that emphasizes plaque volume and type over flow-limiting lesions, do you see FFRCT (HeartFlow) as a complementary tool to Cleerly’s anatomical analysis, or do you believe FFRCT’s physiological assessment has limited relevance in this context? How do you view the role of FFRCT in long-term risk prediction compared to Cleerly’s approach, and do you ever use FFRCT in your own practice?
I ask partly because I just came across a study from the ADVANCE-DK registry that found FFRCT results can predict long-term outcomes in coronary stenosis cases. Welcome your thoughts. Don't know if I can link here, but here is citation.
Jim
Prognostic value of FFRCT in patients with stable chest pain – a 3-year follow-up of the ADVANCE-DK registry | European Heart Journal | Oxford Academic
This is really helpful, as the CAC and CCTA tests are increasingly entering primary care discussions and routine physicals with motivated middle aged types. In future posts feel free to comment on how this sort of knowledge gleaned from testing might help primary prevention discussions. I'm guessing in the asymptomatic patients it might find the most utility in getting people to shift into another diet and lifestyle gear, be more compliant or intensive with statin therapy, increase exercise? The discrepancies between CLEERLY lesions and CCTA lesions by % are pretty discouraging actually, as this would seem to undermine the value of current CCTA interpretations made by humans/radiologists?
I obtained a CCTA and CLEERLY because of very severe statin intolerance and high apoB (better predictor than LDL-C which should be dropped from the guidelines and replaced by apoB) My CLEERLY interpretation downgraded my disease burden tremendously. The original CCTA report was very worrisome. Calcification is a sign of plaque stabilization. My CAC was 2300. CLEERLY demonstrated that I had less than 1% soft plaque. CCTA report called 70+% LAD stenosis, CLEERLY downgraded to 31%. CAC and CCTA can cause much anxiety and is often over-read because of "blooming artifact" caused by calcification. My local cardiologist offered ICA, he was totally unaware of CLEERLY and after presenting CLEERLY report and images to him he ignored the data and offered stress test and possible cath. Both unnecessary. Very grateful for CLEERLY. Bob Hansen MD, Internal Med, Critical Care, Anesthesiology, now retired.
It seems you are advocating for a diagnostic and treatment strategy that goes far beyond Ischemia. Is there outcome data and evidence to support such a strategy, or any interventions (medical or otherwise) that may be invoked downstream of such a strategy?
Thanks for sharing your personal info, even the embarrassing part! :) I look forward to hearing how this has informed your day-to-day lifestyle and medication choices, and whether the knowledge has given you more or less equanimity. I'm also curious to hear your take on the article below. Maybe the improved risk prediction will help doctors more accurately pinpoint who best to target for primary prevention. I do wish the CCT would release the data because their failure to do so leads many folks to reasonably conclude they must be hiding something.
Correct me if I am wrong: 'This test is ONLY a predictor for something that can not be stopped, reversed or cured. And while it MAY be useful longitudinally to chart an assumed future demise, the downstream psychological harm to many patients has the POTENTIAL to cause more damage than good or promote any reasonable understanding of the test results.'
Follow up: In what universe would a sane person disclose: "My LDL-C levels weren’t particularly high but I periodically took rosuvastatin after eating particularly unhealthy meals just to be on the safe side (not a recommended protocol.)" ???
I have been covered by insurance by appealing their denial. I am asymptomatic, 75, not intolerant of statins with a treated LDL in the 50's by statins and diet alone. However I have a CAC over 1000, a very elevated LP(a) @300, mild aortic valve disease with mild thicken and mild calcification. I used the subset data data from the FOURIER study on LP(a) to bolster my case.
Nina Teicholtz and Gary Taubes also have a substack following and their most recent post talked about:
Among healthy, lean folks, 80 participants on keto diets versus 80 participants on regular diets. The LDL cholesterols were 273 versus 123 and after 5 years the heart scan plaque amounts in both groups were the same.
Conclusions Among primary prevention-type patients aged 50–89 years without diabetes and not on statin therapy, the lowest risk for long-term mortality appears to exist in the wide LDL-C range of 100–189 mg/dL, which is much higher than current recommendations. For counselling these patients, minimal consideration should be given to LDL-C concentration.
So, have you looked into calcium dysregulation as it is involved in CVD, Alzheimer’s, Parkinson’s, cancer, diabetes?
ALL of these diseases share this - calcium dysregulation. Others, too.
Search it. Please. Search each disease with calcium dysregulation in PubMed or similar sources.
Add in vitamin K2. Lots of newer insights. Statins interfere with vitamin K2 actions. That’s why statins increase CAC. Again, search this. I can show, but actually searching seems to offer better insights.
It’s contrary to the enormous energy/money/careers into which we’ve poured our time and interests, but it’s there, it’s viable and it’s rather strongly supported. The only thing standing in the way of a paradigm change is that we’ve completely bought into cholesterol as ‘dangerous’ and related misguided ideas. Whole careers are based in them and ENORMOUS amounts of money, so who can change?
It’s fatal…To doctors, pharma, hospitals and our current (really, really broken) medical system. Fatal not bc more folks will die, but bc we would have to completely change and no one wants to (nor can…we’re stuck).
Yes, we want to avoid sudden death, but we’ve headed the wrong way!
BTW, there are claims that castration adds 14 years to a man’s life…so who is signing up?
In statin studies, so-called ‘side effects’ are cited as absolute risks while ‘benefits’ utilize relative risks. This is complete BS. And so few know! See:
We’re fat, sick, malnourished, and poisoned and modern medicine is either a direct guilty participant or indirectly responsible by way of bias.
Let’s use AI to sort out these various hypotheses. But to avoid garbage in, garbage out, ALL data must be included. See article above about statistical manipulations. See what really leads to healthy longevity. And it’s NOT statins, which actually cause calcium dysregulation.
LDL-C is very poor predictor, The study you reference showed "Unlike LDL-C, both T-C/HDL cholesterol (high-density lipoprotein cholesterol) and triglycerides/
HDL cholesterol ratios were independently associated with long-term mortality." These ratios correlate well with apoB (a measure of all potentially atheorgenic lipoprotein particles). Insulin resistance drives atherosclerosis mediated through inflammation and lipoprotein particles, increased endothelial permeability, and destabilization of plaque after plaque creation.
But I am really pointing to a different paradigm. It's about calcium dysregulation and vitamin K2.
Cholesterol, lipids, as primary causes of CVD have been the focuses, and the data (admittedly less than ideal bc we have focused on fats against any other possibilities) support calcium dysregulation and vitamin K2 as much, much more important and accurate.
Search the literature!
Use these parameters and see that an entirely different paradigm is possible and supported!
Calcium metabolism, insufficient Vit K2 and other fat soluble vitamins cannot explain lipoprotein endothelial penetration, retention, plaque creation and plaque disruption. I have exhaustively read the K2 literature and I have created > 200 slides on atherosclerosis and MACE for multiple lectures that I have given. The NMR IR index and Lipoprofile predict CV events in women (see Women;s Health Study Data) more strongly than any other clinical variable. Read this: Association of Lipid, Inflammatory, and Metabolic Biomarkers With Age at Onset for Incident Coronary Heart Disease in Women. Insulin resistance and its associated metabolic effects, including dysfunctional HDL, hypertension, inflammation, endothelial disruption, and lipid changes drive atherosclerosis and subsequent plaque rupture, not calcium metabolism. Autopsy studies, metabolic studies, randomized controlled trials, epidemiologic data, all support this model. Go here to view my most recent lecture, I can send you a PDF of the slides. https://2023.evolutionaryhealthconference.com/replays/
Different models can be supported beyond this though, and the investigation of roles of VK in health are only more recently being published…it’s newer to even go here. VK has long been “stuck” in coagulation roles, but that has been myopic.
And, though these folks find that VK has more roles than calcium regulation that benefit cardiovascular health and endothelial functioning…we’re much more than only cardiovascular beings.
T2D, an epidemic, IS a manifestation of calcium dysregulation:
Thyroid Hormone Targets Matrix Gla Protein Gene Associated With Vascular Smooth Muscle Calcification (2005)
Multiple publications, many newer, correlate VSMC calcifications, CAC and perturbations in creating T3. Not on radar of cardiologists and endocrinology has assumed that T4 conversion to T3 is a constant. Serum measures do not necessarily reflect individual tissue levels of T3.
I mentioned UBIAD1, the enzyme essential to create MK-4 endogenously.
Statins interfere with this. Statins increase CAC. Statin studies are usually cited via relative risks for so-called benefits but absolute risks for detriments (side effects). This is beyond disingenuous. And has fooled many.
Also, EVERY intervention with VK (if they looked) increases insulin sensitivity.
Keep looking. Exhaustively. Expand to these topics. Reconsider.
Thanks, read the links and related articles. Was aware of Rotterdam and similar studies, have been taking K2 for many years, tried to find Natto several years ago, none in my community. Many factors affect insulin sensitivity, K2 clearly one of many. K2 is part of a complex system. Not the only or primary factor.
Natto is found in Asian markets in the freezer section. So you can stock up if you get some. But liver is just as amazing as an excellent source of long chain menaquinones. I believe that I “hate” it, so I don’t eat liver, but I am wrong. Food is cultural….
Also, fermented anything is usually high in K2 and if you select something like yogurt, get full-fat because it’s been shown that removing the fats also greatly reduces the fat soluble vitamins like K2.
We’ve really altered fats in our diets in recent times.
Is there a difference from observer to observer in interpretation ? This sounds very exciting and a non invasive way to see coronaries , the test I’m told is about 1.500$ compared to invasive angiography , seems to be the future . Thank you sir
Unfortunately, lots of seemingly healthy individuals with no symptoms die suddenly from coronary artery disease. Death is their first symptom. You don't get second chances unless you are fortunate enough to have bystanders do CPR, utilized an AED and get you to a Cath lab.
Not sure what "detailed reductionist information is". The CCTA tells us exactly what amount of the disease of concern (CAD) we have. We need unbiased, enlightened MDs to help individuals do the best thing with that information, therein lies the problem.
I appreciate the prompt insightful response. My point is that as we look harder we find more. Not uncommonly I care for elderly frail patients admitted with serious bleeding issues on dual antiplatelet therapy after percutaneous intervention due to extrapolated study findings. Yes of course we are worried about in stent thrombosis. I welcome efforts to inform the clinician in these situations. I also hope that new AI generated information can not only persuade but also dissuade the practitioner when nuanced judgement is required.
This information is exciting to be sure. Cautionary tales abound however. A few basic truths should be kept in mind. First, it’s hard to make a healthy person feel better and attempts to intervene on this population should be viewed with great caution. Second, coronary artery anatomy blockages when approached as a plumbing problem is a simplistic naive world view fraught with unintended consequences. More detailed reductionist information is not necessarily a good thing(if we have learned anything from our cancer screening misadventures).
This study concluded that patients at all initial CAC scores showed dramatically more heart attacks if they did not hold their CAC increase to 15% per year.
My initial CAC was 2300. Clearly it had been moving rapidly. After 2 years of keto my CAC increase was 12.5% per year. (Also pre-diabetic markers disappeared, raw cholesterol numbers degraded but cholesterol ratios improved dramatically .)
That study was small, retrospective, observational with poor lipid control and published in 2004. Needs confirmation from at least one larger study from a different center. Nothing that I am aware of since then supports that conclusion.
Also, I suspect there were very few subjects who had CAC >2K
I will remember your compliment on my "remarkable online presence" the next time I feel more like playing music than writing posts!
My Dad had the invasive scan (not because he was having a heart attack, although he was getting angina pains. I don’t know whether he also had a non-invasive CT scan. I don’t know whether the NHS has Cleerly AI software for further coronary artery analysis. It sounds like very useful equipment though, and it would be brilliant if it was accessible across the globe via internet!
How does Cleerly compare to HeartFlow One analysis?
Cleerly quantifies the anatomy of the coronary arteries.
HeartFlow (aka CT FFR) is looking at the physiology of the coronary arteries.
More and more (with some exceptions) the plumbing paradigm of CAD is taking a back seat to the pimple paradigm.
Volume and type of atherosclerotic burden in the coronaries is more important than whether there are flow-limiting lesions.
Given your ‘pimple' paradigm’
that emphasizes plaque volume and type over flow-limiting lesions, do you see FFRCT (HeartFlow) as a complementary tool to Cleerly’s anatomical analysis, or do you believe FFRCT’s physiological assessment has limited relevance in this context? How do you view the role of FFRCT in long-term risk prediction compared to Cleerly’s approach, and do you ever use FFRCT in your own practice?
I ask partly because I just came across a study from the ADVANCE-DK registry that found FFRCT results can predict long-term outcomes in coronary stenosis cases. Welcome your thoughts. Don't know if I can link here, but here is citation.
Jim
Prognostic value of FFRCT in patients with stable chest pain – a 3-year follow-up of the ADVANCE-DK registry | European Heart Journal | Oxford Academic
This is really helpful, as the CAC and CCTA tests are increasingly entering primary care discussions and routine physicals with motivated middle aged types. In future posts feel free to comment on how this sort of knowledge gleaned from testing might help primary prevention discussions. I'm guessing in the asymptomatic patients it might find the most utility in getting people to shift into another diet and lifestyle gear, be more compliant or intensive with statin therapy, increase exercise? The discrepancies between CLEERLY lesions and CCTA lesions by % are pretty discouraging actually, as this would seem to undermine the value of current CCTA interpretations made by humans/radiologists?
Anyway, looking forward to you next post.
I obtained a CCTA and CLEERLY because of very severe statin intolerance and high apoB (better predictor than LDL-C which should be dropped from the guidelines and replaced by apoB) My CLEERLY interpretation downgraded my disease burden tremendously. The original CCTA report was very worrisome. Calcification is a sign of plaque stabilization. My CAC was 2300. CLEERLY demonstrated that I had less than 1% soft plaque. CCTA report called 70+% LAD stenosis, CLEERLY downgraded to 31%. CAC and CCTA can cause much anxiety and is often over-read because of "blooming artifact" caused by calcification. My local cardiologist offered ICA, he was totally unaware of CLEERLY and after presenting CLEERLY report and images to him he ignored the data and offered stress test and possible cath. Both unnecessary. Very grateful for CLEERLY. Bob Hansen MD, Internal Med, Critical Care, Anesthesiology, now retired.
I incorporate Ischemia into my daily practice.
It seems you are advocating for a diagnostic and treatment strategy that goes far beyond Ischemia. Is there outcome data and evidence to support such a strategy, or any interventions (medical or otherwise) that may be invoked downstream of such a strategy?
Thanks for sharing your personal info, even the embarrassing part! :) I look forward to hearing how this has informed your day-to-day lifestyle and medication choices, and whether the knowledge has given you more or less equanimity. I'm also curious to hear your take on the article below. Maybe the improved risk prediction will help doctors more accurately pinpoint who best to target for primary prevention. I do wish the CCT would release the data because their failure to do so leads many folks to reasonably conclude they must be hiding something.
https://www.medpagetoday.com/opinion/second-opinions/110734?xid=nl_secondopinion_2024-06-23&eun=g2093479d0r
Correct me if I am wrong: 'This test is ONLY a predictor for something that can not be stopped, reversed or cured. And while it MAY be useful longitudinally to chart an assumed future demise, the downstream psychological harm to many patients has the POTENTIAL to cause more damage than good or promote any reasonable understanding of the test results.'
Follow up: In what universe would a sane person disclose: "My LDL-C levels weren’t particularly high but I periodically took rosuvastatin after eating particularly unhealthy meals just to be on the safe side (not a recommended protocol.)" ???
(opinion) 6-2-and even you will not answer!
I have been covered by insurance by appealing their denial. I am asymptomatic, 75, not intolerant of statins with a treated LDL in the 50's by statins and diet alone. However I have a CAC over 1000, a very elevated LP(a) @300, mild aortic valve disease with mild thicken and mild calcification. I used the subset data data from the FOURIER study on LP(a) to bolster my case.
PS see:
https://www.ahajournals.org/doi/10.1161/01.RES.0000181431.04290.bd?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub%20%200pubmed
Thyroid Hormone Targets Matrix Gla Protein Gene Associated With Vascular Smooth Muscle Calcification
There is so much to learn about calcification!
VSMCs are vulnerable.
And endocrinology misunderstands the conversion of T4 to T3.
Another specialty involved in cardiovascular risk that tends to misguided.
Nina Teicholtz and Gary Taubes also have a substack following and their most recent post talked about:
Among healthy, lean folks, 80 participants on keto diets versus 80 participants on regular diets. The LDL cholesterols were 273 versus 123 and after 5 years the heart scan plaque amounts in both groups were the same.
Also, see this:
https://bmjopen.bmj.com/content/bmjopen/14/3/e077949.full.pdf
Conclusions Among primary prevention-type patients aged 50–89 years without diabetes and not on statin therapy, the lowest risk for long-term mortality appears to exist in the wide LDL-C range of 100–189 mg/dL, which is much higher than current recommendations. For counselling these patients, minimal consideration should be given to LDL-C concentration.
So, have you looked into calcium dysregulation as it is involved in CVD, Alzheimer’s, Parkinson’s, cancer, diabetes?
ALL of these diseases share this - calcium dysregulation. Others, too.
Search it. Please. Search each disease with calcium dysregulation in PubMed or similar sources.
Add in vitamin K2. Lots of newer insights. Statins interfere with vitamin K2 actions. That’s why statins increase CAC. Again, search this. I can show, but actually searching seems to offer better insights.
It’s contrary to the enormous energy/money/careers into which we’ve poured our time and interests, but it’s there, it’s viable and it’s rather strongly supported. The only thing standing in the way of a paradigm change is that we’ve completely bought into cholesterol as ‘dangerous’ and related misguided ideas. Whole careers are based in them and ENORMOUS amounts of money, so who can change?
It’s fatal…To doctors, pharma, hospitals and our current (really, really broken) medical system. Fatal not bc more folks will die, but bc we would have to completely change and no one wants to (nor can…we’re stuck).
Yes, we want to avoid sudden death, but we’ve headed the wrong way!
BTW, there are claims that castration adds 14 years to a man’s life…so who is signing up?
In statin studies, so-called ‘side effects’ are cited as absolute risks while ‘benefits’ utilize relative risks. This is complete BS. And so few know! See:
https://www.cureus.com/articles/141648-historical-review-of-the-use-of-relative-risk-statistics-in-the-portrayal-of-the-purported-hazards-of-high-ldl-cholesterol-and-the-benefits-of-lipid-lowering-therapy
We’re fat, sick, malnourished, and poisoned and modern medicine is either a direct guilty participant or indirectly responsible by way of bias.
Let’s use AI to sort out these various hypotheses. But to avoid garbage in, garbage out, ALL data must be included. See article above about statistical manipulations. See what really leads to healthy longevity. And it’s NOT statins, which actually cause calcium dysregulation.
LDL-C is very poor predictor, The study you reference showed "Unlike LDL-C, both T-C/HDL cholesterol (high-density lipoprotein cholesterol) and triglycerides/
HDL cholesterol ratios were independently associated with long-term mortality." These ratios correlate well with apoB (a measure of all potentially atheorgenic lipoprotein particles). Insulin resistance drives atherosclerosis mediated through inflammation and lipoprotein particles, increased endothelial permeability, and destabilization of plaque after plaque creation.
"LDL-C is a very poor predictor..."
Yes, true.
But I am really pointing to a different paradigm. It's about calcium dysregulation and vitamin K2.
Cholesterol, lipids, as primary causes of CVD have been the focuses, and the data (admittedly less than ideal bc we have focused on fats against any other possibilities) support calcium dysregulation and vitamin K2 as much, much more important and accurate.
Search the literature!
Use these parameters and see that an entirely different paradigm is possible and supported!
Search these:
Atherosclerosis/vitamin K2/microcalcifications/diabetes/vascular smooth muscle cells/UBIAD1/
Calcium metabolism, insufficient Vit K2 and other fat soluble vitamins cannot explain lipoprotein endothelial penetration, retention, plaque creation and plaque disruption. I have exhaustively read the K2 literature and I have created > 200 slides on atherosclerosis and MACE for multiple lectures that I have given. The NMR IR index and Lipoprofile predict CV events in women (see Women;s Health Study Data) more strongly than any other clinical variable. Read this: Association of Lipid, Inflammatory, and Metabolic Biomarkers With Age at Onset for Incident Coronary Heart Disease in Women. Insulin resistance and its associated metabolic effects, including dysfunctional HDL, hypertension, inflammation, endothelial disruption, and lipid changes drive atherosclerosis and subsequent plaque rupture, not calcium metabolism. Autopsy studies, metabolic studies, randomized controlled trials, epidemiologic data, all support this model. Go here to view my most recent lecture, I can send you a PDF of the slides. https://2023.evolutionaryhealthconference.com/replays/
Thank you.
Different models can be supported beyond this though, and the investigation of roles of VK in health are only more recently being published…it’s newer to even go here. VK has long been “stuck” in coagulation roles, but that has been myopic.
Please read: Phylloquinone improves endothelial function, inhibits cellular senescence, and vascular inflammation (2024)
And, though these folks find that VK has more roles than calcium regulation that benefit cardiovascular health and endothelial functioning…we’re much more than only cardiovascular beings.
T2D, an epidemic, IS a manifestation of calcium dysregulation:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10305719/
Vitamin K-dependent carboxylation regulates Ca2+ flux and adaptation to metabolic stress in β cells (2023)
There are tons more publications about VK and diabetes and calcium.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11172246/
Vitamin K2 in Health and Disease: A Clinical Perspective (2024)
Further, actual synthesis of vitamin K-dependent proteins - especially matrix gla protein - are independent of VK.
Please see:
https://www.ahajournals.org/doi/10.1161/01.RES.0000181431.04290.bd?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub%20%200pubmed
Thyroid Hormone Targets Matrix Gla Protein Gene Associated With Vascular Smooth Muscle Calcification (2005)
Multiple publications, many newer, correlate VSMC calcifications, CAC and perturbations in creating T3. Not on radar of cardiologists and endocrinology has assumed that T4 conversion to T3 is a constant. Serum measures do not necessarily reflect individual tissue levels of T3.
I mentioned UBIAD1, the enzyme essential to create MK-4 endogenously.
Statins interfere with this. Statins increase CAC. Statin studies are usually cited via relative risks for so-called benefits but absolute risks for detriments (side effects). This is beyond disingenuous. And has fooled many.
Also, EVERY intervention with VK (if they looked) increases insulin sensitivity.
Keep looking. Exhaustively. Expand to these topics. Reconsider.
Thank you.
Thanks, read the links and related articles. Was aware of Rotterdam and similar studies, have been taking K2 for many years, tried to find Natto several years ago, none in my community. Many factors affect insulin sensitivity, K2 clearly one of many. K2 is part of a complex system. Not the only or primary factor.
Natto is found in Asian markets in the freezer section. So you can stock up if you get some. But liver is just as amazing as an excellent source of long chain menaquinones. I believe that I “hate” it, so I don’t eat liver, but I am wrong. Food is cultural….
Also, fermented anything is usually high in K2 and if you select something like yogurt, get full-fat because it’s been shown that removing the fats also greatly reduces the fat soluble vitamins like K2.
We’ve really altered fats in our diets in recent times.
Love “K2 is part of a complex system.”
Is there a difference from observer to observer in interpretation ? This sounds very exciting and a non invasive way to see coronaries , the test I’m told is about 1.500$ compared to invasive angiography , seems to be the future . Thank you sir
Unfortunately, lots of seemingly healthy individuals with no symptoms die suddenly from coronary artery disease. Death is their first symptom. You don't get second chances unless you are fortunate enough to have bystanders do CPR, utilized an AED and get you to a Cath lab.
I've written a lot about the problem with plumbing paradigm of coronary disease (https://theskepticalcardiologist.com/2021/01/24/is-coronary-heart-disease-a-plumbing-problem-or-a-pimple-problem/) which is a disaster of unintended consequences.
Not sure what "detailed reductionist information is". The CCTA tells us exactly what amount of the disease of concern (CAD) we have. We need unbiased, enlightened MDs to help individuals do the best thing with that information, therein lies the problem.
dr. P
I appreciate the prompt insightful response. My point is that as we look harder we find more. Not uncommonly I care for elderly frail patients admitted with serious bleeding issues on dual antiplatelet therapy after percutaneous intervention due to extrapolated study findings. Yes of course we are worried about in stent thrombosis. I welcome efforts to inform the clinician in these situations. I also hope that new AI generated information can not only persuade but also dissuade the practitioner when nuanced judgement is required.
This information is exciting to be sure. Cautionary tales abound however. A few basic truths should be kept in mind. First, it’s hard to make a healthy person feel better and attempts to intervene on this population should be viewed with great caution. Second, coronary artery anatomy blockages when approached as a plumbing problem is a simplistic naive world view fraught with unintended consequences. More detailed reductionist information is not necessarily a good thing(if we have learned anything from our cancer screening misadventures).
I'm sorry for your music but happy for your readers.
Re: The CAC cannot be repeated to gain insights into how effective therapy has been.
Have you considered and rejected the conclusions of https://www.ahajournals.org/doi/10.1161/01.ATV.0000127024.40516.ef
This study concluded that patients at all initial CAC scores showed dramatically more heart attacks if they did not hold their CAC increase to 15% per year.
My initial CAC was 2300. Clearly it had been moving rapidly. After 2 years of keto my CAC increase was 12.5% per year. (Also pre-diabetic markers disappeared, raw cholesterol numbers degraded but cholesterol ratios improved dramatically .)
Should I rethink things?
Thanks for a remarkable online presence.
That study was small, retrospective, observational with poor lipid control and published in 2004. Needs confirmation from at least one larger study from a different center. Nothing that I am aware of since then supports that conclusion.
Also, I suspect there were very few subjects who had CAC >2K
I will remember your compliment on my "remarkable online presence" the next time I feel more like playing music than writing posts!
Dr. P
My Dad had the invasive scan (not because he was having a heart attack, although he was getting angina pains. I don’t know whether he also had a non-invasive CT scan. I don’t know whether the NHS has Cleerly AI software for further coronary artery analysis. It sounds like very useful equipment though, and it would be brilliant if it was accessible across the globe via internet!
Cleerly analysis can be done on any CCTA done anywhere.
Their website lists several sites in SoCal including mine (United Medical Doctors Encinitas)
SimonMed Imaging which is right next to my office has a VPN connection with Cleerly so that studies can be uploaded to the cloud for analysis.
Dr. P