In case you were keeping track, I’ve been getting a CIMT twice a year since starting in ’16. I just got my fourth one yesterday and was certainly curious to see what would come back.
Early on in my cholesterol education I came across an article by Rakesh C. Patel, Does LDL-P Matter?. He had this to say about the test:
My workhorse disease detection is Carotid Intima Media Thickness (CIMT). This test simply put, measures the “lining” of the carotid artery via ultrasound. The thicker the lining is, the greater the risk. It is also a way to assess for plaque (atherosclerosis) of the artery. Having plaque means you have atherosclerosis. I believe it is a significantly better way of looking at risk because we are looking for the actual pathology (1,2).
Given the last two times my thickness decreased on both sides, I figured I’d probably plateau or increase at least a little by this point.
Nope. Looks like the streak is continuing so far…
Have you done a baseline and any follow-up CT calcium scans?
In the program I contribute on, CIMT is considered useful and convenient, if only because you can get it run as often as you like, and cheaply, but the dispositive test is the CT calcium scan, or CAC (coronary arterial calcium), yielding an Agatston calcium score.
It is radiation, so doing it more often than annually is not encouraged. Malik, Zhao & Budoff just yesterday published another paper on the utility of it. Available without doctor’s order for $100 in many places.
And as with CIMT, it is possible to slow, arrest and reverse calcium scores, although you are unlikely to hear that from consensus practitioners, because they don’t know how to do it, think the opposite is true, and tend to prescribe diets and meds that just increase the score. Consequently, they are reluctant to order it.
Yes, I had a CAC in early March last year and another as part of the larger 640 slice CT I did in NY in May. Both came back 0.
As you might’ve guessed, I’m a big fan of Ivor Cummins, who has advanced a lot of knowledge on CAC. Generally, I think it’s one of the most important tests you can have.
re: I’m a big fan of Ivor Cummins, who has advanced a lot of knowledge on CAC. Generally, I think it’s one of the most important tests you can have.
And for some context, as I understand developments there, Ivor heard about CAC from David Bobbet, and David heard about it from Bill Davis, who was an early adopter of the (then) EBT scan.
I think density-volume information is likely to be a better indicator of risk than the simple Agatston. My test was read by Dr. Budoff but unfortunately he only gave me the Agatston number and I have been unable to get the full information. The density relates to plaque stability and apparently increase with the amount of exercise. Since I swim regularly and have a fairly high Agatston I would like to see the alternative calculation but it will have to wait until my next assessment.
Coronary Artery Calcium Volume and Density: Potential Interactions and Overall Predictive Value: The Multi-Ethnic Study of Atherosclerosis.
ncbi.nlm.nih.gov/m/pubmed/28797404/
Abstract
OBJECTIVES: This study sought to determine the possibility of interactions between coronary artery calcium (CAC) volume or CAC density with each other, and with age, sex, ethnicity, the new atherosclerotic cardiovascular disease (ASCVD) risk score, diabetes status, and renal function by estimated glomerular filtration rate, and, using differing CAC scores, to determine the improvement over the ASCVD risk score in risk prediction and reclassification.
BACKGROUND: In MESA (Multi-Ethnic Study of Atherosclerosis), CAC volume was positively and CAC density inversely associated with cardiovascular disease (CVD) events.
METHODS: A total of 3,398 MESA participants free of clinical CVD but with prevalent CAC at baseline were followed for incident CVD events.
RESULTS: During a median 11.0 years of follow-up, there were 390 CVD events, 264 of which were coronary heart disease (CHD). With each SD increase of ln CAC volume (1.62), risk of CHD increased 73% (p < 0.001) and risk of CVD increased 61% (p < 0.001). Conversely, each SD increase of CAC density (0.69) was associated with 28% lower risk of CHD (p < 0.001) and 25% lower risk of CVD (p < 0.001). CAC density was inversely associated with risk at all levels of CAC volume (i.e., no interaction was present). In multivariable Cox models, significant interactions were present for CAC volume with age and ASCVD risk score for both CHD and CVD, and CAC density with ASCVD risk score for CVD. Hazard ratios were generally stronger in the lower risk groups. Receiver-operating characteristic area under the curve and Net Reclassification Index analyses showed better prediction by CAC volume than by Agatston, and the addition of CAC density to CAC volume further significantly improved prediction.
CONCLUSIONS: The inverse association between CAC density and incident CHD and CVD events is robust across strata of other CVD risk factors. Added to the ASCVD risk score, CAC volume and density provided the strongest prediction for CHD and CVD events, and the highest correct reclassification.
Copyright © 2017 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.
Yes, I’ve likewise read in a few places where exercise can increase thickness, and perhaps this is transitory on a scale we don’t yet understand. (ie, perhaps after X days of sedentary behavior, CIMT drops by Y amount…)
That said, I do think there might be value in watching it’s *progression. Thus, for example, you’d probably find it interesting if the CIMT increased despite the degree and extent of exercise remaining relatively constant.
This is awesome, Dave, thanks for sharing. I had my CAC run via my docs order (zero calcium score btw) and I told the radiology dept tech I knew I needed a CIMT to look for soft plaque. That the CAC would only pick up hard plaque
Doc refused to order one, so I’ll be hitting up a CA licensed doc ( I can use my flexible spending card), or just find a place and pay out of pocket (easier) and getting a CIMT.
My latest Feldman attempt (3 days, high fat before my work insurance draw) didn’t give me lower numbers (or my hyper response was higher and it DID give me lower numbers- LOL). My work place changed parameters from LDL to HDL and my ratios are super great.
Thanks again for blazing the path and being a change agent in self testing. I look forward to data collection and hopefully a publication in the future. Onward and I’m cheering you every step.
Thank you for the kind words, Karen! 🙂
And yes, please share back your data when you get done. We even have a central post we’re using now: http://cholesterolcode.com/blood-pool/
Hi Dave,
Have you kept track of your fasting insulin/blood glucose/HOMA-IR since starting this?
Could be yet another example of its all about insulin…
regards,
Paul
Well, I started tracking fasting insulin regularly near the middle of last year. I didn’t do it before that point as it was cost prohibitive given the money spent on all the lipid tests, etc. But now I get it with every lipid test anyway since working out a better cost curve.
My fasting insulin is very low in general at that point and up to now. I suspect it was higher before starting keto, but as it never got tested, I can’t know for sure.
But to your point, I *definitely* believe that insulin is a major factor in intima-media thickness. Check out this study: intima-media thickness
Missing link above?
What do intervention are you doing that you think is connected to the lowered numbers?
Nice catch! — I fixed the link…
Have you done a CT angiogram? My cardiologist said that unlike CAC, this test uses a dye and can detect soft plaques.
In young people, non-calcified plaque may be more prevalent:
Madaj, Paul M., Matthew J. Budoff, Dong Li, John A. Tayek, Ronald P. Karlsberg, and Harold L. Karpman. “Identification of Noncalcified Plaque in Young Persons with Diabetes.” Academic Radiology 19, no. 7 (July 2012): 889–93. https://doi.org/10.1016/j.acra.2012.03.013.
My calcium score was 0. Yet, I had a 99% blockage in my LAD. My symptoms (chest pain during exercise) appeared first last month, 5 months after being on LCHF.
I haven’t done an angiogram, but I did get a 640 slice CT scan at Northshore University Hospital in NY (see Ketofest presentation). What’s great is that you get a high resolution virtual scan of the heart and its cardiovascular system to the point where they can make a 3D model from it. Certainly I’m concerned about both calcified and non-calcified plaque, which is very reason I went to get the test.
Wow! Good thing you caught that 99% blockage! I’d be curious how long it was developing.
Sorry, I noticed your response very late.
Did you need to get a doctor prescription to get that 640 slice CT scan done?
Also, did the test identify any lesions?
I have some 30-40% lesions that were (thankfully) not intervened upon. I need to keep track of their regression (hopefully).
Because of the radiation risk of CTA, I am wondering whether I should get frequent IVUS (intravascular ultrasound) tests. Because I am not currently taking statins, I feel it is necessary to keep track of the lesions. I hope the lesions regress without statins. If they don’t I will take statins.
I am also very curious how long my LAD lesion was developing. Unfortunately, I never did any coronary imaging tests before. I have never done a CIMT either. And no doctor has been able to give me any information about how my lesion progressed beyond “plaques take decades to develop”.
One doctor told me that it is possible that the LAD lesion was small until September 2017 and ruptured after that during the stressful weeks. After the rupture, it may have quickly become much bigger.
All I have is a history of lipid profiles and other bloodwork:
https://docs.google.com/spreadsheets/d/1IpPeuPXV-deXjexaR3uXwGjhBxaY2EuBlrTeR7dGbzE/edit?usp=sharing
My HDL has always been low. The tests in September 2017 came back very unusual perhaps because I was under extreme emotional stress for 4-5 days before the test. Because I was eating low carb, I was expecting my HBA1C to drop. But it increased, I think because of effects of high stress-induced cortisol. I was also expecting my HDL to go up, but it dropped, perhaps due to stress?
– Yes, I had to get my doctor to sign off on the order, but he was fine with it provided I paid for it myself.
– I’m getting my CIMTs every 6 months and paying out of pocket $75/test. For me, it’s well worth it. I’d imagine I’d be doing the same in your shoes as I too would want to have at least a proxy to keep an eye on.
– Your concern about the CT radiation is certainly well taken. I was reluctant myself for that very reason. But I do have an additional motivation many others don’t in that I feel my body of data (no pun intended) would be far more valuable with that baseline. But I’ll concede afterward I felt a lot better just having the information anyway.
– HDL being low would concern me. I tend to find it is a good “status indicator” of what’s going on in the body. I often use the analogy of neighborhood cops on patrol — when you see a lot of them being bored, that’s a good sign — when a lot of them are missing, that’s a bad sign (probably in other places dealing with emergencies — see Reverse Cholesterol Transport). That said, some have genetically lower HDL, which doesn’t seem to apply as much.
Actually, I take back my concern about radiation.
While reading the following paper, I found that various techniques (e.g. precise timing using EKG) can be used to dramatically cut down the radiation of CTA.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3259311/
It seems some facilities have implemented those radiation-cutting techniques.
I just called UCLA radiology and they said that they can do CTA with radiation exposure between 3-4msv as long as the heart rate is between 60-80bpm.
They also have an ultra-low mode 1-2msv, which is less sensitive.
Also, Mass General seems to have a low radiation CTA:
http://www.massgeneral.org/imaging/news/newsarticle.aspx?id=2594
Where did you get your CIMT done? Your CIMT measurements are much more precise. I only got a precision of 0.1mm: 0.6mm in the left and 0.4mm in the right.
Useful information, Abhishek!
I get my measurements through my doctor’s office. I don’t put too much stock in the CIMT right now, we’ll see how it goes long term as I don’t know the standard error deviation. Mainly, I just wanted to be sure it wasn’t skyrocketing up.
Regarding the standard error around a CIMT estimate. I am involved in making ultrasound systems and software that perform CIMT. Your results look very repeatable compared to literature. You must be using the same sonographer, system, measuring at the exact same location, and likely at the same part of the heart cycle (eg end-diastole). Change system, location, or part of cycle and you will have more error. I use this as my reference. https://www.ahajournals.org/doi/full/10.1161/JAHA.114.001492
BTW: Good work. Been trying to reduce my CIMT through LC diet and supplementation as mine is >.9mm (high risk). No luck over 2 years, but no growth either. Will be changing supp strategy.
Sorry, but I just began exploration of the outcomes of Keto diets. I am in the dark about these aspects. Any chance one of you might give a summary to a newcomer? Thanks.
Hi – is there anything in particular you were wondering about? 🙂
Another data point: my wife has been doing keto for 8 months and her low dose CCTA (at UCLA radiology) showed no stenosis.
Nice! Thanks for the data addition!
Interesting to see how the right has a greater improvement to almost align with the left. Will be interesting to see what the next test reveals…
I’m interested as well.
I certainly don’t expect this will go on indefinitely (ala Benjamin Button), but I’d likewise be curious if they remain roughly synchronized.
Have you come across any study evaluating how well CIMT can predict the presence/severity of lesions observed using CT Angiogram?
Possibly. I haven’t put a lot of work into researching into this area, I just track it as another potential metric.
Hi Dave,
Been LCHF for a couple years now and I finally talked my Doc into a good lipid panel (NMR) but nobody told (except for you later) how useless NMR data would be having water fasted 4 days before the test and having burned 20 lbs of fat in previous 6 weeks. Results were dreadful. Trig up to 126 from 60, hdl down to 51 from 60 and ldl-p at >2500. I freaked until I rediscovered you online and you’ve saved my sanity. Went carnivore for 10 days and retested w/ standard lipid panel and trig now 75 and hdl up to 69 giving a ratio or 1.08. Total C was 320 and ldl 258. Needing more ammo against the Pfizer marketing, I requested a CIMT but medicare won’t help and out of pocket would be $800 so I settled or a carotid duplex ultrasound (today). No official results yet but tech said I looked pretty normal for my age (70). CAC will be available for $100 in Feb. and will get that then. You think the CIMT is far superior to CAC?
Well just wanted to say thank you for all you do. Really saved my sanity and have great stores of ammo for going to doc next Monday.
Best Regards,
Jim Lynn
Hi Jim! Yes, I suppose it doesn’t come up much likely because most of the population doesn’t multi-day fast. A bit of a niche subject!
Glad you figured out what it was, and re-tested to verify the results. 🙂
Regarding the CIMT – it (and the carotid doppler too), have a few benefits like being able to test at a higher frequency than CAC (due to it just being an ultrasound), but CAC measures extensive disease and if I remember right predicts mortality outcomes better. So they both have their strengths.
For myself, I prefer to get frequent CIMTs and carotid dopplers, and then a less frequent CAC if possible to cover my bases. Dave does the same.