.4 years. Comparing patients with and without statin exposure, statin therapy was associated with reduced risk of MACE in patients with CAC (adjusted subhazard ratio: 0.76; 95% confidence interval: 0.60 to 0.95; p = 0.015), but not in patients without CAC (adjusted subhazard ratio: 1.00; 95% confidence interval: 0.79 to 1.27; p = 0.99). The effect of statin use on MACE was significantly related to the severity of CAC (p <0.0001 for interaction), with the number needed to treat to prevent 1 initial MACE outcome over 10 years ranging from 100 (CAC 1 to 100) to 12 (CAC>100).
CONCLUSIONSIn a largescale cohort without baseline ASCVD, the presence and severity of CAC identified patients most likely to benefit from statins for the primary prevention of cardiovascular diseases.
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30409567
Most calculation algorithms assess risk of developing cardiovascular disease (CVD), that is heart, stroke or blood vessel disease. Might show up as angina, heart attack, arrhythmia, transient ischemic attack, full blown stroke, etc. Might be mild or might be fatal.
Thanks for that. So no much evidence for much statin benefit with a CAC of zero.
I did a little more digging and found this.
https://www.ahajournals.org/doi/10.1161/hc4601.099464
Older than our OP and a surprisingly high one in ten had score of zero.
Yes a high score might convince to take but finding out that you are the one in ten may be more useful, avoiding medication that would be of little chance to be of benefit.
Does that follow by your thinking as well?
I’m trying to cut down on thinking, I’m retired now. But yeah, I agree with the potential value of finding out one has a zero score.
More time to think!
Now it’s a hobby!
Congrats. Enjoy. How’s the lake look today?
Welcoming to the statin club…me! It’s been fun to read this and other threads, as I went down the same reaction cycle as so many others:
Eh, I just said fuck it and started taking them.
Is there a club meeting or handshake!?
My doctor was very slow to prescribe statins. I’d say two years or more of high levels. But once I started, they’ve been incredibly successful at dramatically lowering my cholesterol. Whether that translates to me living longer is hard to know.
Here is the rub, I think. For some (not meaning you, @Maserschmidt, just thinking of it reading this, the end point of interest is the lipid panel. For those people a thought process can emerge that the statin accomplishing the lipid goal obviates the need to exercise.
If I had to choose exercise with lipids still cruddy, or lipids fine with a statin but no exercise, I think I’d pick exercising as more impactful. I think.
Obviously not really either or but functionally that way to some.
It depends on which age is meant by “a certain age.” A colleague of mine put in a way that sounded pithy to me, and IMHO demonstrates the right approach to statins. “You take statins in your 40s, 50s, and 60s, so that you can reach your 70s, 80s, and 90s.” The implication being that taking statins in your 80s, 90s, and 100s with the goal of reaching your 110s and 120s doesn’t make much sense, at least for a significant number of people. As a physician with a patient panel that consists entirely of people who live in nursing homes, one of the most frequent orders I write for newly admitted patients is “discontinue lipitor.”
Of course this is mostly for people who have Alzheimer’s dementia, muscle wasting, and labs that return with an LDL in the 10, or 20s on a statin and in the 30s off statins.
And it is clear that cardiorespiratory fitness is, independent of its impact on lipids, of HUGE impact on both life expectancy and quality of life. (Even greater when combined with modest amounts of strength training.)
Yeah, the whole “Better Living thru Pharmaceuticals” thing.
I started on a low-dose statin about 4-5 years ago but did not change my lifestyle much - still active as prior, but did change some eating habits. But, yeah, I can see how someone would just say at the Golden Corral buffet “Screwit! This is what Liptor is for!”
43 year old here, with significantly discouraging numbers, and am starting on crestor.
I’m curious… my doc and sources online say “once you’re on it, you’re on it for good,” but I can’t tell if that’s because once you stop your levels will revert to what they were before (ie, stop taking the drug and stop experiencing its benefit), or if taking the drug causes physiological changes that leave you worse off that before if you stop. Any insight here?
After my stent I was put on a statin, despite the fact that my labs were very good. My cardiologist said that taking a statin for one year following the procedure would statistically increase my chances of survival.
After the year was up I stopped taking it. While on a statin I had leg cramps 4 nights out of each seven. It was horrible. Once I stopped the statin the cramps stopped.
There is no mechanism I am aware of that would cause physiologic changes to make one worse off when one stops. And no general need to increase the dose over the years which would be consistent with such a process.
OTOH, statistically if someone was going to be able adequately impact their numbers by nutrition and exercise choices they would have been more likely to do it before going on the medication. If anything people unfortunately often reduce risk reducing behaviors once on medication. Plus the algorithm for being on medication weighs more toward being on it with advancing age (higher risk of a cardiovascular event over the next ten years).
That said, if someone started medication when they were obese unfit and eating crap, having been so for most of their life, and then switched to a healthy diet with regular exercise losing 10 to 15% of their body mass, they might be able to stop and maintain adequate numbers. Yeah that does not happen very often.
That makes sense, and is what I figured/hoped.
There was just a piece of my brain that panicked when I heard “you can’t stop taking it”… what if the apocalypse comes and they stop manufacturing statins (or some fresh hell in health care leaves me uninsured or unable to afford them)? Will I drop dead from some horrible withdrawal symptoms? Seems like, no, but I’ll likely be just as unhealthy as I am now (barring some significant lifestyle changes) but also with added complications of age.